Abstract
Objective
Ginseng intake and zinc homeostasis are potential protective factors against Alzheimer's disease (AD), but their interrelationship in cognition remains unclear. This study examined the association of ginseng intake and serum zinc with AD-related cognitive function in older adults.
Methods
We conducted a cross-sectional study of 160 community-dwelling older adults. Ginseng intake was assessed through structured interviews, and serum zinc levels were measured by inductively coupled plasma-mass spectrometry. Cognitive function, focusing on delayed episodic memory (an early AD-related marker) and non-memory cognition, was assessed using the Korean version of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD-K) neuropsychological battery. Multiple linear regression analyses were conducted to evaluate independent predictors.
Results
Ginseng intake was significantly associated with higher serum zinc levels (P = 0.002) and better delayed episodic memory (P = 0.005). Higher serum zinc levels were also significantly associated with better delayed episodic memory (P = 0.023) in separate regression models. However, in a simultaneous model including both ginseng and serum zinc, ginseng intake remained a significant independent predictor of delayed episodic memory (P = 0.017), whereas the association between zinc and memory was attenuated.
Conclusion
Ginseng intake was associated with better AD-related memory in older adults and may be related to the zinc pathway as an upstream factor. These findings suggest that ginseng may be associated with higher zinc bioavailability while also showing associations with memory that appear independent of zinc homeostasis, supporting its potential value as a nutritional strategy for maintaining cognitive function in early AD.
Keywords: Ginseng, Zinc, Delayed episodic memory, Alzheimer's disease, Cognition
Graphical abstract
1. Introduction
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that represents a growing global health burden [1]. Despite ongoing advances in therapeutics, effective preventive strategies remain essential, particularly those targeting modifiable lifestyle factors including nutrition [2]. Decline in delayed episodic memory represents one of the earliest and most specific cognitive hallmarks of AD pathology and often precedes broader cognitive and functional deterioration by several years [[3], [4], [5], [6], [7], [8]]. Accordingly, identifying nutritional factors associated with preservation of delayed episodic memory in older adults may have important implications for early prevention of AD.
Panax ginseng, a widely consumed herbal medicine in East Asia, has garnered significant attention for its neuroprotective potential [9]. Prior studies, including our own, have suggested that regular ginseng intake shows a positive association with cognitive performance, particularly in AD-related domains such as delayed episodic memory [10,11]. However, the biological basis for this association remains incompletely understood. Although antioxidant and anti-inflammatory properties have been proposed, it remains unclear whether ginseng influences cognition directly via neuronal mechanisms or indirectly by modulating metabolic or nutritional pathways [12,13].
Zinc is a strong candidate nutritional factor in this context. It functions as an important neuromodulator in the brain, especially within the hippocampus—a region central to memory consolidation and highly vulnerable to AD pathology [14,15]. In parallel, our previous neuroimaging study demonstrated a significant link between reduced serum zinc concentrations and greater in vivo amyloid-beta (Aβ) deposition, a key pathological feature of AD [16]. However, maintaining optimal zinc status may be particularly challenging for older adults. Aging is frequently accompanied by a decline in systemic zinc levels, which has been attributed, at least in part, to impaired intestinal absorption [17]. In particular, expression of Zrt- and Irt-like protein 4 (ZIP4), a major transporter responsible for intestinal zinc uptake, has been reported to decrease with age [18].
Because age-related impairment in zinc absorption may limit the effectiveness of zinc intake alone, a physiological modulator that enhances zinc transport may be important for maintaining zinc homeostasis in older adults. Recent experimental findings suggest a potential biological link between ginseng and zinc metabolism. Ginsenosides have been reported to directly upregulate the expression of zinc transporters, such as ZIP4, in intestinal epithelial cells, thereby facilitating zinc influx and restoring intracellular zinc pools [19]. This suggests that ginseng may act as a bio-enhancer for zinc, potentially helping to improve zinc bioavailability in older adults.
