Abstract
INTRODUCTION
This study aimed to determine the associations between parkinsonism and Parkinson's disease (PD) with cognitive impairment and dementia in a multi‐country cohort in Latin America, using data from the 10/66 Dementia Research Group.
METHODS
This population‐based prospective cohort study was conducted in six Latin American countries, including 11,321 participants 65 years of age or older living in urban and rural areas.
RESULTS
At baseline, the prevalence of cognitive impairment in people with parkinsonism and PD was 33% and 26%, respectively. Parkinsonism (odds ratio [OR] 2.2 [95% confidence interval [CI] 1.9–2.6] and PD (OR 1.9 [95% CI 1.4–2.4]) were individually associated with baseline cognitive impairment and incident dementia. The pooled sub‐hazard ratios for dementia in fixed‐effect meta‐analysis were 1.5 (95% CI 1.2–1.9) for parkinsonism and 1.5 (95% CI 1.0–2.2) for PD.
DISCUSSION
Parkinsonism and PD were cross‐sectionally associated with cognitive impairment and prospectively associated with incident dementia. These findings underscore the importance of routine screening for cognitive impairment in individuals with parkinsonism and PD, to facilitate early detection and intervention strategies that mitigate adverse outcomes.
Highlights
The present study is one of the first longitudinal investigations into the association of parkinsonism and Parkinson's disease (PD) with cognitive impairment and dementia incidence in Latin America.
Parkinsonism and PD showed strong cross‐sectional associations with cognitive impairment, with consistent estimates across countries, independent of demographic factors.
Parkinsonism and PD were linked to a significantly higher incidence of dementia over a 4‐year follow‐up period.
Findings emphasize the need for routine cognitive screening in Parkinsonism and PD.
Keywords: cognitive impairment, dementia, Latin America, Parkinson's disease, parkinsonism
1. BACKGROUND
Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder globally, contributing substantially to disability and mortality in aging populations, with ≈6.1 million cases reported in 2016. 1 Beyond its hallmark motor symptoms, PD frequently involves a wide spectrum of non‐motor symptoms, among which cognitive impairment is particularly prominent. 2 This is particularly relevant in Latin America, where demographic aging is accelerating and is projected to drive a marked increase in the prevalence of PD. 3 In this context, it is crucial to understand transitional states and the underlying factors that can lead to dementia in PD. 4
Cognitive impairment is up to six times more prevalent in individuals with PD than in healthy age‐matched populations, and it is recognized as one of the most significant non‐motor features of the disease, often associated with accelerated progression to dementia. 5 , 6 Longitudinal studies indicate that up to 80% of patients with PD will develop dementia over the disease course; however, little is known about the main risk factors and pattern of change of the cognitive deficits. 2 Understanding the association between PD and cognitive impairment is crucial for addressing the cognitive health challenges in aging populations. 7 , 8
This knowledge gap is particularly evident in studies involving Latino populations, who remain underrepresented in neurodegenerative research. Most evidence to date has originated from high‐income countries (HICs) and is often concentrated in specialized referral centers, which may not reflect population‐based estimates or capture the diversity of cognitive trajectories in broader, community‐dwelling cohorts. 8 Only a few studies from Latin America have reported on the prevalence and factors contributing to cognitive impairment in PD. 4 Despite growing recognition of this issue, determining the prevalence and incidence of cognitive impairment in PD patients in Latin America remains challenging. 9 , 10 The absence of comprehensive evidence hinders resource allocation, treatment program development, and research studies aimed at fully understanding the impact of cognitive decline in this region. 1 , 11 High‐quality, context‐specific data are urgently needed to support individuals affected by PD in Latin America and to guide effective prevention and care strategies.
To date, no study has assessed the current status of cognitive impairment in people with PD and parkinsonism in a large population‐based study from multiple countries in Latin America using the same methodology. In this study, we analyzed data from an ≈4‐year prospective community‐based cohort to determine the prevalence of cognitive impairment in people with parkinsonism and PD and their association with incident dementia in people living in six Latin American countries.
2. METHODS
The present study was reported according to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) checklist for cohort studies (Table S1). 12
2.1. Data source
The primary analyses in this study focused on community‐dwelling participants 65 years of age or older, who were part of the 10/66 Dementia Research Group study. 13 The 10/66 study is a multinational longitudinal cohort of older adults 65 years of age or older from low‐ and middle‐income countries (LMICs). 14 The present study involved six Latin American countries: Cuba, Dominican Republic, Puerto Rico, Venezuela, Mexico, and Peru. All countries included data from urban catchment sites, whereas Mexico and Peru included both urban and rural catchment sites. The individuals included in the study provided written informed consent. 13
The protocol and cohort profile of the study are published elsewhere. 13 , 14 In brief, participants undertook the baseline phase survey between 2003 and 2008, which had a response rate ranging from 74% to 98%. The participants were followed up ≈4 years later, between 2007 and 2011, in the incidence phase. 13
2.2. Study sample
The present analysis included 10/66 study participants from the following Latin American countries: Cuba (n = 2905), Dominican Republic (n = 1888), Peru (n = 1906), Venezuela (n = 1386), Mexico (n = 1999), and Puerto Rico (n = 1606). The cross‐sectional analysis included 11,321 baseline participants, which excluded 1544 participants with incomplete data on parkinsonism/PD, mild cognitive impairment (MCI), and key covariates. Participants who were not lost to follow‐up and not cognitively impaired at baseline were included in the longitudinal analysis (n = 9552).
