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General Psychiatry logoLink to General Psychiatry
. 2025 Aug 7;38(4):e102020. doi: 10.1136/gpsych-2024-102020

The China Alzheimer Report 2025

Nan Zhi 1,0,0, Rujing Ren 2,0,0, Jinlei Qi 3,0,0, Xinya Liu 4,0,0, Zike Yun 1, Shaohui Lin 5, Yisong Hu 6, Haixia Li 2, Xinyi Xie 1, Jintao Wang 2, Jianping Li 2, Yikang Zhu 5, Mengyi Gao 5, Junjie Yang 5, Yiran Wang 5, Yurong Jing 4, Jieli Geng 1, Wenwei Cao 1, Qun Xu 1, Xiaoping Yu 2, Yuan Zhu 2, Ying Zhou 7, Lin Wang 7, Chao Gao 2, Binyin Li 2, Shengdi Chen 2, Fang Yuan 8, Ronghua Dou 9, Xiaoyun Liu 10, Xuena Li 11, Yafu Yin 12, Yan Chang 13, Gang Xu 14, Yanting Zhong 3, Chunbo Li 5,*, Ying Wang 4,*, Maigeng Zhou 3,*, Gang Wang 1,
PMCID: PMC12336476  PMID: 40792123

Abstract

With the sustained growth of the economy and significant changes in social demographics, the issue of elderly-related diseases has increasingly drawn attention, particularly. Alzheimer’s disease (AD), as a representative disease of neurodegenerative diseases, has become a major challenge, affecting the health and quality of life of the elderly population severely. In recent years, the incidence, prevalence and mortality rates of AD have increased in China, imposing substantial economic burdens on families, society and the entire healthcare system. To proactively address this challenge and respond to the national ‘Healthy China Action’ initiative, leading experts from authoritative institutions jointly authored the China Alzheimer Report 2025. Building on previous editions, this report updates epidemiological data on AD in China, thoroughly analyses the latest economic burdens of the disease and comprehensively evaluates the current status of AD diagnosis and treatment services, as well as the allocation of public health resources in our country. Its release reflects China’s progress in AD research and prevention, underscores societal concern for elderly health and aims to provide scientific guidance and data support for AD prevention, diagnosis and treatment. It also facilitates academic exchanges and cooperation, enhancing public awareness and promoting active participation in elderly healthcare, towards achieving ‘healthy ageing’ in China.

Keywords: Cognition Disorders

Introduction

According to data released by the Ministry of Civil Affairs at the end of 2022, China’s population aged 60 and above reached 280.04 million, accounting for 19.8% of the total population, and those aged 65 and above numbered 209.78 million, representing 14.9%. This marked a severe ageing phase. Diseases related to this ageing trend have seen significant rises in incidence, prevalence and mortality, posing heavy societal pressures.1 Notably, Alzheimer’s disease (AD) cases are increasing, with a growing socioeconomic burden, becoming a major disease and societal issue threatening Chinese urban and rural residents.2,4 In 2019, China reported 13.14 million cases of Alzheimer’s disease and related dementias (ADRD), accounting for 25.5% of the global total, with a prevalence rate of 788.3/100 000. ADRD-related deaths totalled 320 715 (19.8% of the global total), and China contributed 23.6% to the global ADRD disease burden, equivalent to 25.28 million person-years.3 Building on previous reports,2 3 5 6 this report expands its scope to provide a comprehensive analysis of epidemiological data, diagnostics, biomarkers, therapeutic advancements, public health support, international cooperation and digital technology applications in AD. It presents the latest incidence, mortality and prevalence trends spanning from 1990 to 2021, detailing updates that showcase China’s recent achievements and future directions in the research and management of AD.

Data source and analysis

This study leverages data from the Global Burden of Disease (GBD) study and China’s provincial disease burden study (not including Taiwan). It employs multiple reliable sources and a standardised methodology to analyse the disease burden across multiple countries from 1990 to 2024.7 Mortality data are sourced from the Chinese Disease Surveillance Point System and the Centers for Disease Control and Prevention (CDC)’s death registration system, while morbidity data stem from historical monitoring, surveys and published literature.8 Key sources include chronic disease surveillance, national health surveys and service evaluations. Detailed data sources are available at the GBD Global Health Data Exchange Index (http://ghdx.healthdata.org). Diseases are classified using the International Classification of Diseases and Related Health Problems, 10th revision (ICD-10), with ADRD coded as F00–F03.91 and G30–G31.9. Prior research indicates AD comprises 63%–70% of dementia cases.9 The processes for assessing the burden of disease, which encompass cause-specific death estimation, disease prevalence estimation, years lived with disability (YLD) estimation, years of life lost due to premature mortality (YLL) estimation and disability-adjusted life years (DALYs) calculation, align with the methodologies described in the 2022 Alzheimer’s Disease report3 and pertinent GBD literature.10

To characterise the 2021 distribution of ADRD in China and provinces, this study employed DALY, YLL and YLD to assess disease burden, comparing urban–rural death causes and DALY rankings, and contrasting China’s findings with global data. Age-specific rates for mortality, prevalence, YLL, YLD and DALY were used to analyse age-related ADRD burden, categorising patients into nine age groups: 40–44, 45–49, 50–54, 55–59, 60–64, 65–69, 70–74, 75–79 and ≥80 years of age. Standardisation was based on the GBD 2019 world standard population. Provincial ADRD burden distributions in 2021 are presented in subsequent tables.

To update the progress on AD treatments since the ‘China Alzheimer Report 2021’, the authors conducted a search for studies related to AD treatments conducted in China from August 2021 to December 2024, using the Participant, Intervention, Comparison, Outcome, and Study Design (PICOS) framework. The inclusion criteria included: (1) Western and traditional Chinese medicines and non-drug interventions (marketed drugs, clinical trial drugs (domestic and international)); (2) Single-centre or multicentre trials registered on domestic (www.chictr.org.cn) or international (https://clinicaltrials.gov/) platforms; (3) patients with AD, including Chinese; (4) Published or registered between 1 August 2021 and 31 December 2024. The exclusion criterion was trials without a control group for intervention. The search process and results are shown in figure 1. The search yielded 107 trials with updated progress: 16 on Aβ (β-amyloid) protein, 26 on neuromodulation, 24 on traditional Chinese medicine, 5 on cell therapy, 8 on surgical treatment and 28 on other targets (figure 2).

Figure 1. Flowchart of the report search process. CNKI, China National Knowledge Infrastructure.

Figure 1

Figure 2. Newly registered therapy trials for Alzheimer’s disease. (1) Secondary indication: Left to right: Flos gossypii flavonoids tablet, anti-depression drug, rosiglitazone, canagliflozin, canagliflozin, lacosamide and levetiracetam, cholestyramine, piperazine ferulate tablets; (2) AD pathology: Left to right: CNP520, GV-971, lecanemab, gantenerumab, 50561, SHR1707, donanemab, SHR1707, GV-971, GV-971, citicoline, donepezil+GV-971, protein polymer alitol (ALEETO), remternetug, CM383, donepezil dihydroxynaphthalate; (3) Neuromodulation: Left to right: Theta burst TMS, rTMS, light therapy, light therapy, tACS, tACS+40 Hz sound, 4 Hz tACS, VNS, TMS, HD-tDCS, tDCS+cognitive training, rTMS, tES, TUS, photobiomodulation, photobiomodulation, 10 Hz rTMS, taVNS, taVNS, TMS, TMS, TMS, TMS, TMS, TMS, tACS; (4) Traditional Chinese medicine: Left to right: Kangshuailao Pian, acupuncture, Smart soup, EAS, Astragalus, Astragalus, yangxieqingnao Pian, Weilibai Capsule, acupuncture, Shenggonghuanglianjiedu Fang, Huanshao Dan+acupuncture, Tai chi+Huanshao Dan, EAS, acupuncture+cognitive training, Polygonum cuspidatum Yizhi granules, Bushen Huazhuo formula, Regulating Heart and Kidney, electroacupuncture+TMS, nourishing blood oral liquid, Shenghui Yizhi Tang, Wujia Yizhi granules, Electroacupuncture, Astragalus Membranaceus Root, acupuncture; (5) Cell therapy: Left to right: Allogenic adipose MSC Exos, mast cell activation, recombinant human serum albumin, regulatory T cells injection, stem cell-derived small extracellular vesicles; (6) Other: Left to right: ant-osteoporosis, cognitive training+aerobic exercise, faecal microbial transplant, probiotics, lifestyle, dental health management, periodontal therapy, cognitive training, nutrition+exercise+cognitive training, Yeast β-glucan, cognitive training, music therapy, tRNS, faecal microbial transplant, Probio-M8, remote ischaemic conditioning, music therapy, olfactory training, ketogenic diet, experimental sleep deprivation; (7) Surgery: Left to right: deep cervical lymphatic vessel vein anastomosis and lymphatic trunk decompression, deep cervical lymphaticovenous anastomosis, cervical lymphatic vein bypass surgery, cervical deep lymphatic vein anastomosis, deep cervical lymphaticovenous anastomosis, deep cervical lymphaticovenous anastomosis surgery, deep cervical lymphovenous bypass, lymphaticovenous anastomosis. AD, Alzheimer’s disease; EAS, electrical acupoint stimulation; Exos, exosomes; HD, high definition; MSC, mesenchymal stem cell; rTMS, repetitive TMS; tACS, transcranial alternating current stimulation; taVNS, transcutaneous auricular VNS; tDCS, transcranial direct current stimulation; tES, transcranial electrical stimulation; TMS, transcranial magnetic stimulation; tRNS, transcranial random noise stimulation; TUS, transcranial ultrasound stimulation; VNS, vagus nerve stimulation.