Despite this biologically plausible link, clinical research integrating ginseng intake and zinc status remains scarce. Previous studies have largely examined ginseng [9] and zinc [20] separately, without addressing whether their associations with cognition are overlapping or independent. To our knowledge, no prior clinical investigation has examined whether the cognitive benefits of ginseng are mediated by, or independent of, serum zinc levels in older adults. Therefore, this study investigated the interrelationship among ginseng intake, serum zinc, and AD-related cognitive function in non-demented older adults. We aimed to determine whether ginseng intake and serum zinc levels show shared or independent associations on delayed episodic memory.
2. Materials and methods
2.1. Participants
This study is part of the General Lifestyle and Alzheimer's Disease (GLAD) study, an ongoing prospective cohort study initiated in 2020. As of September 2022, the present analysis included 160 non-demented older adults aged 65 to 90 years, comprising 93 cognitively normal (CN) adults and 67 with mild cognitive impairment (MCI). Recruitment was conducted among individuals attending a dementia screening program at the memory clinic of Hallym University Dongtan Sacred Heart Hospital, Hwaseong, Republic of Korea, who were subsequently invited for an eligibility assessment. Additional participants were enrolled from the community through referrals from other subjects, acquaintances, friends, or family members.
The CN group consisted of subjects with a Clinical Dementia Rating (CDR) [21] score of 0 and without a diagnosis of MCI or dementia. All participants in the MCI group met the current consensus criteria for amnestic MCI, including memory complaints confirmed by an informant, objective memory impairment, preservation of global cognitive performance, independence in functional activities, and the absence of dementia. In the objective memory impairment assessment, the age-, education-, and sex-adjusted z-score was < −1.0 on at least one of 4 episodic memory tests in the Korean version of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) neuropsychological battery [22,23]: Word List Memory (WLM), Word List Recall (WLR), Word List Recognition (WLRc), and the Constructional Recall (CR) test [[22], [23], [24]]. All MCI subjects had a CDR score of 0.5.
The exclusion criteria included major psychiatric disorders, significant neurological or medical illness, or a comorbidity likely to influence cognitive performance. Individuals with illiteracy, significant sensory impairments, or severe communication or behavioral difficulties that could interfere with evaluation were also excluded. Participants currently receiving investigational drugs were not included. The study protocol was approved by the Institutional Review Board of Hallym University Dongtan Sacred Heart Hospital and conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from all participants.
2.2. Clinical assessments
All participants underwent standardized clinical evaluations performed by psychiatrists with over 10 years of clinical experience, using an assessment framework that integrates the CERAD clinical and neuropsychological battery [22,23]. Neuropsychological assessment based on the CERAD neuropsychological battery [24] was administered by psychometrists who had received formal training. Cognitive performance was evaluated across both memory (delayed recall) and non-memory domains. The delayed episodic memory score (EMS), reflecting early AD-related cognitive change [[3], [4], [5], [6], [7], [8]], was calculated by summing the scores from three delayed memory tasks: WLR, WLRc, and CR. Non-memory cognition was assessed using a composite score derived from verbal fluency, the modified Boston Naming Test, and constructional praxis.
Vascular risk factors, including hypertension, diabetes mellitus, dyslipidemia, coronary heart disease, transient ischemic attack, and stroke, were identified through structured interviews conducted by trained psychometrists with both participants and informants. A vascular risk score (VRS) was calculated as the proportion of present risk factors relative to the total number assessed [25]. Information was cross-checked with reliable informants to improve accuracy.
2.3. Assessment of ginseng intake and other dietary patterns
Ginseng consumption was systematically assessed for all participants. Information collected included the type of ginseng (white or red ginseng in any formula containing ginseng extract), the age at which intake began, and intake frequency expressed as days per month [11]. Because the actual amount of ginseng varies across commercial products and precise quantification per item is rarely feasible, ‘ginseng intake' was operationally defined as follows: subtracting the age at initial ginseng intake from the age at study entry, adding 1 year to reflect the intake of the first year, and then multiplying the result by the annual intake, calculated by multiplying the number of days of ginseng intake in a month by 12 months [11].