2.3. Measures
The 10/66 study was originally designed to assess the epidemiology and impact of dementia in LMICs; however, the study expanded to several other non‐communicable diseases. To achieve this, the survey obtained information on demographics, chronic diseases, disability, health service utilization, and socioeconomic status by trained research staff using standardized study protocols and procedures. 13 , 14 The relevant variables for this analysis are described below.
RESEARCH IN CONTEXT
Systematic review: We searched Medline (Ovid) for articles investigating the cross‐sectional and prospective associations of cognitive impairment and dementia in Latinos with parkinsonism and Parkinson's disease (PD), published from January 1990 to August 2024. Previous data in Latin America are scarce, with no published primary studies on this topic.
Interpretation: The present study is the first longitudinal study examining the association of parkinsonism and PD with cognitive impairment and the incidence of dementia in Latin America, which is also a less explored area in low‐ and middle‐income countries globally. We found that parkinsonism and PD were strongly associated with cognitive impairment cross‐sectionally, with generally similar estimates in individual countries and independent of demographic factors.
Future directions: Although no therapies are currently available to delay or prevent cognitive decline in PD, it remains crucial from a research perspective to identify individuals at risk before the onset of cognitive decline.
2.4. Definition of parkinsonism and Parkinson's disease
All participants underwent a structured interview, a physical and neurological examination, and an informant interview. This comprehensive assessment obtained data on self‐reported chronic diseases (e.g., stroke) and neurological symptoms and signs (e.g., tremors), facilitating the diagnosis of parkinsonism and PD. 13 , 14 A detailed description of the diagnostic algorithm of parkinsonism and PD adopted for this study was published previously. 9 In summary, parkinsonism was defined as the presence of bradykinesia plus at least one additional motor feature: rigidity, rest tremor, or postural instability, following the United Kingdom Parkinson's Disease Society Brain Bank diagnostic criteria. 15 , 16 Parkinson's disease was diagnosed as a subset of parkinsonism cases requiring the presence of bradykinesia and at least three supportive criteria, in addition to the exclusion of alternative diagnoses and the absence of atypical features. A comprehensive description of the diagnostic criteria can be found in Table S2.
2.5. Definition of cognitive impairment and dementia
Cognitive impairment was defined as meeting the criteria for MCI and/or dementia for this analysis. Mild cognitive impairment was diagnosed according to the criteria of Petersen et al. for MCI. In summary, MCI was operationalized to include: (1) objective cognitive impairment beyond what is expected for age, determined using composite scores from cognitive assessments; (2) subjective cognitive complaints based on participant responses; (3) no or minimal impairment in activities of daily living (ADLs); and (4) absence of dementia confirmed by diagnostic criteria. Detailed descriptions of the assessments and operationalization are provided in the 10/66 Dementia Research Group study methodology. 10 Dementia was diagnosed using the cross‐culturally validated 10/66 dementia diagnosis algorithm, for which strong concurrent and predictive validity has been demonstrated. 14 , 17 , 18 Dementia diagnoses were established following (1) a structured clinical interview; (2) a cognitive test battery including (a) the Community Screening Instrument for Dementia (CSI‐D) (b) a semantic verbal fluency task, and (c) the modified Consortium to Establish a Registry for Alzheimer's Disease (CERAD) 10‐word list learning task with delayed recall; and (3) an informant interview (CSI‐D) for evidence of cognitive and functional decline. 13 , 18 , 19
2.6. Covariates
The following covariates were included in the analysis: age (years), sex (male or female), educational level (none, incomplete primary, completed primary, secondary, or tertiary), and number of physical illnesses (categorized as none, one to two, or three or more). Physical illnesses were drawn from a list of nine conditions: arthritis or rheumatism; persistent cough; breathlessness or asthma; high blood pressure; heart trouble or angina; stomach or intestinal problems; faints or blackouts; paralysis or limb weakness; and skin disorders (e.g., pressure sores, leg ulcers). These illnesses were selected to capture a broad range of age‐related comorbidities that could influence cognitive and functional status.
Several conditions (e.g., arthritis, paralysis, heart trouble) are directly related to potential immobility, whereas others reflect general health burden. Skin disorders specifically were considered as markers of prolonged immobility. Number of household assets and level of care dependency were included to describe the study population and serve as indicators of socioeconomic status and overall health severity.