Figure 2

Epidemiology and disease burden of ADRD in China

Prevalence of ADRD in China in 2021

Prevalence of ADRD by gender

As shown in table 1, in 2021, the number of individuals with ADRD in China reached 16 990 827 (14 488 494 to 19 672 741), of which the male prevalence was 846.3/100 000 (706.3/100 000 to 980.9/100 000) and the female prevalence was 1558.9/100 000 (1341.1/100 000 to 1801.8/100 000). The prevalence of female patients with ADRD was about 1.8 times that of male patients with ADRD. After age standardisation, the standardised prevalence rate for women (1025.1/100 000) remained significantly higher than that for men (731.2/100 000).

Table 1. Prevalence of Alzheimer’s disease and related dementias in China in 2021.
Gender Prevalence (cases) Prevalence (/100 000) Standardised prevalence (/100 000)
Male 6 162 198 (5 142 286 to 7 141 800) 846.3 (706.3 to 980.9) 731.2 (618.5 to 851.6)
Female 10 828 629 (9 315 735 to 12 515 957) 1558.9 (1341.1 to 1801.8) 1025.1 (879.0 to 1186.8)
Total 16 990 827 (14 488 494 to 19 672 741) 1194.2 (1018.3 to 1382.7) 900.8 (770.9 to 1043.2)
Prevalence of ADRD by age groups

In 2021, the number and prevalence of ADRD among both men and women showed a trend of continuous increase with age in the population aged 40 and above, reaching the highest in the age group of 80 and above. In the age group of 80 and older, the number of male patients reached 2 161 446, with a prevalence rate of 16 517.7/100 000; the number of female patients reached 5 055 154, with a prevalence rate of 25 527.2/100 000. In all age groups, the number of female patients and the prevalence rate were higher than those of males.

Prevalence of ADRD by provinces and municipalities

In 2021, the provinces and municipalities in China with higher prevalence rates of ADRD were mainly concentrated in East China, the Southwest and some parts of the Northeast regions, including Shanghai (1528.5/100 000), Sichuan (1477.6/100 000), Liaoning (1460.3/100 000), Jiangsu (1453.8/100 000) and Chongqing (1445.5/100 000). After age standardisation, the top five provinces and municipalities in terms of standardised prevalence rates were Henan (975.6/100 000), Hebei (965.8/100 000), Jilin (964.5/100 000), Yunnan (943.3/100 000) and Fujian (933.7/100 000) (see online supplemental table 1).

China’s trends in prevalence of ADRD from 1990 to 2021

From 1990 to 2021, the total prevalence rate of ADRD in China increased by 249.1%, from 342.1/100 000 to 1194.2/100 000. After age standardisation, the overall standardised prevalence rate showed a fluctuating yet slow upward trend. Specifically, the standardised prevalence rate for females increased by 30.6%, from 785.2/100 000 to 1025.1/100 000; for males, it increased by 27.3%, from 574.5/100 000 to 731.2/100 000. The prevalence and standardised prevalence rates for ADRD among females were consistently higher than those among males.

Incidence of ADRD in China in 2021

Incidence of ADRD by gender

As shown in table 2, in 2021, the estimated number of new cases of ADRD in China was approximately 2 914 112, with a range of estimates between 2 504 728 and 3 350 743. The incidence rate for males was 148.0/100 000 (124.8/100 000 to 171.4/100 000); for females, the incidence rate was 264.4/100 000 (229.4/100 000 to 302.5/100 000). The incidence rate for females was approximately 1.8 times that of males. After age standardisation, the standardised incidence rate for females (171.8/100 000) remained higher than for males (126.5/100 000).

Table 2. Incidence of Alzheimer’s disease and related dementias in China in 2021.
Gender Incidence (cases) Incidence (/100 000) Standardised incidence (/100 000)
Male 1 077 297 (908 448 to 1 248 194) 148.0 (124.8 to 171.4) 126.5 (107.8 to 145.6)
Female 1 836 815 (1 593 651 to 2 101 343) 264.4 (229.4 to 302.5) 171.8 (150.1 to 195.9)
Total 2 914 112 (2 504 728 to 3 350 743) 204.8 (176.0 to 235.5) 151.5 (131.2 to 173.2)

Incidence of ADRD by age groups

In 2021, both the number of cases and the incidence rate of ADRD among males and females aged 40 and above in the population showed a continuous upward trend with increasing age. Specifically, the incidence rate rose rapidly in the 70–74 age group and peaked in the age group of 80 and above. In the age group of 80 and above, the number of male cases reached 376 535 with an incidence rate of 2877.5/100 000. Moreover, the number of female cases was 758 068 with an incidence rate of 3828.0/100 000. Across all age groups, the number of cases and the incidence rate among females were higher than among males.

Incidence of ADRD by provinces and municipalities

In 2021, the provinces and municipalities in China with higher incidence rates of ADRD were mainly concentrated in East China, the Southwest and some Northeast regions, including Sichuan (255.1/100 000), Shanghai (252.3/100 000), Liaoning (250.8/100 000), Chongqing (250.6/100 000) and Jiangsu (245.8/100 000). After age standardisation, the top five provinces and municipalities in terms of standardised incidence rates were Yunnan (158.8/100 000), Jilin (158.4/1 00 000), Henan (158.0/100 000), Qinghai (157.9/100 000) and Hebei (157.1/100 000). In contrast, some regions in North China and East China had relatively lower standardised incidence rates (see online supplemental table 1).

China’s trends in incidence of ADRD from 1990 to 2021

From 1990 to 2021, the crude incidence rate of ADRD in China increased by 242.5%, from 59.8/100 000 to 204.8/100 000. After age standardisation, the standardised incidence rate generally exhibited a fluctuating and slow upward trend. The standardised incidence rate for females increased by 26.9%, from 135.4/100 000 to 171.8/100 000, while for males, it increased by 26.2%, from 100.2/100 000 to 126.5/100 000. The incidence rate and standardised incidence rate of ADRD among females were consistently higher than those among males.

Deaths due to ADRD in China in 2021

Deaths due to ADRD by gender

As shown in table 3, in 2021, the number of female deaths caused by ADRD in China significantly surpassed that of males. The 2021 female death rate was 47.4/100 000 (11.9/100 000 to 126.2/100 000), and the male death rate was 22.5/100 000 (5.3/100 000 to 64.0/100 000), with the female rate being more than twice that of males. After age standardisation, the standardised mortality rate for females remained higher than that for males (33.9/100 000 compared with 25.9/100 000).

Table 3. Deaths due to Alzheimer’s disease and related dementias in China in 2021.
Gender Deaths (cases) Death rate (/100 000) Standardised death rate (/100 000)
Male 163 535 (38 523 to 465 891) 22.5 (5.3 to 64.0) 25.9 (6.2 to 72.1)
Female 329 239 (82 440 to 876 441) 47.4 (11.9 to 126.2) 33.9 (8.5 to 89.6)
Total 492 774 (125 051 to 1 371 493) 34.6 (8.8 to 96.4) 30.9 (7.8 to 84.3)

Deaths due to ADRD by age groups

Age group analysis of ADRD deaths and rates among the population over 40 years old in 2021 showed a rise with advancing age and reached the highest point in the 80 years and over age group. Deaths for men in the over 80 years age group totalled 102 135, and the death rate was 780.5/100 000; deaths for women in this age group totalled 243 253, and the death rate was 1 228.4/100 000. In all age groups, the death rate due to ADRD was higher for women than for men.

Deaths due to ADRD by provinces and municipalities

In 2021, provinces and municipalities with higher crude ADRD death rates included mainly Shanghai (43.8/100 000), Jiangsu (43.4/100 000), Sichuan (41.4/100 000) and Chongqing(41.0/100 000). After age standardisation, the top five provinces and cities in terms of the ADRD death rate were: (1) Hebei province (38.1/100 000), Henan province (35.4/100 000), Jilin province 34.9/100 000), Guangdong province (33.4/100 000) and Zhejiang province (33.3/100 000). Additionally, some western and eastern regions of China had relatively lower standardised death rates (see online supplemental table 1).

China’s trends in deaths due to ADRD from 1990 to 2021

From 1990 to 2021, the overall crude death rate for ADRD in China increased by 239.2%, from 10.2/100 000 to 34.6/100 000. After age standardisation, the standardised death rate for ADRD in China remained generally stable, with minimal fluctuations ranging from 29.5/100 000 to 31.5/100 000. By gender, the crude and standardised death rates for ADRD in females were consistently higher than those in males.

Years of life lost due to ADRD in China in 2021

YLL due to ADRD by gender

As shown in online supplemental table 2, in 2021, YLL due to ADRD in China reached 6 623 417 (1 651 040 to 18 668 886), with the YLL of females significantly higher than that of males. The YLL rate for males was 328.2/100 000 (76.2/100 000 to 942.2/100 000) and for females was 609.5/100 000 (154.6/100 000 to 1643.4/100 000), which was about 1.9 times the rate of males. After age standardisation, the standardised YLL rate for females (415.9/100 000) remained higher than that for males (320.3/100 000).

YLL due to ADRD by age groups

In 2021, both men and women exhibited a trend of increasing YLL and YLL rates with age among the population aged 40 and above, peaking in the age group of 80 and above. Among individuals aged 80 and above, the YLL for men reached 1 087 308, with a YLL rate of 8309.1/100 000; for women, the YLL reached 2 474 608, with a YLL rate of 12 496.1/100 000. Across all age groups, the YLL and YLL rate for women were higher than those for men.