2.4. Blood test
Venous blood samples were obtained from participants in the morning after an overnight fast. Serum albumin concentrations were measured using a Roche COBAS c702 analyzer with the manufacturer-provied reagents (Roche Diagnostics, Mannheim, Germany). Serum zinc levels were determined using inductively coupled plasma-mass spectrometry (ICP-MS) on a PerkinElmer ELAN DRC-e system (PerkinElmer, Waltham, MA, USA).
2.5. APOE genotyping
Whole blood was collected into EDTA-coated vacutainer tubes for DNA extraction. Genomic DNA was isolated using QIAamp DSP DNA Blood mini kits (QIAGEN, Hilden, Germany) on the QIAcube HT System (QIAGEN). Apolipoprotein E (APOE) genotyping was carried out using the Seeplex ApoE ACE Genotyping Kit (Seegene, Seoul, Korea) and the ProFlex PCR system (ThermoFisher Scientific, Waltham, MA, USA), following the manufacturers' protocols. PCR products were analyzed via capillary electrophoresis using the QIAxcel Advanced System (QIAGEN). Genotypes (ε2/ε2, ε2/ε3, ε2/ε4, ε3/ε3, ε3/ε4, or ε4/ε4) were determined based on the electrophoretic patterns. Participants carrying at least one ε4 allele were classified as APOE ε4 (APOE4)-positive.
2.6. Statistical analysis
Baseline demographic and clinical profiles were compared between ginseng consumers and non-consumers, with independent t-tests applied to continuous variables and chi-square or Fisher's exact tests used for categorical variables. To determine the independent and combined associations of ginseng intake and serum zinc with cognitive performance, we employed multiple linear regression analyses. Confounding factors were addressed through sequential adjustment: an unadjusted Model 1 and a fully adjusted Model 2, which controlled for age, sex, APOE4 carrier status, education level, clinical diagnosis, and VRS.
To explore the interrelationship between ginseng intake and serum zinc in relation to memory—specifically, whether their associations overlap or are independent—we adopted a comparative modeling approach:
-
1.
Separate Models: Ginseng intake and serum zinc levels were first analyzed in separate regression models to establish their individual associations with cognition.
-
2.
Simultaneous Model: Both variables were then entered simultaneously into the same fully adjusted model. We examined whether the association of serum zinc with memory was attenuated in the presence of ginseng intake. This comparison was intended as an exploratory analysis of attenuation rather than a formal test of causal hierarchy; persistence of the ginseng association together with attenuation of the zinc association would be consistent with ginseng carrying explanatory information that overlaps with, but also extends beyond, serum zinc.
All analyses were performed in SPSS version 28 (IBM Corp., Armonk, NY, USA). A two-sided P-value below 0.05 was considered statistically significant.
3. Results
3.1. Participant characteristics
The study participants comprised 160 older adults, consisting of 80 individuals in the ginseng intake group and 80 in the non-intake group. Detailed demographic and clinical characteristics are presented in Table 1. Nutritional status was adequate across the cohort, as reflected by serum albumin concentrations consistently exceeding the clinical malnutrition threshold (< 3.5 g/dL) [26].
Table 1.