2.7. Statistical analysis
The present study analyzed data from the baseline and incidence phases of the 10/66 study. The baseline characteristics of participants were reported overall, by individual countries and cognitive status. The prevalence of cognitive impairment by parkinsonism and PD status at baseline was calculated overall and by age group (65–69, 70–74, 75–79, and ≥80 years).
The baseline cross‐sectional associations between parkinsonism or PD and cognitive impairment were assessed using logistic regression models. Logistic regression models were adjusted for age, sex, and education. Models were fitted separately for each country and combined via a fixed effect meta‐analysis, and estimates were illustrated in a forest plot.
TABLE 1.
Cohort characteristics at baseline, overall, and by individual country.
| Baseline characteristics | Cuba (n = 2564) | Dominican Republic (n = 1876) | Peru (n = 1897) | Venezuela (n = 1381) | Mexico (n = 1998) | Puerto Rico (n = 1605) |
Overall (n = 11321) |
|---|---|---|---|---|---|---|---|
| Age, years, mean (SD) | 75.1 (7.1) | 74.9 (7.3) | 74.8 (7.4) | 72.3 (6.6) | 74.3 (6.7) | 76.1 (7.3) | 74.7 (7.1) |
| Sex | |||||||
| Male | 926 (36.1) | 645 (34.4) | 730 (38.5) | 500 (36.2) | 735 (36.8) | 518 (32.3) | 4054 (35.8) |
| Female | 1638 (63.9) | 1231 (65.6) | 1167 (61.5) | 881 (63.8) | 1263 (63.2) | 1087 (67.7) | 7267 (64.2) |
| Marital status | |||||||
| Never married | 239 (9.3) | 132 (7.0) | 209 (11.0) | 131 (9.5) | 105 (5.3) | 103 (6.4) | 919 (8.1) |
| Married/cohabiting | 1153 (45.0) | 561 (29.9) | 1084 (57.1) | 676 (49.0) | 1007 (50.4) | 798 (49.7) | 5279 (46.6) |
| Widowed | 780 (30.4) | 736 (39.2) | 515 (27.1) | 401 (29.0) | 763 (38.2) | 516 (32.1) | 3711 (32.8) |
| Divorced/separated | 392 (15.3) | 447 (23.8) | 89 (4.7) | 173 (12.5) | 123 (6.2) | 188 (11.7) | 1412 (12.5) |
| Education level | |||||||
| None | 66 (2.6) | 372 (19.8) | 119 (6.3) | 113 (8.2) | 554 (27.7) | 59 (3.7) | 1283 (11.3) |
| Some, did not complete primary | 558 (21.8) | 961 (51.2) | 230 (12.1) | 298 (21.6) | 862 (43.1) | 282 (17.6) | 3191 (28.2) |
| Completed primary | 837 (32.6) | 348 (18.6) | 720 (38.0) | 708 (51.3) | 350 (17.5) | 336 (20.9) | 3299 (29.1) |
| Completed secondary | 670 (26.1) | 129 (6.9) | 508 (26.8) | 196 (14.2) | 124 (6.2) | 584 (36.4) | 2211 (19.5) |
| Tertiary (college) | 433 (16.9) | 66 (3.5) | 320 (16.9) | 66 (4.8) | 108 (5.4) | 344 (21.1) | 1337 (11.8) |
| Number of assets | |||||||
| First quartile—least assets | 365 (14.2) | 592 (31.6) | 151 (8.0) | 33 (2.4) | 375 (18.8) | 418 (26.0) | 1934 (17.1) |
| Second quartile | 855 (33.3) | 413 (22.0) | 1117 (58.9) | 898 (65.0) | 842 (42.1) | 0 (0.0) | 4125 (36.4) |
| Third quartile | 860 (33.5) | 693 (36.9) | 175 (9.2) | 0 (0.0) | 164 (8.2) | 1187 (74.0) | 3079 (27.2) |
| Fourth quartile—most assets | 484 (18.9) | 178 (9.5) | 454 (23.9) | 450 (32.6) | 617 (30.9) | 0 (0.0) | 2183 (19.3) |
| Number of illnesses | |||||||
| No illnesses | 1,136 (44.3) | 571 (30.4) | 865 (45.6) | 575 (41.6) | 831 (41.6) | 583 (36.3) | 4561 (40.3) |
| One to two illnesses | 1,165 (45.4) | 890 (47.4) | 771 (40.6) | 500 (36.2) | 824 (41.2) | 680 (42.4) | 4830 (42.7) |
| Three or more illnesses | 263 (10.3) | 415 (22.1) | 261 (13.8) | 306 (22.2) | 343 (17.2) | 342 (21.3) | 1930 (17.0) |
| Dependency (need for care) | |||||||
| Much of the time | 162 (6.3) | 77 (4.1) | 82 (4.3) | 30 (2.2) | 86 (4.3) | 110 (6.9) | 547 (4.8) |
| Some of the time | 91 (3.5) | 85 (4.5) | 75 (4.0) | 72 (5.2) | 109 (5.5) | 85 (5.3) | 517 (4.6) |
| Does not need care | 2311 (90.1) | 1714 (91.4) | 1740 (91.7) | 1279 (92.6) | 1803 (90.2) | 1410 (87.9) | 10257 (90.6) |
| Disease status | |||||||
| A. Parkinsonism | 159 (6.2) | 192 (10.2) | 139 (7.3) | 84 (6.1) | 178 (8.9) | 138 (8.6) | 890 (7.9) |
| A.1‐ Parkinsonism and cognitive impairment | 35 (42.7) | 50 (33.1) | 32 (29.0) | 14 (24.6) | 45 (32.8) | 39 (35.4) | 215 (33.2) |
| B. Parkinson's Disease (PD) | 95 (3.7) | 46 (2.5) | 38 (2.0) | 37 (2.7) | 50 (2.5) | 32 (2.0) | 298 (2.6) |
| B.1‐ PD and cognitive impairment | 30 (31.6) | 9 (19.6) | 8 (21.1) | 7 (18.9) | 12 (24.0) | 12 (37.5) | 78 (26.2) |
| C. Cognitive Impairment | 386 (15.1) | 254 (13.5) | 243 (12.8) | 104 (7.5) | 304 (15.2) | 290 (18.1) | 1581 (14.0) |
Data are n (%) unless indicated otherwise.