YLL due to ADRD by provinces and municipalities

In 2021, the provinces and municipalities in China with higher YLL rates for ADRD were mainly concentrated in East China, the Southwest and some parts of the Northeast regions, including Jiangsu (565.8/100 000), Sichuan (554.3/100 000), Chongqing (552.1/100 000), Jilin (544.9/100 000) and Shanghai (544.6/100 000). After age standardisation, the top five provinces and municipalities in terms of standardised YLL rates were Hebei (461.6/100 000), Henan (432.6/100 000), Jilin (426.3/100 000), Zhejiang (407.2/100 000) and Guangdong (406.9/100 000), mainly concentrated in the central and eastern regions (see online supplemental table 1).

China’s trends in YLL due to ADRD from 1990 to 2021

From 1990 to 2021, the crude YLL rate due to ADRD in China increased by 188.4%, from 161.4/100 000 to 465.5/100 000. During this period, the crude YLL rate for males increased by 189.9%, from 113.2/100 000 to 328.2/100 000; for females, it increased by 186.6%, from 212.7/100 000 to 609.5/100 000. After age standardisation, the overall standardised YLL rate displayed a stable trend, with the total standardised YLL rate fluctuating within a range of 362.5/100 000 to 389.7/100 000. The crude YLL rate and standardised YLL rate for ADRD among females were consistently higher than those among males.

Years lived with disability due to ADRD in China in 2021

YLD due to ADRD by gender

As shown in online supplemental table 3, in 2021, YLD due to ADRD in China reached 3 460 316 (2 394 430 to 4 631 824), and the YLD for females was significantly higher than that for males. The YLD rate for males was 162.7/100 000 (112.3/100 000 to 218.6/100 000), and for females, it was 327.6/100 000 (224.0/100 000 to 439.0/100 000), which is about twice that of males. After age standardisation, the standardised YLD rate for females (216.4/100 000) remained higher than that of males (143.7/100 000).

YLD due to ADRD by age groups

In 2021, both men and women in the population aged 40 and above exhibited a trend of increasing YLD and YLD rates with age, with a particularly rapid increase in the 70–74 age group, peaking in the age group of 80 and above. For the age group of 80 and above, the YLD for men reached 437 732, with a YLD rate of 3345.1/100 000; for women, the YLD reached 1 098 632, with a YLD rate of 5 547.8/100 000. In all age groups, the number of YLDs and the YLD rates for women were higher than those for men.

YLD due to ADRD by provinces and municipalities

In 2021, the provinces and municipalities in China with higher YLD rates for ADRD were mainly concentrated in East China, the Southwest and some parts of the Northeast regions, including Shanghai (314.3/100 000), Sichuan (299.9/100 000), Liaoning (297.5/100 000), Jiangsu (296.0/100 000) and Chongqing (292.6/100 000). After age standardisation, the top five provinces and municipalities in terms of standardised YLD rates were Henan (202.0/100 000), Hebei (199.3/100 000), Jilin (199.2/100 000), Yunnan (193.5/100 000), and Guangdong (192.0/100 000) (see online supplemental table 1).

China’s trends in YLD due to ADRD from 1990 to 2021

From 1990 to 2021, the crude YLD rate due to ADRD in China increased by 254.0%, from 68.7/100 000 to 243.2/100 000. After age standardisation, the overall standardised YLD rate exhibited a fluctuating but slow upward trend. Among these, the standardised YLD rate for females increased by 29.9%, from 166.6/100 000 to 216.4/100 000; for males, it increased by 26.9%, from 113.2/100 000 to 143.7/100 000. Both the crude and standardised YLD rates for ADRD among females were consistently higher than those among males.

Disability-adjusted life years due to ADRD in China in 2021

DALYs due to ADRD by gender

As shown in table 4, in 2021, DALY due to ADRD in China reached 10 083 733 (10 071 548 to 22 194 978), of which 34.3% was disability-related burden, and 65.7% was premature death-related burden. The DALY rate for females was approximately 1.9 times that of male patients. The DALY rate for males was 490.2/100 000 (233.6/100 000 to 1097.4/100 000); for females, it was 936.0/100 000 (455.5/100 000 to 1950.3/100 000). After age standardisation, the standardised DALY rate for females (631.6/100 000) remained higher than that for males (463.4/100 000).

Table 4. DALYs due to Alzheimer’s disease and related dementias in China in 2021.
Gender DALY (person-years) DALY rate (/100 000) Standardised DALY rate (/100 000)
Male 3 574 164 (1 700 783 to 7 990 410) 490.2 (233.6 to 1097.4) 463.4 (214.4 to 1045.4)
Female 6 509 569 (3 163 773 to 13 547 879) 936.0 (455.5 to 1950.3) 631.6 (305.0 to 1308.1)
Total 10 083 733 (10 071 548 to 22 194 978) 707.9 (347.7 to 1560.0) 562.4 (270.4 to 1227.8)

DALY, disability-adjusted life year.

DALYs due to ADRD by age groups

In 2021, both male and female DALY numbers and rates for ADRD in China showed a trend of continuous increase with age, with a rapid rise in the 70–74 age group and peaking in the 80 and above age group. In the age group of 80 and above, the DALY count for males reached 1 523 335, with a DALY rate of 11 636.3/100 000; for females, the DALY count reached 3 566 627, with a DALY rate of 18 020.1/100 000. In all age groups, the DALY count and rate for females were higher than those for males.

DALYs due to ADRD by provinces and municipalities

In 2021, the provinces and municipalities in China with higher DALY rates for ADRD were primarily concentrated in East China, the Southwest and some parts of the Northeast regions, including Jiangsu (860.7/100 000), Shanghai (857.9/100 000), Sichuan (853.3/100 000), Chongqing (843.6/100 000) and Liaoning (840.1/100 000). After age standardisation, the provinces and municipalities with higher standardised DALY rates were mainly concentrated in the central and eastern regions, with the top five being Hebei (660.0/100 000), Henan (633.7/100 000), Jilin (624.6/100 000), Guangdong (598.1/100 000) and Zhejiang (587.1/100 000), while some areas in East China and the West had relatively lower standardised DALY rates (see online supplemental table 1).

China’s trends in DALYs due to ADRD from 1990 to 2021

From 1990 to 2021, the crude DALY rate for ADRD in China increased by 208.2%, from 229.7/100 000 to 707.9/100 000. During this period, the crude DALY rate for males increased by 206.0%, from 160.2/100 000 to 490.2/100 000; for females, it increased by 208.0%, from 303.9/100 000 to 936.1/100 000. After age standardisation, the overall standardised DALY rate showed a stable trend, with the total standardised DALY rate fluctuating within a narrow range of 530.7/100 000 to 562.4/100 000. The crude and standardised DALY rates for ADRD among females were consistently higher than those among males.

ADRD comparison between the world and China

China bears a disproportionate share of the global ADRD burden, contributing nearly 30% of global cases, deaths and DALYs in 2021, with consistently higher age-standardised prevalence, incidence and mortality rates compared with worldwide averages. Detailed comparative data are presented in table 5.

Table 5. Comparison of Alzheimer’s disease and related dementias burden between the world and China in 2021.

Indicator Global China China’s share of global total
Prevalence
 Cases 57 010 854
(49 508 597 to 65 155 679)
16 990 827
(14 488 494 to 19 672 741)
29.8%
 Age-standardised rate (/100 000) 696.0
(604.4 to 796.7)
900.8
(770.9 to 10 430.2)
Incidence
 Cases 9 837 055
(8 620 519 to 11 163 699)
2 914 112
(2 504 728 to 3 350 743)
29.6%
 Age-standardised rate (/100 000) 119.7
(104.9 to 135.8)
151.5
(131.2 to 173.2)
Deaths
 Cases 1 955 864
(498 907 to 5 118 038)
492 744
(125 051 to 1 371 493)
25.2%
 Age-standardised rate (/100 000) 25.2
(6.4 to 65.6)
30.9
(7.8 to 84.3)
YLL
 Person-years 24 750 579
(6 224 336 to 63 537 378)
6 623 417
(1 651 040 to 18 668 886)
26.8%
 Age-standardised rate (/100 000) 309.0
(78.8 to 786.1)
377.5
(96.7 to 1056.5)
YLD
 Person-years 11 582 108
(7 961 941 to 15 296 793)
3 460 316
(2 394 430 to 4 631 824)
29.9%
 Age-standardised rate (/100 000) 141.9
(97.7 to 187.2)
185.6
(128.0 to 246.8)
DALY
 Person-years 36 357 131
(17 253 011 to 77 446 245)
10 083 733
(10 071 548 to 22 194 978)
27.7%
 Age-standardised rate (/100 000) 451.3
(213.2 to 957.5)
562.4
(270.4 to 1227.8)

All values are presented as numbers (95% uncertainty interval) unless specified.

DALY, disability-adjusted life years; YLD, years lived with disability; YLL, years of life lost.