Demographic and clinical characteristics of the participants according to ginseng intake status.
| Overall | No ginseng intake | Ginseng intake | P | |
|---|---|---|---|---|
| n | 160 | 80 | 80 | |
| Age, years | 72.53 (5.88) | 72.54 (6.27) | 72.51 (5.51) | 0.979a |
| Female, n (%) | 111 (69.38) | 54 (67.50) | 57 (71.25) | 0.607b |
| Education, years | 9.79 (4.44) | 9.33 (4.67) | 10.25 (4.18) | 0.189a |
| APOE4 positive, n (%) | 33 (20.63) | 17 (21.25) | 16 (20.00) | 0.845b |
| Clinical diagnosis, MCI, n (%) | 67 (41.88) | 37 (46.25) | 30 (37.50) | 0.262b |
| VRS | 23.54 (18.26) | 24.58 (17.18) | 22.50 (19.32) | 0.472a |
| MMSE | 25.66 (3.29) | 25.36 (3.61) | 25.95 (2.93) | 0.260a |
| Ginseng type, n (%) | — | |||
| red | 75 (46.88) | — | 75 (93.75) | |
| white | 5 (3.12) | — | 5 (6.25) | |
| Age at initiation of ginseng intake, years | — | — | 61.74 (10.55) | — |
| Duration of ginseng intake, years | — | — | 9.12 (9.37) | — |
| Serum zinc, μg/dL | 80.80 (11.31) | 78.16 (10.44) | 83.44 (11.59) | 0.003a |
| Malnutrition, n (%) | 0 (0.00) | 0 (0.00) | 0 (0.00) | — |
| Albumin, g/dL | 4.58 (0.26) | 4.57 (0.28) | 4.58 (0.24) | 0.831a |
| CERAD-K neuropsychological tests | ||||
| Delayed EMS | 19.83 (5.96) | 18.66 (6.43) | 21.00 (5.24) | 0.013a |
| NMS | 34.21 (6.34) | 33.78 (7.03) | 34.65 (5.59) | 0.385a |
Abbreviations: APOE4, apolipoprotein E ε4 allele; MCI, mild cognitive impairment; VRS, vascular risk score; MMSE, mini-mental state examination; CERAD-K, Korean version of the Consortium to Establish a Registry for Alzheimer's Disease; EMS, episodic memory score; NMS, non-memory score.
Data are expressed as mean (standard deviation), unless otherwise indicated.
Age at initiation and duration of ginseng intake are presented only among ginseng users, as these variables are not defined for non-users.
by student t-test.
by chi-square test.
3.2. Association of ginseng intake with cognitive function
The relationship between ginseng intake and cognitive performance was evaluated through multiple linear regression, controlling for age, sex, APOE4 carrier status, education, clinical diagnosis, and VRS. Greater ginseng intake was significantly associated with higher delayed episodic memory scores (β = 0.158, P = 0.005) compared to the non-intake group (Table 2, Table S1, Figs. 1A and 2A). In contrast, no significant association was observed between ginseng intake and non-memory cognition (β = 0.034, P = 0.579; Table 2). These findings suggest that the cognitive benefit of ginseng is specific to the AD-related memory domain.
Table 2.
Multiple linear regression analyses of the association between ginseng intake and cognition domains.
| Delayed EMS |
NMS |
|||
|---|---|---|---|---|
| β | P | β | P | |
| Model 1 | ||||
| Ginseng intake | 0.197 | 0.013 | 0.069 | 0.385 |
| Model 2 | ||||
| Ginseng intake | 0.158 | 0.005 | 0.034 | 0.579 |
Values are presented as standardized regression coefficients (β) and P-values. Abbreviations: APOE ε4, apolipoprotein E ε4 allele; EMS, episodic memory score; NMS, non-memory score; VRS, vascular risk score.
Model 1: Unadjusted model. Model 2: Adjusted for age, sex, APOE ε4 carrier status, education level, clinical diagnosis, and VRS.
Fig. 1.
Associations of ginseng intake and serum zinc level with delayed episodic memory in non-demented older adults. (A, B) Bar plots of adjusted means for (A) delayed episodic memory score (EMS) and (B) serum zinc level according to ginseng intake status; error bars indicate standard errors. (C) Partial regression plot of serum zinc level against delayed EMS, with both axes representing residuals. All values were adjusted for age, sex, APOE4 carrier status, education level, clinical diagnosis, and vascular risk score (VRS) (n = 160). Standardized regression coefficients (β) and P values are shown for each association. EMS, episodic memory score; VRS, vascular risk score.