Next, we conducted a time‐to‐event analysis to examine the associations between parkinsonism and dementia, as well as PD and dementia, while accounting for dementia‐free death as a competing risk event. The event of interest was the onset of dementia, defined as the time from interview to the date of dementia onset, here assumed to be the midpoint between the baseline examination and the follow‐up examination or postmortem interview. For those participants who did not develop dementia during follow‐up, person‐years were calculated from the baseline examination to either the date of death in persons deceased without dementia or the time of the follow‐up interview in those people who did not develop dementia. Given the competing risk of death without dementia, we employed Fine and Gray's proportional sub distribution hazards model 20 to estimate sub‐hazard ratios (sHRs). This approach allowed us to account for the possibility that some participants died before developing dementia, which could otherwise bias traditional survival analyses. In this framework, dementia‐free death does not lead to simple right‐censoring but is instead treated as a competing risk, influencing the probability of dementia occurrence over time. To assess the proportionality assumption, we tested time interactions for all covariates. The results indicated no violation of the proportional sub‐hazards assumption.
Competing risk models were run separately in each site and then pooled together by fixed‐effect meta‐analysis, using inverse‐variance weighting together with an estimation of heterogeneity using the Higgins I2. Higgins I2 was computed to estimate the proportion of between‐site variability in the estimates accounted for by heterogeneity as opposed to sampling error (up to 40% heterogeneity is conventionally considered negligible, whereas up to 60% reflects moderate heterogeneity). The first model was unadjusted; the second model adjusted for age, gender, and education level; and the third model adjusted for age, gender, education level, and number of physical illnesses.
Statistical significance was defined as a p‐value < 0.05 (two‐tailed) in all analyses. Analyses were carried out in Stata SE 18 and R Studio 4.3. The corresponding analytic code can be accessed by contacting the corresponding author.
3. RESULTS
3.1. Cohort characteristics
The 10/66 cohort included 12,865 participants aged ≥65 years living in Latin America. Excluding incomplete data on parkinsonism/PD, MCI, and key covariates (Figure S1) at baseline, the total number of participants for analysis was 11,321. The mean age (SD) of this cohort was 74.7 (± 7.1) years and 36% were male (Table 1). Most participants were married or cohabitating (47%), and most completed some level of primary education (29%), had one or two illnesses (43%), and were not dependent on any care need (91%). The prevalence of parkinsonism and PD was 7.9% (n = 890) and 2.6% (n = 298), respectively. The number of participants included in each country ranged from 1897 (Peru) to 2564 (Cuba). Demographic factors were largely similar across countries but there was some variation in clinical factors. For instance, the prevalence of parkinsonism ranged from 6.1% (Venezuela) to 10.2% (Dominican Republic) and the prevalence of PD ranged from 2% (Puerto Rico) to 3.7% (Cuba). The overall prevalence of cognitive impairment was 14.0% (n = 1581; Cuba = 15.1%, Dominican Republic = 13.5%, Peru = 12.8%, Venezuela = 7.5%, Mexico = 15.2%, and Puerto Rico = 18.1%). Baseline differences between participants who were followed and those lost to follow‐up are summarized in Table S3. Participants who were lost to follow‐up had similar age and gender distributions but differed significantly in marital status, education level, number of illnesses, and level of dependency compared to those who completed follow‐up.