Diagnostic approaches for ADRD in China

Neuroimaging examination

Routine imaging technologies

Both magnetic resonance imaging (MRI) and computed tomography (CT) are essential tools in diagnosing AD, assessing brain atrophy and pinpointing the causes of cognitive disorders, with MRI being favoured for its superior clarity in imaging brain tissue. For AD suspects, adding an oblique coronal T1-weighted imaging for medial temporal lobe atrophy (MTA) scoring is recommended.11 Hippocampal MTA is an early AD marker. For those unable to undergo MRI, multislice CT thin-section scanning is an alternative.12 Resting-state and task-based functional MRI (fMRI) can reveal brain network differences among dementia types, aiding early AD screening and diagnosis. Studies using brain network metrics in machine learning models achieve high accuracy in distinguishing AD from controls, but they vary in mild cognitive impairment (MCI) classification.13 Currently, fMRI is mainly used in AD research, rather than for clinical diagnosis. A new gradient echo imaging technique by Wayne State University’s Haacke minimises scan time while maintaining high signal-to-noise ratios in neurodegenerative diseases like AD and Parkinson’s disease.14

Molecular imaging technology

In 2018, the National Institute on Ageing and the Alzheimer’s Association introduced the Amyloid-β/ Tau/Neurodegeneration (A/T/N) framework for AD research.15 At the 2023 Alzheimer’s Association Conference, the Amyloid-β/Tau/Neurodegeneration /Vasular brain injury/Inflammation/α-Synuclein (ATNVIS) framework was unveiled as an update.16 Both frameworks emphasise the role of positron emission tomography (PET) technology in diagnosing AD, from preclinical stages to dementia. PET imaging with Aβ-PET, Tau-PET and fluorodeoxyglucose positron emission tomography provides insights into ATN changes, aiding in early diagnosis and prognosis (see online supplemental table 4). However, in China, PET’s clinical application is limited due to high costs, lack of insurance coverage, scarcity of molecular probes and limited imaging devices.17 A health economic evaluation is urgently needed to assess its widespread clinical feasibility.

Neuropsychological assessments

Neuropsychological assessment, crucial for diagnosing cognitive disorders, evaluating treatment outcomes and predicting prognosis, is typically conducted by qualified professionals under the guidance of doctors. It encompasses cognitive and non-cognitive evaluations. Recently, with the advancement and popularisation of digital technology, some computer-assisted neuropsychological assessment methods have emerged, filling some gaps in traditional assessment methods.

Electronic screening tools

Computerised cognitive testing can be categorised into three types: transplanted, research-oriented and adjusted.18 The transplanted type directly transfers paper-based test content to computers without altering it. Jiang et al confirmed the diagnostic validity, efficiency (resulting in a 40% time savings) and value of electronic versions of tests such as the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA) and activities of daily living (ADL).19 The research-oriented type is designed based on neuropsychological research predictive of cognitive impairment, such as Wang’s team’s language analysis software for MCI and early AD diagnosis through fluency indicators.20 The adjusted type uses computer tools to enhance test reliability and accuracy, such as using ChatGPT for speech and text analysis to diagnose AD.

Compared with paper-based testing, computerised screening offers advantages such as reduced psychological and measurement bias, wider audience adaptability, virtual reality-enhanced interest and accuracy, portability and real-time variable recording.21 The 2023 ‘China Digital Memory Clinic Clinical Application Guidelines’ advocate for digital memory clinics. International markets offer tools such as Cogstate22 and Mindstreams,23 whereas domestic tools, including CatCog,24 CoCoSc25 and the Multidimensional Assessment System, need further verification. Future trends include developing multi-terminal, multi-scenario and multi-dimensional tools tailored for older Chinese adults. However, computerised screening faces challenges such as acceptance among the elderly, technical factors and potential misdiagnosis, necessitating integration with clinical results.

Fluid biomarkers

An ideal body fluid marker of AD should have high sensitivity and specificity (≥80%), which can reflect AD’s pathophysiological characteristics during disease development, and exhibit good clinical practicability. They roughly come from three sources: cerebrospinal fluid (CSF), blood and urine.

CSF biomarkers test

Currently, the conditional clinical memory clinics in China routinely carry out the detection of β-amyloid protein (Aβ), total tau protein (T-tau), and phosphorylated tau protein (P-tau) in the CSF of patients suspected of having AD. CSF Aβ biomarkers predominantly consist of Aβ42 and Aβ40. CSF Aβ42 levels are significantly decreased in sporadic AD, offering 86% sensitivity and 81% specificity for diagnosing AD in patients with MCI26 and predicting early AD onset. The Aβ42/Aβ40 ratio enhances sensitivity and specificity in differentiating AD from other neurological disorders compared with measurements of individual Aβ42 or Aβ40. CSF tau biomarkers mainly include T-tau and P-tau (P-tau181, P-tau231, P-tau217). P-tau levels in CSF and plasma increase early in AD, potentially outperforming tau-PET imaging in detecting early AD pathological changes. CSF T-tau levels rise by approximately 300% in AD,27 with a sensitivity of 0.77 and a specificity of 0.86,26 although T-tau also elevates in conditions such as Lewy body dementia and stroke. P-tau proteins, particularly P-tau217, more accurately reflect AD pathology, with increased levels indicating the transition from MCI to AD and cognitive decline. P-tau217 is considered the most promising AD biomarker.28 Jia et al’s seminal longitudinal study29 revealed dynamic CSF and imaging biomarker patterns during AD progression from asymptomatic to symptomatic stages, elucidating early physiological and pathological changes and the correlation between cognitive decline and peripheral biomarkers.

Blood biomarker tests

PET scans and CSF biomarker testing have high predictive value for diagnosing, but their characteristics restrict clinical use, including high cost, limited sample availability and invasiveness. Blood biomarkers of AD, including amyloid precursor protein (APP), Tau, neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP), show promising potential in clinical research. In 2023, blood biomarkers were included as diagnostic criteria in a draft of the latest AD diagnostic guidelines presented at the Alzheimer’s Association International Conference,16 demonstrating high diagnostic accuracy.

Aβ-related biomarkers

In patients with familial AD, total plasma Aβ or Aβ42 levels are elevated, while in patients, these levels increase early on and then decrease as significant cognitive impairment emerges. The plasma Aβ42/Aβ40 ratio correlates with the CSF Aβ42/Aβ40 ratio and Aβ-PET, making it more valuable for predicting the transition from normal cognition to MCI or AD.27 However, some studies suggest that the plasma Aβ42/Aβ40 ratio may be less robust compared with the CSF Aβ42/Aβ40 ratio.30

Tau protein-related biomarkers

Plasma T-tau levels overlap significantly across diagnostic groups, limiting diagnostic value. Weak correlations between blood and CSF T-tau levels suggest that most blood T-tau originates from peripheral sources (approximately 20% from central ones), which hinders the detection of neurodegenerative changes. The levels of P-tau are associated with Aβ, tau, the degree of neurodegeneration, CSF biomarker levels and PET values, predicting changes in these measures.31 Plasma P-tau231 and P-tau217 indicate early Aβ changes, with P-tau231 potentially the earliest AD biomarker. As Clinical Dementia Rating (CDR) scores increase from 0 to 3, P-tau181 levels continue to rise. In patients with MCI, plasma P-tau181 and P-tau217 have been proven to accurately predict cognitive decline and the risk of progressing to AD dementia over the next 2–6 years.30 However, elevated plasma P-tau levels in comorbidities (eg, chronic kidney disease, hypertension) may cause false positives.32

Neurofilament light chain

NfL is a marker of neuronal axon damage and can be detected in both CSF and plasma (serum), which is currently the most promising biomarker for neurodegeneration (N). Increased NfL levels above the threshold indicate a faster cognitive decline,33 so NfL may serve as a predictor of cognitive deterioration. Noteworthily, in individuals over 60 years old, the impact of age on serum NfL levels becomes increasingly significant, while factors such as kidney function and blood volume also have a certain degree of influence on serum NfL levels.34

Glial fibrillary acidic protein

GFAP is a marker of reactive astrogliosis. Unlike other blood biomarkers for AD, serum GFAP is far superior to CSF GFAP in identifying the worsening of brain Aβ pathology.35 Recent studies36 show that GFAP could be an early biomarker for AD, detectable earlier than P-tau181 and NfL.37 Additionally, serum GFAP levels can distinguish AD from frontotemporal dementia, and predict the cognitive decline of cognitively unimpaired (CU) individuals30 and the conversion from MCI to dementia.

Non-invasive urine biomarkers

The ‘Chinese expert consensus on brief screening of prodromal Alzheimer’s disease (2023)’ has included urine biomarkers in the peripheral biomarkers.38 Urine can reflect the pathological features of AD, with metabolites, proteins and nucleic acids potentially serving as AD biomarkers. The AD7C-neurofilament protein in urine serves as an AD biomarker, exhibiting high sensitivity (89.3%) and specificity (84.7%).39 Guo et al reported that urinary formic acid had an area under the curve (AUC) of 0.797 in early AD screening, with a sensitivity of 66.7% and a specificity of 78.9%.40 Other potential urinary biomarkers include Aβ42 and P-S396-tau in urinary exosomes, urinary monocyte chemoattractant protein-1 and dysregulated arginine metabolism.41 Their diagnostic value still requires further clinical evidence for validation.