Fig. 2.
Comparison of the associations among ginseng intake, serum zinc level, and delayed episodic memory. Path diagrams show these associations in (A) separate models, with ginseng intake and serum zinc level entered independently, and (B) a simultaneous model including both predictors. All models were adjusted for age, sex, APOE4 carrier status, education level, clinical diagnosis, and VRS (n = 160). Arrows represent statistical associations derived from multiple linear regression analyses, not proven causal pathways. Standardized regression coefficients (β) and P values are shown for each path. Solid arrows indicate significant associations (P < 0.05); dashed arrows, non-significant. EMS, episodic memory score; VRS, vascular risk score.
3.3. Comparative associations of ginseng intake and serum zinc with delayed episodic memory
To elucidate the interrelationship between ginseng, zinc, and memory, we performed comparative regression modeling. First, we examined the individual associations in separate models. Ginseng intake was significantly associated with higher serum zinc concentrations (β = 0.243, P = 0.002; Table 3, Table S1, Figs. 1B and 2A). Higher serum zinc concentrations were also significantly associated with better performance in delayed EMS (β = 0.119, P = 0.023; Table 4, Table S1, Figs. 1C and 2A) when analyzed without adjusting for ginseng. However, in the simultaneous multivariate model including both ginseng intake and serum zinc, ginseng intake remained significantly associated with delayed episodic memory (β = 0.139, P = 0.017; Table 5, Table S1, Fig. 2B), whereas the association between serum zinc and memory was attenuated and no longer significant (β = 0.073, P = 0.208; Table 5, Table S1, Fig. 2B) in the presence of ginseng.
Table 3.
Multiple linear regression analyses of the association between ginseng intake and serum zinc level.
| Serum zinc level |
||
|---|---|---|
| β | P | |
| Model 1 | ||
| Ginseng intake | 0.234 | 0.003 |
| Model 2 | ||
| Ginseng intake | 0.243 | 0.002 |
Values are presented as standardized regression coefficients (β) and P-values. Abbreviations: APOE ε4, apolipoprotein E ε4 allele; EMS, episodic memory score; NMS, non-memory score; VRS, vascular risk score.
Model 1: Unadjusted model. Model 2: Adjusted for age, sex, APOE ε4 carrier status, education level, clinical diagnosis, and VRS.
Table 4.
Multiple linear regression analyses of the association between serum zinc and cognition domains.
| Delayed EMS |
NMS |
|||
|---|---|---|---|---|
| β | P | β | P | |
| Model 1 | ||||
| Serum zinc | 0.175 | 0.014 | 0.120 | 0.096 |
| Model 2 | ||||
| Serum zinc | 0.119 | 0.023 | 0.052 | 0.367 |
Values are presented as standardized regression coefficients (β) and P-values. Abbreviations: APOE ε4, apolipoprotein E ε4 allele; EMS, episodic memory score; NMS, non-memory score; VRS, vascular risk score.
Model 1: Unadjusted model. Model 2: Adjusted for age, sex, APOE ε4 carrier status, education level, clinical diagnosis, and VRS.
Table 5.
Multiple linear regression analyses of the association between ginseng intake, serum zinc and cognition domains.
| Delayed EMS |
NMS |
|||
|---|---|---|---|---|
| β | P | β | P | |
| Model 1 | ||||
| Ginseng intake | 0.168 | 0.039 | 0.049 | 0.551 |
| Serum zinc | 0.090 | 0.268 | 0.110 | 0.179 |
| Model 2 | ||||
| Ginseng intake | 0.139 | 0.017 | 0.028 | 0.655 |
| Serum zinc | 0.073 | 0.208 | 0.072 | 0.265 |
Values are presented as standardized regression coefficients (β) and P-values. Abbreviations: APOE ε4, apolipoprotein E ε4 allele; EMS, episodic memory score; NMS, non-memory score; VRS, vascular risk score.