Characteristics of the baseline participants by cognitive impairment status are shown in Table S4. The overall prevalence of cognitive impairment in the baseline participants was 14%. The mean age of the participants with cognitive impairment was higher as compared to participants with no cognitive impairment (78.5 vs 74.1 years, p < 0.001). The majority of the participants with cognitive impairment were either married/cohabiting or widowed, and nearly one‐third of the participants with cognitive impairment did not complete primary education. Nearly 44% of the participants with cognitive impairment lived with one to two illnesses.
The prevalence of cognitive impairment in participants with parkinsonism and PD was 33.2% and 26.2%, respectively. In terms of age group (Figure 1), the prevalence of cognitive impairment in both parkinsonism and PD was highest in participants 80 years of age or older, 34.9% and 39.8%, respectively.
FIGURE 1.
Prevalence of cognitive impairment by parkinsonism and Parkinson's disease (PD) status and age group at baseline. Figure shows the percentage of individuals with and without cognitive impairment among those diagnosed with parkinsonism and PD, stratified by age group (65–69, 70–74, 75–79, ≥80 years). For each diagnostic category, the distribution of cognitive impairment and non–cognitive impairment cases is presented as a proportion of the total within that group.
3.2. Cross‐sectional associations between parkinsonism, Parkinson's disease, and cognitive impairment
In logistic regression models adjusted for age, sex, education level, and number of physical illnesses, parkinsonism (Figure 2A) and PD (Figure 2B) were strongly associated with cognitive impairment. The pooled odds ratio (OR) from the meta‐analysis for cognitive impairment in parkinsonism cases was 2.19 (95% confidence interval [CI]: 1.9–2.6) and for PD cases was 1.85 (95% CI: 1.4–2.4). Individual country analyses generally reported similar associations, with the strongest association being in Venezuela, with 2.90 (95% CI: 1.5–5.3). The OR for cognitive impairment in PD cases was 1.85 (95% CI: 1.4–2.4). Individual country analyses generally reported varied associations by country, with Dominican Republic showing the weakest association at 1.2 (95% CI: 0.6–2.5), and Puerto Rico the strongest at 2.4 (95% CI: 1.1–5.2).
FIGURE 2.
Odds ratios (95% confidence intervals [CIs]) of the cross‐sectional association between parkinsonism (A), Parkinson's disease (B), and cognitive impairment in baseline participants.
3.3. Prospective associations between parkinsonism, Parkinson's disease, and dementia
Dementia‐free follow‐up status of the participants is described by country in Table S5. In summary, follow‐up outcomes varied across the 10/66 Latin American cohort. The percentage of participants interviewed ranged from 60.5% in the Dominican Republic to 75.2% in Cuba. Incident dementia rates varied from 5.8% in Peru to 11.5% in the Dominican Republic and Venezuela. Median follow‐up times ranged from 3.0 years in Mexico and Peru to 5.0 years in the Dominican Republic.
In competing risk models, both parkinsonism and PD at baseline were associated with incident dementia after different levels of adjustment for age, sex, education level, and number of illnesses (Table 2). In the pooled meta‐analysis, participants with parkinsonism had a 2.3 times higher sHR of developing dementia during the follow‐up period (sHR 2.3, 95% CI: 1.9–2.8, I2 0.0%), compared to participants without parkinsonism (Table 2). This association was attenuated after adjusting for potential confounders, including age, sex, education level, and number of physical illnesses, with a fully adjusted sHR of 1.5. The association remained after adjusting for potential confounders (pooled fully adjusted sHR 1.5, 95% CI: 1.2–1.9). The hazard estimates varied between the study sites. Peru (sHR 1.9, 95% CI: 1.0–3.7) and Venezuela (sHR 1.9, 95% CI: 1.0–3.6) had the highest sHR, whereas Mexico (sHR 1.3, 95% CI: 0.7–2.2) and Puerto Rico (sHR 1.3, 95% CI: 0.8–2.6) had the lowest observed estimations (adjusted for age, sex, education level, and number of illnesses). PD was associated with a 1.5 times increased risk of developing dementia (95% CI: 1.0–2.2, I2 14.4%) in the pooled meta‐analysis adjusted for age, sex, education level, and number of illnesses (Table 2). Site‐specific analysis showed the highest sHR in Venezuela (sHR 3.3, 95% CI: 1.6–6.7) and the lowest in Peru (sHR 0.5, 95% CI: 0.1–3.7).
TABLE 2.