Other fluid biomarkers

Many promising fluid biomarkers are currently being investigated in clinical studies. The study by Jia et al42 confirmed that Aβ42, T-tau and P-tau181 in peripheral blood neuron-derived exosomes can distinguish patients with AD from healthy individuals. Additionally, exosomal synaptic proteins can be used as biomarkers for predicting AD and MCI 5–7 years before the onset of cognitive impairment.43 Proteomics analysis suggested that a combination of six proteins in neuron-derived exosomes can accurately distinguish patients with AD from healthy controls (AUC=0.978).44 Some studies have achieved antibody-free detection of Aβ and tau aggregate activity in the plasma of patients with AD, using a newly developed AD aggregate activity detector. This confirmed that Aβ aggregate activity could identify patients with AD and distinguish them from CU individuals or those with non-AD dementia (AUC=0.85–0.86).45 Shen’s team discovered that the onset and progression of AD are accompanied by specific autoantigen-antibody reactions.46 They were the first to identify seven AD-specific serum autoantibodies with diagnostic value: MAPT, DNAJC8, KDM4D, SERF1A, CDKN1A, AGER and ASXL1. Further analysis revealed that the AUC of these seven antibodies combined for diagnosing AD reached 0.94. Their levels can also reflect the cognitive function of patients with AD, with higher predictive accuracy for mild cognitive decline. Their effectiveness in predicting cognitive decline surpassed that of CSF-Aβ and p-tau. Wang et al47 pioneered the first integrated analysis of the subgingival microbiome and gingival crevicular fluid metabolome in individuals with AD and amnestic MCI, uncovering that periodontal microbial imbalance and metabolic alterations might play a role in the onset and progression of AD. Variations in the abundance of microbial communities and metabolites could emerge as promising biomarkers for AD in the future.48

Genetic tests

In China, clinical guidelines do not recommend gene testing for all patients with AD, as there are numerous issues and confounding factors associated with its purpose, methods and interpretation. AD is mostly sporadic, with familial cases accounting for approximately 5%, and early-onset AD comprising only about 1%. The most studied genes include PSEN1, PSEN2 and APP, with PSEN1 mutations being the most common, making up 75%–80%. A study by Xuanwu Hospital in Beijing found 13.12% of 404 familial AD families carry mutations in these genes.49 In addition to these pathogenic genes, over 70 genetic loci are associated with AD.50 ApoE ε4 is the most significant genetic risk factor and is key for the conversion from MCI to AD.51 For the elderly with a family history of AD, carrying ApoE ε4 significantly increases the risk. Studies have also identified other genes, such as CR1, TREM2 and ACE, with higher mutation frequencies in late-onset familial AD.52

In the past, APP gene mutations were primarily associated with early-onset AD. Recently, Wang’s group reported the APP Shanghai mutation (APP E674Q), linking it to late-onset AD, which filled a gap in APP mutation research in China.53 PSEN2 mutations are also associated with late-onset AD, suggesting that gene testing for patients with AD with a family history of dementia is recommended, particularly the use of gene panels or whole-exome sequencing or whole-genome sequencing for autosomal dominant AD families.54

Ongoing clinical trials of potential diagnostic tools

Currently, some biomarkers have successfully entered the domestic clinical trial stage. For instance, the (Roche) Elecsys CSF immunoassay kit assists in diagnosing AD by detecting CSF β-amyloid (Aβ1–42), phosphorylated tau protein (181P) and total tau protein, either individually or in combination. This assay kit has already been launched in the European Union and the USA and is considered a ‘breakthrough device’. It can early identify patients with cognitive decline and is a reliable predictive method for monitoring the progression of MCI to AD. The Elecsys Amyloid Plasma Panel is the first blood-based biomarker product for diagnosing AD to receive the US Food and Drug Administration ‘Breakthrough Device’ designation. This method can identify patients who need confirmatory testing by measuring P-tau181 and apolipoprotein E4 in human plasma. This test is currently undergoing multicentre clinical validation within China. In addition, previous Chinese researchers discovered a protein, TRPC6, encoded by the transient receptor potential canonical 6 (TRPC6) gene, which can block the binding of the substrate APP to secretase and specifically inhibit Aβ production. TRPC6 messenger RNA levels in peripheral blood cells were significantly reduced in patients with MCI and AD. TRPC6 could potentially be an early biomarker for diagnosing AD.55 Since 2021, the TRPC6 blood testing product from Maozhi Biotechnology has been undergoing clinical trials at centres for multiple cognitive disorders, with the aim of gaining market approval.

Treatment of AD and related clinical trials

Therapeutic approaches for AD

Currently, the main drugs available on the market include donepezil, galantamine, rivastigmine, memantine and sodium mannitolate capsules (GV-971), all primarily aimed at improving the clinical symptoms of AD. Recently, octohydroaminoacridine succinate tablets, a novel acetylcholinesterase inhibitor with proven significant cognitive improvement (Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS-Cog)) and lower adverse events in Phase III trials (NCT01569516), are now seeking market authorisation to offer patients with AD a new hopeful treatment option. In parallel, novel drugs targeting disease-modifying therapies (DMTs) for AD, particularly monoclonal antibodies targeting Aβ and tau proteins, have become a major focus of AD treatment research. Additionally, neuroregulatory therapies and traditional Chinese medicine treatments have also made rapid progress. However, it should be noted that the quality of clinical research reports related to AD urgently needs improvement and should adhere strictly to the CONSORT (Consolidated Standards of Reporting Trials) guidelines for reporting.

Anti-Aβ therapy

Aβ monoclonal antibody drugs are representative of DMTs for AD, thought to intervene in the production, aggregation and clearance of Aβ to delay the onset and progression of early AD. Recently, significant progress has been made in clinical trials of Aβ monoclonal antibody treatments for AD.56

Aducanumab

Developed by Biogen, aducanumab is the first drug designed for DMT in patients with mild AD. On 11 December 2022, Wang’s team at Ruijin Hainan Hospital conducted a clinical study (ChiCTR2200066153) of patients with mild AD using aducanumab monoclonal antibody, marking the first clinical therapy of aducanumab for AD in China. The Phase III (EMERGE, NCT02484547) study showed that after 78 weeks of treatment with aducanumab, the primary clinical endpoint, the CDR-Sum of Boxes score, decreased by 22%, the secondary endpoints—MMSE, ADAS-Cog13 and Alzheimer’s disease cooperative study–activities of daily living for mild cognitive impairment (ADCS-ADL-MCI) scores—decreased by 18%, 27% and 40%, respectively, showing a significant difference compared with the control group. In the Phase III (ENGAGE) study, aducanumab failed to achieve the primary and secondary clinical endpoints.57 Amyloid-related imaging abnormalities (ARIA) with oedema are the most common adverse event observed with the 10 mg/kg dose of aducanumab treatment.58

Lecanemab

In January 2024, the National Medical Products Administration of China officially approved lecanemab for marketing in China. Phase IIb and III clinical trials demonstrated that after 18 months of treatment, lecanemab significantly reduced Aβ deposition in the brain and slowed the decline in cognitive function and quality of life scores, with the rate of decline in clinical dementia scores reduced by approximately 27%, indicating substantial long-term efficacy. However, lecanemab led to infusion-related reactions in 26.4% of participants, and 12.6% experienced ARIA, such as oedema or effusion.59 According to statistics, approximately 2000 patients in China have received treatment with lecanemab, following the USA and Japan. This reflects the widespread acceptance and promising outlook in China. Chinese clinicians’ clinical experience suggests ARIA incidence in Chinese patients with AD may be lower than the global Clarity AD study data, but this needs validation. A prospective real-world study (ChiCTR2400087134) in China aims to assess monoclonal antibody safety and efficacy in patients with AD, including ARIA data. Its results will offer targeted evidence for the Chinese population. Meanwhile, the Yuyuan Community Health Service Centre in Shanghai has successfully achieved a breakthrough in applying lecanemab at the community level by effectively integrating community resources.60 The centre has also innovatively introduced the ‘Yuyuan Model’, which is actively promoting the adoption and application of lecanemab in China.

Donanemab

Donanemab is a humanised IgG1 antibody targeting a specific epitope (the N-terminal pyroglutamate at position 3). The results of the Phase III clinical trial (TRAILBLAZER-ALZ 2) indicated that donanemab slowed the decline in the primary endpoint of the integrated AD Assessment Scale by 35% compared with the control group.61 It also slowed the decline in the key secondary endpoint, CDR, by 36%. Participants with low or moderate tau pathology have greater cognitive benefits, and 47% of patients with early-stage AD showed no further worsening of clinical AD symptoms after treatment with donanemab. Similar to other monoclonal antibodies of the same class, the primary adverse reaction of donanemab is ARIA with oedema. Currently, donanemab has become the second approved anti-Aβ antibody marketed in China by the National Medical Products Administration of China, effective 18 December 2024.

SHR-1707

SHR-1707 is the first humanised anti-Aβ monoclonal antibody in China to treat early AD. It has completed Phase I clinical trials in healthy individuals in China and Australia. Meanwhile, recruitment for the Phase II clinical trial (NCT06199037) has now commenced.

Anti-Tau therapy

Globally, numerous clinical trials targeting tau pathology in AD have yielded limited clinical success. Anti-tau monoclonal antibodies have either failed to meet primary endpoints in early-stage AD (NCT02880956 and NCT03352557) or have shown only modest improvements in cognition and reductions in biomarkers, without demonstrating clear clinical efficacy (NCT03828747 and NCT03186989). In addition to anti-tau monoclonal antibodies designed to eliminate pathological Tau, certain pharmaceuticals are formulated to impede the aggregation of Tau proteins. For instance, a Phase 3 study (NCT01689246) involving Chinese researchers aimed to assess the safety and efficacy of leuco-methylthioninium bis, a selective inhibitor of Tau protein aggregation, in modifying the disease progression of patients with mild-to-moderate AD. However, the primary analysis yielded negative results. Collectively, these findings underscore that tau-targeted therapies have not yet provided transformative clinical benefits, necessitating continued exploration of the underlying mechanisms and refinement of trial designs.

Other disease-modifying therapies for AD

AR1001, an orally administered small-molecule drug, demonstrates high selectivity for phosphodiesterase-5 inhibition and employs a multifaceted mechanism to address AD pathology. Specifically, it targets three critical pathological hallmarks of AD: (1) reducing Aβ plaque deposition, (2) suppressing the hyperphosphorylation of Tau protein and (3) exerting anti-inflammatory effects by modulating neuroinflammatory pathways. Currently, China is actively participating in an ongoing Phase 3 clinical trial (NCT05531526), which is of significant interest. The primary objective of this study is to evaluate the efficacy and safety of AR1001 in patients with early-stage AD. A total of 150 participants with early AD are expected to be enrolled in China for this trial. The results of this study are highly anticipated, as they may offer valuable insights into the potential of AR1001 as a novel therapeutic option for the early stages of AD.