Model 1: Unadjusted model. Model 2: Adjusted for age, sex, APOE ε4 carrier status, education level, clinical diagnosis, and VRS.
4. Discussion
The present study demonstrated that regular ginseng intake was significantly associated with better performance in delayed episodic memory, a specific cognitive marker for early AD-related decline. A key finding is the different pattern of association between ginseng intake and serum zinc in relation to memory. In our multivariate analysis, the association between serum zinc and memory was substantially attenuated when ginseng intake was taken into account, whereas ginseng intake remained significantly and independently associated with delayed episodic memory. This pattern may suggest that the association of serum zinc with memory overlaps in part with that of ginseng intake. Ginseng may therefore be associated with better zinc status while also showing associations with memory that appear at least partly independent of the zinc pathway, although these interpretations warrant confirmation in longitudinal and mechanistic studies.
The observation that ginseng intake was associated with higher serum zinc levels is central to interpreting this ‘shared channel’. Aging is frequently accompanied by a decline in the efficiency of intestinal micronutrient absorption, which can contribute to systemic zinc deficiency even when dietary intake is sufficient [18,27]. Ginseng may help counteract this age-related reduction by supporting intestinal zinc absorption. This interpretation is consistent with recent mechanistic evidence showing that ginsenosides have been shown to upregulate the expression of the zinc transporter ZIP4 in the intestinal epithelium [19]. By facilitating the influx of zinc into the systemic circulation, ginseng may help restore the zinc pool required for neuronal function. Thus, the attenuation of the zinc effect in the combined model may, in part, reflect a role of ginseng in supporting the zinc pathway. However, this attenuation should be interpreted with caution and does not establish a causal or hierarchical relationship, as it may also reflect overlapping information between ginseng intake and serum zinc.
In addition to this shared pathway, the finding that ginseng retained its independent association with memory indicates that its relationship with memory may extend beyond the zinc pathway. Apart from zinc-related effects, such as modulating synaptic plasticity and long-term potentiation via zinc release [14,15], ginseng may also act through several zinc-independent mechanisms well documented in the experimental literature. Ginsenosides, particularly Rg1 and Rb1, enhance hippocampal neurotrophic signaling through the CREB–BDNF pathway, thereby promoting neurogenesis, synaptogenesis, and long-term potentiation relevant to episodic memory consolidation [12,13]. In parallel, they suppress microglia-mediated neuroinflammation, attenuate Aβ aggregation and tau hyperphosphorylation, and improve central cholinergic and cerebrovascular function—effects that operate independently of systemic zinc status [12,28,29]. Together, these convergent pathways provide a biologically plausible basis for the association of ginseng with memory that remained after adjustment for serum zinc. Ginseng intake may therefore be associated with better memory through both zinc-related and zinc-independent mechanisms.
It is noteworthy that these benefits were specific to delayed episodic memory and did not extend to non-memory cognition. This domain-specific pattern may be related to the particular vulnerability of the hippocampus to both zinc dyshomeostasis and AD-related pathology. The hippocampus contains a high density of zinc-containing neurons in the prosencephalon [14]. Accordingly, it may be particularly susceptible to functional impairment under conditions of zinc deficiency and may also be more responsive to the restoration of zinc homeostasis associated with ginseng intake [15]. This domain-specificity highlights the potential relevance of ginseng intake for early AD prevention, where hippocampal memory decline is a key feature.