Sub‐hazard ratios for incident dementia in persons with Parkinsonism and PD at baseline.
| Country | Model 1 b | Model 2 c | Model 3 d |
|---|---|---|---|
| Parkinsonism | |||
| Cuba | 2.1 (1.2–3.5) | 1.4 (0.8–2.5) | 1.4 (0.8–2.4) |
| Dominican Republic | 2 (1.3–3.1) | 1.5 (0.9–2.4) | 1.5 (0.9–2.5) |
| Peru | 2.8 (1.5–5.1) | 2.1 (1.1–4.0) | 1.9 (1.0–3.7) |
| Venezuela | 3.3 (2–5.6) | 2 (1.2–3.6) | 1.9 (1.0–3.6) |
| Mexico | 1.8 (1.1–3.1) | 1.3 (0.8–2.2) | 1.3 (0.7–2.2) |
| Puerto Rico | 2.3 (1.4–3.8) | 1.4 (0.8–2.5) | 1.3 (0.8–2.6) |
| Pooled sHR a | 2.3 (1.9–2.8) | 1.6 (1.3–2.0) | 1.5 (1.2–1.9) |
| Parkinson's disease | |||
| Cuba | 2.1 (1.1–4.1) | 1.7 (0.9–3.4) | 1.7 (0.9–3.4) |
| Dominican Republic | 1.0 (0.4–2.8) | 0.9 (0.3–2.5) | 0.9 (0.3–2.6) |
| Peru | 0.6 (0.1–4.5) | 0.5 (0.1–3.8) | 0.5 (0.1–3.7) |
| Venezuela | 4.6 (2.4–8.8) | 3.3 (1.6–6.8) | 3.3 (1.6–6.7) |
| Mexico | 1.2 (0.4–3.8) | 1.1 (0.4–3.5) | 1.2 (0.4–3.6) |
| Puerto Rico | 1.4 (0.5–4.2) | 1.0 (0.3–3.0) | 1.2 (0.3–3.1) |
| Pooled sHR |
2.1 (1.5–3.0) I2 = 54.5% |
1.6 (1.1–2.3) I2 = 34.9% |
1.5 (1.0–2.2) I2 = 14.4% |
I2 = 0.0% for all the models.
Model 1 = unadjusted.
Model 2 = adjusted for age, sex, and education.
Model 3 = adjusted for age, sex, education, and number of physical illnesses.
4. DISCUSSION
4.1. Summary of findings
This multinational, community‐based cohort study provides current estimates of cognitive impairment among individuals with parkinsonism and PD, and examines its longitudinal association with dementia incidence across six Latin American countries. We found that cognitive impairment was highly prevalent among individuals with parkinsonism (33%) and PD (26%) compared to 14% in the overall sample. Both parkinsonism and PD were strongly associated with cognitive impairment cross‐sectionally, with consistent estimates across individual countries and independent of demographic factors. Older adults with parkinsonism had a 1.9‐ to 2.6‐fold higher likelihood of cognitive impairment, whereas those with PD had a 1.4‐ to 2.4‐fold higher risk compared to non‐cases. Furthermore, both parkinsonism and PD predicted a significantly increased incidence of dementia over a median 4‐year follow‐up. To our knowledge, this is the first longitudinal population‐based study assessing the association between parkinsonism, PD, and cognitive impairment and subsequent dementia risk in Latin America.
4.2. Comparison with previous literature
The timing, profile, and rate of cognitive decline in PD vary widely, ranging from normal cognition to dementia. 21 At the time of PD diagnosis, cognitive impairment prevalence is estimated to range between 20% and 42%; however, as disease progresses, cognitive impairment becomes increasingly common, with up to 50% of patients developing some form of cognitive impairment over time. 21 , 22 , 23 , 24 , 25
A meta‐analysis by Baiano et al. (2020) reported a global prevalence of MCI in PD of 40%. 23 In contrast, our study found a lower cognitive impairment prevalence (26%), despite being defined to include both MCI and dementia. Given this broader definition, one might expect our prevalence to be higher than in studies assessing MCI or dementia alone. The observed discrepancy may be attributable to two key methodological factors. First, our population‐based sample likely includes individuals at earlier stages of PD, before cognitive deficits are clinically apparent. However, as we lacked measures of disease severity or duration, we are unable to confirm this hypothesis. Future studies should explicitly assess disease stage to elucidate this further. Second, nearly 90% of the studies included in Baiano's meta‐analysis were conducted in clinical settings, where patients often present with more advanced disease or greater symptom burden, leading to higher reported cognitive impairment rates. In contrast, our study drew from community‐dwelling samples in six Latin American countries, reducing the risk of selection bias and enabling the inclusion of milder or undiagnosed cases.
These methodological differences likely account for the lower cognitive impairment prevalence in our study. As such, direct comparisons across studies should be interpreted cautiously, taking into account differences in disease duration, assessment methods, and cohort setting. 26 , 27 , 28 , 29 , 30 Overall, both the prevalence and strength of association between cognitive impairment, parkinsonism, and PD appear to vary significantly depending on study design, with higher estimates typically seen in hospital‐based cohorts and in samples including more advanced disease. 31 , 32 , 33
In terms of dementia risk, our pooled meta‐analysis found that PD was associated with a 1.5‐fold increased risk of developing dementia (95% CI: 1.0–2.2) over an ≈4‐year follow‐up. Although this association reached statistical significance in the pooled sample, individual country analyses revealed variability in effect size and significance. This heterogeneity may reflect differences in local health care infrastructure, diagnostic practices, or sociodemographic factors. Future research should account for these factors and prioritize larger, more representative country‐specific samples to validate these findings.