Neuromodulation therapy

Emerging neuromodulation techniques, grounded in AD pathophysiology and brain network modulation models, offer promising therapeutic avenues, though clinical optimisation remains crucial. Repetitive transcranial magnetic stimulation demonstrates efficacy in improving cognitive function (MMSE, MoCA, ADAS-Cog), episodic memory and psychiatric symptoms (reduced behavioral pathology in Alzheimer’s Disease Rating Scale scores) in patients with moderate-to-severe AD, particularly with high-frequency protocols, while low-frequency stimulation shows limited impact. Adverse effects are mild (scalp pain, headache) and transient, with most cases gradually subsiding once the stimulation is halted.62,64 Transcranial alternating current stimulation at 40 Hz enhances MMSE and ADAS-Cog scores in individuals with mild-to-moderate AD, with transient changes in the Aβ40/Aβ42 ratio; however, long-term benefits require validation in larger trials.65 Near-infrared light therapy significantly improves cognitive and functional scores (ADAS-Cog, MMSE, ADL) in mild-to-moderate AD, with over 57% achieving clinically meaningful improvements.66 Deep brain stimulation targeting the Meynert basal nuclei yields short-term MMSE gains but lacks sustained efficacy, correlating with reduced salience network activity and altered hippocampal-frontoparietal connectivity.67 Future directions emphasise intermittent stimulation, gamma modulation and closed-loop systems, necessitating rigorous validation of efficacy and safety. Collectively, parameter optimisation (frequency, duration, target), adverse effect monitoring and long-term outcomes remain critical for translating neuromodulation into standardised AD therapies.

Lymphatic-venous anastomosis

In 2018, a study published in Nature68 clarified the association between the meningeal lymphatic system and AD. Following this, domestic researchers have actively pursued further investigations into this area. One report noted that after performing a cervical lymphatic-venous anastomosis (CLVA) on a 70-year-old patient with cognitive impairment, the patient showed significant improvement in cognitive function within 4 months post-operation.69 Based on this, a research team led by Zhang (the principal investigator of the trial) conducted a clinical trial (ChiCTR2400084617) to improve cerebral lymphatic drainage using microsurgical techniques for lymphatic reconstruction via CLVA. The approach leverages both the local drainage effect and the systemic influence of the lymphatic system to accelerate the clearance of cerebral metabolic waste, particularly pathological proteins, thereby slowing neurodegenerative changes and the progression of AD. This trial is highly anticipated and holds promise for offering novel insights into treating AD. By the end of 2024, at least 500 cases had been publicly reported in case reports and media coverage on mainstream public online platforms in China. However, continued observation of patients undergoing this procedure, along with close monitoring of ongoing research, is critical to ensuring its safe and effective implementation.

Stem cell and exosome therapy

Wang et al reported the world’s first clinical trial using allogenic human adipose mesenchymal stromal cells-derived exosomes (ahaMSCs-Exos) administered intranasally for the treatment of AD.70 Participants were assigned to three different dose groups: low, medium and high. They received intranasal administration of ahaMSCs-Exos two times a week for 12 weeks, followed by follow-up assessments at weeks 16, 24, 36 and 48. Compared with baseline, the medium-dose group (4×108 particles) showed a decrease of 2.33 (1.19) points in the ADAS-cog score and an increase of 2.38 (0.58) points in the MoCA Basic score at week 12. There were no statistically significant differences in Aβ or tau deposition changes among the three participant groups. The medium-dose group showed a possible trend of reduced hippocampal atrophy, which requires further exploration and validation in clinical trials. No adverse events were reported in this trial.

Other therapies

Emerging research on AD suggests potential benefits from complementary approaches, including Chinese medicine (eg, anthocyanins, acupuncture and herbal formulations) with improved cognitive metrics, alongside non-pharmacological therapies like vitamin D3, memory training and multimodal interventions (see details in online supplemental material).

Public health resources for the prevention and treatment of AD

Current status and service provision of specialised clinics for AD

Memory clinics aim to expedite the early diagnosis, identification and treatment of cognitive disorders, such as AD, while offering family care education and caregiver training. These clinics provide specialised care in a shorter timeframe and serve as vital units for health education and chronic disease monitoring.71 By 2022, China had 273 such clinics.72

The ‘China Alzheimer’s Disease Report 2023’ revealed significant awareness growth, with 80% of patients and families recognising early AD symptoms. The 1-year consultation rate is 32.6%, and the 2-year rate is 71.6%, indicating improved timely access to medical care.

Government support and policy orientation

Government support

As China’s population ages, the risk of cognitive impairment increases, posing a significant societal threat with potential national implications. Both the government and society are increasingly focusing on cognitive impairment diseases, such as AD. The ‘Healthy China 2030 Plan’ emphasised the need to improve interventions for AD. In September 2020, the National Health Commission issued a plan to explore specialised dementia prevention and treatment services, aiming to raise public awareness to 80% in pilot regions by 2022. Additionally, the plan called for the establishment and enhancement of AD prevention and treatment networks, ensuring that 80% of elderly adults in communities undergo cognitive function screening. A multidisciplinary team, comprising general practitioners, volunteers, social workers and psychotherapists, should provide services for individuals with MCI and dementia. The ‘National Nursing Development Plan (2021–2025)’ further emphasised the provision of convenient and professional care for elderly adults with disabilities and dementia.73 Another notice set criteria for national medical-nursing demonstration institutions, stipulating that over 50% of residents must be elderly individuals with disabilities or dementia.74 In June 2023, the release of the ‘Notice on the Promotion and Prevention of Alzheimer’s Disease (2023–2025)’ marked the initiation of a nationwide campaign to prevent and control AD.75

Long-term care insurance

Since 2016, long-term care insurance (LTCI) has been piloted in 15 cities in China, expanding to 49 cities by the end of 2022. It has covered 169 million people and benefited 1.95 million.76 The initiative aims to establish a social insurance system funded through mutual aid, which supports daily and medical care for individuals who are long-term disabled or suffer from dementia. Notably, only six pilot cities (Shanghai, Shangrao, Chengdu, Nantong, Qingdao and Guangzhou) have included patients with dementia within the scope of LTCI coverage. Most pilot cities have established specialised dementia care units within institutions; for example, Qingdao offers short-term, daycare and long-term care services,77 while Shanghai introduces cognitive care units with flexible bed capacity. LTCI has not only alleviated financial pressure on patients with dementia and their families but has also garnered strong approval and enhanced caregivers’ skills through its in-home services.

Resource allocation status for AD

Resource allocation for AD in China spans specialised geriatric hospitals, rural/urban pension institutions with dementia-friendly designs, community-home care systems for screening and management, as well as non-governmental organisation-led initiatives including volunteer groups, public welfare projects and self-help networks. However, rural gaps and service disparities persist (see details in the online supplemental material).

Limitation

A limitation of this study is that, despite its title being ‘2025 AD Report’, the data and tables presented are actually based on epidemiological information from 2021. The prolonged duration required for global data collection, quality assurance and model validation within the data processing frameworks of the GBD initiative and national health agencies inevitably leads to a 2–3-year lag in data release. Consequently, it is comprehensible that the 2021 data were the most current information available at the time of conducting this study in 2024. To guarantee the accuracy and reliability of our findings, we carried out meticulous cross-verification of the original data sources during the study’s preparation phase in 2024, aiming to use the most up-to-date and comprehensive data available.

Conclusion

This report, an update to previous editions, summarises the latest epidemiological data on AD in China. It thoroughly analyses the economic burden of the disease and evaluates the current status of diagnosis, treatment services and public health resource allocation. The report highlights China’s progress and commitment to AD research, prevention and control, emphasising society’s focus on elderly health. Additionally, it provides professional evidence to support governments and departments in developing targeted health policies and intervention strategies.

Supplementary material

online supplemental file 1
gpsych-38-4-s001.pdf (388.3KB, pdf)
DOI: 10.1136/gpsych-2024-102020

Biography

Nan Zhi obtained her medical doctor's degree in neurology from Peking Union Medical College, China, in 2011. She focused on the pathogenesis mechanism of cognitive impairment in ischaemic cerebral vascular disease during her medical training by building animal models of cerebral small vessel disease. Now, she is an attending physician at the Department of Neurology, Shanghai Renji Hospital, affiliated with Shanghai Jiao Tong University School of Medicine, China. Her current main research interests include vascular and neurodegenerative-related cognitive impairment diseases, especially Alzheimer’s disease. Her main research findings have been published in journals such as General Psychiatry and The European Journal of Neurology.

graphic file with name gpsych-38-4-g001.gif

Footnotes

Funding: This report was supported by a grant from Brain Science and Brain-Like Intelligence Technology of the Ministry of Science and Technology of China (2021ZD0201804).

Provenance and peer review: Not commissioned; externally peer reviewed.

Patient consent for publication: Not applicable.

Ethics approval: Not applicable.