This study has several strengths, including the novel integration of nutritional epidemiology with hierarchical regression modeling to elucidate the ‘Ginseng-Zinc-Cognition’ axis. Nevertheless, several limitations warrant consideration. First, because of the cross-sectional nature of this study, causality cannot be inferred. Longitudinal studies are required to determine whether ginseng intake temporally precedes an increase in serum zinc and subsequent cognitive preservation. Second, brain AD pathology biomarkers, such as Aβ or tau protein, were not assessed in this study. Future studies incorporating these biomarkers are needed to clarify the link between ginseng-induced metabolic optimization and AD pathology. Third, there was a possibility of recall bias regarding ginseng intake history. To mitigate this, ginseng intake was assessed using intensive face-to-face interviews by trained researchers rather than relying on self-administered questionnaires. In addition, data accuracy was cross-verified through informant interviews whenever feasible. Fourth, unmeasured supplement use is a genuine limitation, and firmly separating ginseng- and supplement-derived zinc is best addressed by future designs, either by matching ginseng consumers and non-consumers for supplement use or by enrolling non-users and examining longitudinally whether ginseng intake alone is associated with changes in serum zinc and memory. However, the association of ginseng intake with memory persisted after adjustment for serum zinc, a pattern not readily explained by supplement-derived zinc. Finally, the association of ginseng intake with cognition may vary depending on the dose of ginseng. While previous trials suggest that high-dose ginseng improves cognitive performance [30], accurate quantification in observational studies is challenging. Further clinical studies administering defined ginseng doses in older adult populations are needed to establish optimal intake guidelines.
Our findings provide a rationale for a potential combinational strategy in AD prevention. Given that aging may be accompanied by reduced zinc absorption related to downregulated transporters such as ZIP4, zinc supplementation alone may have limited efficacy in older adults. Our results raise the possibility that co-administration of ginseng could complement zinc supplementation. By potentially enhancing zinc absorption while also providing zinc-independent neuroprotection, ginseng may help improve the effectiveness of zinc in this population. Future clinical trials may therefore examine whether a ‘ginseng plus zinc’ combination approach offers benefits over zinc monotherapy. This approach could be particularly beneficial for non-demented older adults with low baseline zinc levels, offering a potential nutritional intervention to delay the onset of AD.
In conclusion, our study suggests that ginseng intake was associated with better AD-related cognitive function and may be related to the zinc pathway as an upstream factor. These findings are consistent with the hypothesis that ginseng could be associated with zinc bioavailability, potentially counteracting the age-related decline in zinc absorption, while its association with cognition may also involve mechanisms independent of zinc. From a preventive perspective, ginseng intake may represent a promising nutritional factor for cognitive health in older adults, although longitudinal studies are needed to confirm these associations in the earliest stages of AD.
Data availability statement
The study data are not freely accessible because the IRB of the Hallym University Dongtan Sacred Heart Hospital prevents public sharing of such data for privacy reasons. However, the data are available on reasonable request after IRB approval. Requests for data access can be submitted to an independent administrative coordinator by e-mail (yoon4645@gmail.com).
Ethics statement
This study protocol was approved by the institutional review board of the Hallym University Dongtan Sacred Heart Hospital (2020-12-004, 1 December 2020) and was conducted in accordance with the recommendations of the current version of the Declaration of Helsinki. The subjects or their legal representatives gave informed consent.
Funding
This study was supported by the grants from the Korean Society of Ginseng. The funding sources had no role in the study design, data collection, data analysis, data interpretation, writing of the manuscript, or decision to submit it for publication.
Declaration of competing interest
The authors have no conflict of interest to report.
Acknowledgements
We thank the GLAD study subjects and their caregivers.
Footnotes
Supplementary data to this article can be found online at https://doi.org/10.1016/j.jgr.2026.101119.
Appendix A. Supplementary data
The following is the Supplementary data to this article:
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The study data are not freely accessible because the IRB of the Hallym University Dongtan Sacred Heart Hospital prevents public sharing of such data for privacy reasons. However, the data are available on reasonable request after IRB approval. Requests for data access can be submitted to an independent administrative coordinator by e-mail (yoon4645@gmail.com).