As PD progresses, the risk of dementia increases significantly—up to 6‐fold compared to the general population—with the most pronounced risk observed in those manifesting PD cognitive impairment. 31 , 34 For example, at the time of PD diagnosis, 15%–40% of patients meet the criteria for PD cognitive impairment, 32 , 35 a proportion that escalates to 20%–57% within 3 to 5 years. 36 , 37 In our cohort, individuals with PD had more than twice the risk of cognitive impairment compared to those without PD, and this association was consistent across countries.
Few longitudinal studies have examined dementia in PD, although evidence suggests that most patients who survive will develop dementia. 38 , 39 Currently, the majority of individuals affected by dementia live in LMICs, with projections indicating that these nations will experience the most accelerated surge in dementia cases over the forthcoming decades. 40 , 41 , 42 Longitudinal cohort studies can produce a more accurate estimate of the risk of dementia in PD because of their prospective nature and relative freedom from survival bias. 43 For instance, in a United Kingdom ‐based prospective study, the incidence of dementia after 5 years was 17.5 per 1000 person‐years, and by age ≥70 years, the incidence of dementia was 39.7 per 1000 person‐years. 44 In another prospective study from the United Kingdom and Taiwan, the incidence of dementia was six times higher in patients with PD than in controls. 43 , 45
In our study, the cumulative risk of incident dementia exceeded 50% among PD cases across all six countries. These findings are consistent with observations from HICs such as the Netherlands, Spain, and France, while also providing novel insights into underrepresented populations in Latin America. 46 The limited availability of robust data from LMICs complicates cross‐national comparisons and underscores the need for more inclusive global research.
In addition, it is important to note that direct comparisons with data from HICs may be challenging due to differences in diagnostic definitions and cognitive assessments across studies, reinforcing the need for harmonized and culturally sensitive diagnostic criteria in global neuroepidemiology.
4.3. Implications for clinical practice and research
Accurate identification and monitoring of cognitive impairment in individuals with PD can pose significant challenges, particularly due to overlapping motor and cognitive symptoms, the influence of dopaminergic therapy, and the difficulty in attributing functional decline solely to cognitive impairment. 47 , 48 Information on long‐term clinical outcomes in PD is not only of significant importance to the patient and their caregivers but also for identifying potential modifiable factors that could potentially halt or slow clinical progression. 49 Findings of our study indicate a strong association of parkinsonism and PD with cognitive impairment and subsequent dementia, even after adjusting for age, sex, education, and comorbidities. This highlights the importance of parkinsonism and PD as independent risk factors for cognitive decline. 50 Overall, our results emphasize the need for comprehensive cognitive screening and monitoring in patients with PD, even in the early stages, and especially in LMICs where such practices are less common.
4.4. Strength and limitations
Our study has several strengths. First, there are few large‐scale cohort studies investigating the relationship between PD and cognitive impairment; thus we provide first‐hand evidence on the cross‐sectional association between PD and cognitive impairment and incident dementia in Latin America. Second, assessments were conducted using a harmonized protocol and structured interview specifically designed for older populations, which enhances cross‐country comparability by minimizing variations that arise from the use of different clinical–cognitive assessment methods across populations. In addition, the large sample size enhances the significance of our findings, particularly in this understudied population. However, some limitations must be acknowledged. First, the use of self‐reported measures and clinical–cognitive assessments conducted by general clinicians or trained interviewers may introduce underreporting, misclassification, and selection bias. Previous studies have shown that the accuracy of parkinsonism and PD diagnoses is higher when assessed by movement disorder specialists compared to general clinicians, which may have influenced diagnostic precision in this study. Similarly, in a longitudinal population‐based study, it is also subject to selection bias, particularly due to differential non‐response associated with factors such as economic status and education, potentially leading to an underestimation of prevalence estimates. Second, we observed distinct patterns of loss to follow‐up that may have introduced bias in different directions. Participants lost due to death tended to have greater illness burden and dependency at baseline, which may have led to underestimation of dementia incidence. In contrast, those lost due to refusal or inability to contact had baseline profiles similar to those retained and may include healthier individuals who relocated or deprioritized participation, potentially introducing a healthy volunteer bias. These differential attrition patterns should be considered when interpreting longitudinal findings. Third, our study lacked data on disease duration at baseline or measurements of disease severity; consequently, the frequency of cognitive impairment might be higher in individuals with longer disease duration, who are also more likely to progress to dementia during the follow‐up period. Finally, given the observational nature of the study, the causal nature of the relationship cannot be inferred.
Overall, although no therapies are currently available to delay or prevent cognitive decline in PD, it remains crucial from a research perspective to identify individuals at risk before the onset of cognitive decline. Early identification and characterization of cognitive decline trajectories in these groups will be essential to inform targeted interventions and the development of evidence‐based strategies aimed at mitigating or delaying the transition from cognitive impairment to dementia in PD.