References

  • 1.Ministry of Civil Affairs, People’s Republic of China The communique on the development of the national cause for aging in 2022 was released. 2022. [6-Dec-2024]. https://www.mca.gov.cn/n152/n166/c1662004999979996644/content.html Available. Accessed.
  • 2.Ren R, Qi J, Lin S, et al. The China Alzheimer report 2022. Gen Psychiatr. 2022;35:e100751. doi: 10.1136/gpsych-2022-100751. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Ren RJ, Yin P, Wang ZH, et al. China Alzheimer disease report 2021. J Diagn Concepts Pract. 2021;20:317–37. [Google Scholar]
  • 4.Jia L, Du Y, Chu L, et al. Prevalence, risk factors, and management of dementia and mild cognitive impairment in adults aged 60 years or older in China: a cross-sectional study. Lancet Public Health. 2020;5:e661–71. doi: 10.1016/S2468-2667(20)30185-7. [DOI] [PubMed] [Google Scholar]
  • 5.Xiao J, Li J, Wang J, et al. China Alzheimer’s disease: facts and figures. Human Brain. 2023;2:1–13. [Google Scholar]
  • 6.Wang G, Qi J, Liu X, et al. China Alzheimer report 2024. Journal of Diagnostics Concepts & Practice. 2024;23:219–56. [Google Scholar]
  • 7.GBD 2021 Forecasting Collaborators Burden of disease scenarios for 204 countries and territories, 2022-2050: a forecasting analysis for the global burden of disease study 2021. Lancet. 2024;403:2204–56. doi: 10.1016/S0140-6736(24)00685-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Global burden of disease study 2021 (gbd 2021) data resources. 2021. [6-Dec-2024]. https://ghdx.healthdata.org/gbd-2021 Available. Accessed.
  • 9.Silva MVF, Loures CMG, Alves LCV, et al. Alzheimer’s disease: risk factors and potentially protective measures. J Biomed Sci. 2019;26:33. doi: 10.1186/s12929-019-0524-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Avan A, Hachinski V. Global, regional, and national trends of dementia incidence and risk factors, 1990–2019: a Global Burden of Disease study. Alzheimers Dement. 2023;19:1281–91. doi: 10.1002/alz.12764. [DOI] [PubMed] [Google Scholar]
  • 11.Aging and cognitive impairment branch of shanghai society of aging and degenerative diseases. Expert consensus on neuroimaging diagnosis of dementia and cognitive impairment (2023) Journal of Diagnostics Concepts & Practice. 2024;23:30–9. [Google Scholar]
  • 12.Wang G, Lv FJ. Advice on diagnostic process of neuroimaging in dementia and cognitive impairment. J Chongqing Med Univ. 2017;42:684–6. [Google Scholar]
  • 13.Pistono A, Senoussi M, Guerrier L, et al. Language network connectivity increases in early Alzheimer’s disease. J Alzheimers Dis. 2021;82:447–60. doi: 10.3233/JAD-201584. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Haacke EM, Chen Y, Utriainen D, et al. Strategically Acquired Gradient Echo (STAGE) imaging, part III: technical advances and clinical applications of a rapid multi-contrast multi-parametric brain imaging method. Magn Reson Imaging. 2020;65:15–26. doi: 10.1016/j.mri.2019.09.006. [DOI] [PubMed] [Google Scholar]
  • 15.Jack CR, Jr, Bennett DA, Blennow K, et al. NIA-AA research framework: toward a biological definition of Alzheimer’s disease. Alzheimers Dement. 2018;14:535–62. doi: 10.1016/j.jalz.2018.02.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Revised criteria for diagnosis and staging of alzheimer’s disease: alzheimer’s association workgroup. 2024. [6-Dec-2024]. https://aaic.alz.org/diagnostic-criteria.asp#drafts Available. Accessed. [DOI] [PMC free article] [PubMed]
  • 17.Chinese Society of Nuclear Medicine A brief report on the results of the national survey of nuclear medicine in 2020. Chin J Nucl Med Mol Imaging. 2020;40:747–9. [Google Scholar]
  • 18.Meng QY, Yin HR, Wang S, et al. Research progress of computerized cognitive screening test in elderly patients with mild cognitive impairment. Chin J Nurs. 2019;54:1023–7. [Google Scholar]
  • 19.Jiang PJ, Tan XL, Yu TT, et al. Application of early recognition screening and diagnostic scale of dementia and cognitive impairment based on electronization. Chin J Alzheimer’s Dis Relat Disord. 2021;4:116–20. [Google Scholar]
  • 20.Wang H-L, Tang R, Ren R-J, et al. Speech silence character as a diagnostic biomarker of early cognitive decline and its functional mechanism: a multicenter cross-sectional cohort study. BMC Med. 2022;20:380. doi: 10.1186/s12916-022-02584-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Xuan LM, Zhuan SW, Chen MT, et al. Research progress of virtual reality technology in senile dementia patients. J Nurs. 2019;26:17–9. [Google Scholar]
  • 22.Stricker NH, Lundt ES, Edwards KK, et al. Comparison of PC and iPad administrations of the cogstate brief battery in the mayo clinic study of aging: assessing cross-modality equivalence of computerized neuropsychological tests. Clin Neuropsychol. 2019;33:1102–26. doi: 10.1080/13854046.2018.1519085. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 23.Dwolatzky T, Dimant L, Simon ES, et al. Validity of a short computerized assessment battery for moderate cognitive impairment and dementia. Int Psychogeriatr. 2010;22:795–803. doi: 10.1017/S1041610210000621. [DOI] [PubMed] [Google Scholar]
  • 24.Xie HQ, Wang YK, Huang SY, et al. Development of a computerized adaptive testing system for cognitive impairment screening. Chin J Geriatr Care. 2017;15:30–2. [Google Scholar]
  • 25.Wong A, Fong C-H, Mok V-T, et al. Computerized cognitive screen (CoCoSc): a self-administered computerized test for screening for cognitive impairment in community social centers. J Alzheimers Dis. 2017;59:1299–306. doi: 10.3233/JAD-170196. [DOI] [PubMed] [Google Scholar]
  • 26.Tian JZ, Xie HG, Wang LN, et al. Chinese guideline for the diagnosis and treatment of Alzheimer’s disease dementia. Chin J Geriatri. 2020;40:269–83. [Google Scholar]
  • 27.Bjerke M, Engelborghs S. Cerebrospinal fluid biomarkers for early and differential Alzheimer’s disease diagnosis. J Alzheimers Dis. 2018;62:1199–209. doi: 10.3233/JAD-170680. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Ossenkoppele R, van der Kant R, Hansson O. Tau biomarkers in Alzheimer’s disease: towards implementation in clinical practice and trials. Lancet Neurol. 2022;21:726–34. doi: 10.1016/S1474-4422(22)00168-5. [DOI] [PubMed] [Google Scholar]
  • 29.Jia J, Ning Y, Chen M, et al. Biomarker changes during 20 years preceding Alzheimer’s disease. N Engl J Med. 2024;390:712–22. doi: 10.1056/NEJMoa2310168. [DOI] [PubMed] [Google Scholar]
  • 30.Hansson O, Edelmayer RM, Boxer AL, et al. The Alzheimer’s Association appropriate use recommendations for blood biomarkers in Alzheimer’s disease. Alzheimers Dement. 2022;18:2669–86. doi: 10.1002/alz.12756. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Karikari TK, Ashton NJ, Brinkmalm G, et al. Blood phospho-tau in Alzheimer disease: analysis, interpretation, and clinical utility. Nat Rev Neurol. 2022;18:400–18. doi: 10.1038/s41582-022-00665-2. [DOI] [PubMed] [Google Scholar]
  • 32.Mielke MM, Dage JL, Frank RD, et al. Performance of plasma phosphorylated tau 181 and 217 in the community. Nat Med. 2022;28:1398–405. doi: 10.1038/s41591-022-01822-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33.Smirnov DS, Ashton NJ, Blennow K, et al. Plasma biomarkers for Alzheimer’s disease in relation to neuropathology and cognitive change. Acta Neuropathol. 2022;143:487–503. doi: 10.1007/s00401-022-02408-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Koini M, Pirpamer L, Hofer E, et al. Factors influencing serum neurofilament light chain levels in normal aging. Aging (Albany NY) 2021;13:25729–38. doi: 10.18632/aging.203790. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35.Benedet AL, Milà-Alomà M, Vrillon A, et al. Differences between plasma and cerebrospinal fluid glial fibrillary acidic protein levels across the Alzheimer disease continuum. JAMA Neurol. 2021;78:1471–83. doi: 10.1001/jamaneurol.2021.3671. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36.Milà-Alomà M, Ashton NJ, Shekari M, et al. Plasma p-tau231 and p-tau217 as state markers of amyloid-β pathology in preclinical Alzheimer’s disease. Nat Med. 2022;28:1797–801. doi: 10.1038/s41591-022-01925-w. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37.Stocker H, Beyer L, Perna L, et al. Association of plasma biomarkers, p‐tau181, glial fibrillary acidic protein, and neurofilament light, with intermediate and long‐term clinical Alzheimer’s disease risk: results from a prospective cohort followed over 17 years. Alzheimer’s &Amp; Dementia. 2023;19:25–35. doi: 10.1002/alz.12614. [DOI] [PubMed] [Google Scholar]
  • 38.Dementia and Cognitive Disorders Group, Neurology Branch of Chinese Medical Association, Cognitive Disorders Professional Committee, Neurology Branch of Chinese Medical Doctor Association Chinese expert consensus on brief screening of prodromal Alzheimer’s disease (2023) Chin J Neuromedicine. 2023;22:433–44. [Google Scholar]
  • 39.Ma L, Wang R, Han Y, et al. Development of a novel urine Alzheimer-associated neuronal thread protein ELISA kit and its potential use in the diagnosis of Alzheimer’s disease. J Clin Lab Anal. 2016;30:308–14. doi: 10.1002/jcla.21856. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Wang Y, Wang Y, Zhu J, et al. Systematic evaluation of urinary formic acid as a new potential biomarker for Alzheimer’s disease. Front Aging Neurosci. 2022;14:1046066. doi: 10.3389/fnagi.2022.1046066. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41.Wang R, He J. Study on urine biomarkers in early screening of Alzheimer disease in China. J Neurosci Ment Health. 2022;22:685–90. [Google Scholar]
  • 42.Jia L, Qiu Q, Zhang H, et al. Concordance between the assessment of Aβ42, T‐tau, and P‐T181‐tau in peripheral blood neuronal‐derived exosomes and cerebrospinal fluid. Alzheimers Dement. 2019;15:1071–80. doi: 10.1016/j.jalz.2019.05.002. [DOI] [PubMed] [Google Scholar]
  • 43.Jia L, Zhu M, Kong C, et al. Blood neuro-exosomal synaptic proteins predict Alzheimer’s disease at the asymptomatic stage. Alzheimers Dement. 2021;17:49–60. doi: 10.1002/alz.12166. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Cai H, Pang Y, Wang Q, et al. Proteomic profiling of circulating plasma exosomes reveals novel biomarkers of Alzheimer’s disease. Alzheimers Res Ther. 2022;14:181. doi: 10.1186/s13195-022-01133-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 45.Jia J, Li T, Yang J, et al. Detection of plasma Aβ seeding activity by a newly developed analyzer for diagnosis of Alzheimer’s disease. Alzheimers Res Ther. 2022;14:21. doi: 10.1186/s13195-022-00964-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46.Fang L, Jiao B, Liu X, et al. Specific serum autoantibodies predict the development and progression of Alzheimer’s disease with high accuracy. Brain Behav Immun. 2024;115:543–54. doi: 10.1016/j.bbi.2023.11.018. [DOI] [PubMed] [Google Scholar]
  • 47.Qiu C, Zhou W, Shen H, et al. Profiles of subgingival microbiomes and gingival crevicular metabolic signatures in patients with amnestic mild cognitive impairment and Alzheimer’s disease. Alzheimers Res Ther. 2024;16:41. doi: 10.1186/s13195-024-01402-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 48.2024 Alzheimer’s disease facts and figures. Alzheimers Dement. 2024;20:3708–821. doi: 10.1002/alz.13809. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 49.Jia L, Fu Y, Shen L, et al. PSEN1, PSEN2, and APP mutations in 404 Chinese pedigrees with familial Alzheimer’s disease. Alzheimer’s & Dementia. 2020;16:178–91. doi: 10.1002/alz.12005. [DOI] [PubMed] [Google Scholar]
  • 50.Bellenguez C, Küçükali F, Jansen IE, et al. New insights into the genetic etiology of Alzheimer’s disease and related dementias. Nat Genet. 2022;54:412–36. doi: 10.1038/s41588-022-01024-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 51.Lu XX, Lv Q, Pu JL, et al. Mutation analysis of presenilin-1 gene in Alzheimer’s disease patients and the effects of its mutation on expression of presenilin-1 and amyloid precursor protein. Chin J Neurol. 2013;46:5–9. [Google Scholar]
  • 52.Xie X-Y, Zhao Q-H, Huang Q, et al. Genetic profiles of familial late-onset Alzheimer’s disease in China: The Shanghai FLOAD study. Genes Dis. 2022;9:1639–49. doi: 10.1016/j.gendis.2021.05.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 53.Zhang Y, Xie X, Chen B, et al. E674Q (Shanghai APP mutant), a novel amyloid precursor protein mutation, in familial late-onset Alzheimer’s disease. Genes Dis. 2024;11:1022–34. doi: 10.1016/j.gendis.2023.02.051. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 54.Che XQ, Xie XY, Wang G, et al. Clinical strategies for genetic testing of Alzheimer’s disease and related cognitive impairments. J Chongqing Med Univ. 2021;46:804–8. [Google Scholar]
  • 55.Lu R, Wang J, Tao R, et al. Reduced TRPC6 mRNA levels in the blood cells of patients with Alzheimer’s disease and mild cognitive impairment. Mol Psychiatry. 2018;23:767–76. doi: 10.1038/mp.2017.136. [DOI] [PubMed] [Google Scholar]
  • 56.Xiao JW, Ren RJ, Wang G. Anti-amyloid-β monoclonal antibodies for Alzheimer’s disease: clinical practice and progress. Chin J Alzheimer’s Dis Relat Disord. 2023;6:7–11. [Google Scholar]
  • 57.Budd Haeberlein S, Aisen PS, Barkhof F, et al. Two randomized phase 3 studies of aducanumab in early Alzheimer’s Disease. J Prev Alzheimers Dis. 2022;9:197–210. doi: 10.14283/jpad.2022.30. [DOI] [PubMed] [Google Scholar]
  • 58.Salloway S, Chalkias S, Barkhof F, et al. Amyloid-related imaging abnormalities in 2 phase 3 studies evaluating aducanumab in patients with early Alzheimer disease. JAMA Neurol. 2022;79:13–21. doi: 10.1001/jamaneurol.2021.4161. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 59.van Dyck CH, Swanson CJ, Aisen P, et al. Lecanemab in early Alzheimer’s disease. N Engl J Med. 2023;388:9–21. doi: 10.1056/NEJMoa2212948. [DOI] [PubMed] [Google Scholar]
  • 60.Li X, Jing Y, Li Y, et al. Full-process management model for cognitive impairment based on the concept of integrated care. Chin Prim Health Care. 2025;39:12–6. [Google Scholar]
  • 61.Sims JR, Zimmer JA, Evans CD, et al. Donanemab in early symptomatic Alzheimer disease: the TRAILBLAZER-ALZ 2 randomized clinical trial. JAMA. 2023;330:512–27. doi: 10.1001/jama.2023.13239. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 62.Liu C, Han T, Xu Z, et al. Modulating gamma oscillations promotes brain connectivity to improve cognitive impairment. Cereb Cortex. 2022;32:2644–56. doi: 10.1093/cercor/bhab371. [DOI] [PubMed] [Google Scholar]
  • 63.Jiang W, Wu Z, Wen L, et al. The efficacy of high- or low-frequency transcranial magnetic stimulation in Alzheimer’s disease patients with behavioral and psychological symptoms of dementia. Adv Ther. 2022;39:286–95. doi: 10.1007/s12325-021-01964-8. [DOI] [PubMed] [Google Scholar]
  • 64.Zhou X, Wang Y, Lv S, et al. Transcranial magnetic stimulation for sleep disorders in Alzheimer’s disease: a double-blind, randomized, and sham-controlled pilot study. Neurosci Lett. 2022;766:136337. doi: 10.1016/j.neulet.2021.136337. [DOI] [PubMed] [Google Scholar]
  • 65.Zhou D, Li A, Li X, et al. Effects of 40 Hz transcranial alternating current stimulation (tACS) on cognitive functions of patients with Alzheimer’s disease: a randomised, double-blind, sham-controlled clinical trial. J Neurol Neurosurg Psychiatry. 2022;93:568–70. doi: 10.1136/jnnp-2021-326885. [DOI] [PubMed] [Google Scholar]
  • 66.Chen L, Xue J, Zhao Q, et al. A pilot study of near-infrared light treatment for Alzheimer’s disease. J Alzheimers Dis. 2023;91:191–201. doi: 10.3233/JAD-220866. [DOI] [PubMed] [Google Scholar]
  • 67.Jiang Y, Yuan T-S, Chen Y-C, et al. Deep brain stimulation of the nucleus basalis of Meynert modulates hippocampal-frontoparietal networks in patients with advanced Alzheimer’s disease. Transl Neurodegener. 2022;11:51. doi: 10.1186/s40035-022-00327-9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 68.Da Mesquita S, Louveau A, Vaccari A, et al. Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease. Nature New Biol. 2018;560:185–91. doi: 10.1038/s41586-018-0368-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 69.Li X, Zhang C, Fang Y, et al. Promising outcomes 5 weeks after a surgical cervical shunting procedure to unclog cerebral lymphatic systems in a patient with Alzheimer’s disease. Gen Psychiatr. 2024;37:e101641. doi: 10.1136/gpsych-2024-101641. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 70.Xie X, Song Q, Dai C, et al. Clinical safety and efficacy of allogenic human adipose mesenchymal stromal cells-derived exosomes in patients with mild to moderate Alzheimer’s disease: a phase I/II clinical trial. Gen Psychiatr. 2023;36:e101143. doi: 10.1136/gpsych-2023-101143. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 71.Ren RJ, Wang G, Chen SD. Thinking and prospect of constructing standardized memory clinic in China. J Intern Med Concepts Pract. 2015;10:90–1. [Google Scholar]
  • 72.Alzheimer’s Disease China (ADC) ADC national memory clinic map. 2023. [6-Dec-2024]. https://www.adc.org.cn/index.php/page/371.html Available. Accessed.
  • 73.The Medical Administration Hospital Authority Notice of the national health commission on the issuance of the national nursing development plan (2021–2025) 2022. [6-Dec-2024]. https://www.gov.cn/zhengce/zhengceku/2022-05/09/content_5689354.htm Available. Accessed.
  • 74.Department of Ageing Health Interpretation of the notice of the national health commission on issuing the work program of the demonstration project of combining medical and nursing care. 2022. [6-Dec-2024]. https://www.nhc.gov.cn/lljks/c100157/202204/52e1963853a64b8e82c3e8fdf4a1473d.shtml Available. Accessed.
  • 75.General Office of the National Health Commission Notice of the general office of the national health commission on the promotion and prevention of alzheimer’s disease (2023–2025) 2023. [6-Dec-2024]. https://www.gov.cn/zhengce/zhengceku/202306/content_6886277.htm Available. Accessed.
  • 76.Wang X. The long-term care insurance program has benefited 1.95 million people over the past six years. 2023
  • 77.Zhang XY, Chen X, Chen C. Text analysis of long-term care insurance system pilot city policy in China. Journal of Panzhihua College. 2023;40:11–7. [Google Scholar]

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DOI: 10.1136/gpsych-2024-102020

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