CONFLICT OF INTEREST STATEMENT
The authors declare that there are no additional disclosures or conflicts of interest to report. Author disclosures are available in the Supporting Information.
CONSENT STATEMENT
Written informed consent was obtained from all participants and their study partners. This project was approved by local institutional review boards and the King's College London Research Ethics Committee. The full protocol for the 10/66 population‐based surveys is available in an open‐access publication.
Supporting information
Supporting Information
Supporting Information
ACKNOWLEDGMENTS
This is a secondary analysis of data collected by the 10/66 Dementia Research Group. We extend our deepest gratitude to all the participants and families who dedicated their time and effort to our research project. We thank the principal investigators, data custodians, and responsible parties for research governance at each site including Martin Prince (United Kingdom), Juan Llibre Rodriguez (Cuba), Daisy Acosta (Dominican Republic), Mariella Guerra (Peru), Aquiles Salas (Venezuela), Ana Luisa Sosa (Mexico), K.S. Jacob (Vellore, India), Joseph D. Williams (Chennai, India), Ivonne Jimenez (Puerto Rico), and Yueqin Huang (China). The 10/66 Dementia Research Group's research has been supported by funding from the Wellcome Trust Health Consequences of Population Change Programme (GR066133 – Prevalence phase in Cuba and Brazil; GR080002 – Incidence phase in Peru, Mexico, Argentina, Cuba, Dominican Republic, Venezuela, and China), the World Health Organization (India, Dominican Republic, and China), the Alzheimer's Association (IIRG‐04‐1286; 24HPE‐1287320; ALZSI‐25‐1464205), the Puerto Rico State Legislature (Puerto Rico), and FONACIT/CDCH/UCV (Venezuela). The study also has funding from the European Research Council (ERC‐2013‐ADG 340755 LIFE2YEARS1066). Secondary data analysis on parkinsonism and Parkinson's disease in 10/66 Latin American countries is supported by the Michael J. Fox Foundation (MJFF‐020770). The content is solely the responsibility of the authors and does not represent the official views of the funders.
Khan N, Arruabarrena MM, Kim DJ, et al. Cognitive impairment and dementia in Latin American individuals with parkinsonism and Parkinson's disease: A 10/66 Dementia Research Group study. Alzheimer's Dement. 2025;21:e70371. 10.1002/alz.70371
[Correction added on August 14, 2025, after first online publication: The name of the 16th author of this paper was misspelled and has been corrected from ‘Christina Jeyachandran’ to ‘Christine Jeyachandran’].
REFERENCES
- 1. Feigin VL, Krishnamurthi RV, Theadom AM, et al. Global, regional, and national burden of neurological disorders during 1990‐2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet Neurol. 2017;16:877‐897. doi: 10.1016/S1474-4422(17)30299-5 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. Geurtsen GJ, Hoogland J, Goldman JG, et al. Parkinson's disease mild cognitive impairment: application and validation of the criteria. J Parkinsons Dis. 2014;4:131. doi: 10.3233/JPD-130304 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3. Kim DJ, Isidro‐Pérez AL, Doering M, et al. Prevalence and incidence of Parkinson's disease in Latin America: a meta‐analysis. Mov Disord. 2024;39:105‐118. doi: 10.1002/MDS.29682 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Ribeiro FS, Teixeira‐Santos AC, Leist AK. The prevalence of mild cognitive impairment in Latin America and the Caribbean: a systematic review and meta‐analysis. Aging Ment Health. 2022;26:1710. doi: 10.1080/13607863.2021.2003297 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5. Aarsland D, Batzu L, Halliday GM, et al. Parkinson disease‐associated cognitive impairment. Nat Rev Dis Primers. 2021;7(1):47. doi: 10.1038/S41572-021-00280-3 [DOI] [PubMed] [Google Scholar]
- 6. Åström DO, Simonsen J, Raket LL, et al. High risk of developing dementia in Parkinson's disease: a Swedish registry‐based study. Sci Rep. 2022;12:1‐7. doi: 10.1038/s41598-022-21093-8 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7. Leroi I, McDonald K, Pantula H, Harbishettar V. Cognitive impairment in parkinson disease: impact on quality of life, disability, and caregiver burden. J Geriatr Psychiatry Neurol. 2012;25:208‐214. doi: 10.1177/0891988712464823 [DOI] [PubMed] [Google Scholar]
- 8. Aarsland D, Kurz MW. The epidemiology of dementia associated with Parkinson's disease. Brain Pathol. 2010;20:633. doi: 10.1111/J.1750-3639.2009.00369.X [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9. Llibre‐Guerra JJ, Prina M, Sosa AL, et al. Prevalence of Parkinsonism and Parkinson disease in urban and rural populations from Latin America: a community based study. Lancet Reg Health Am. 2022;7. doi: 10.1016/J.LANA.2021.100136 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10. Sosa AL, Albanese E, Stephan BCM, et al. Prevalence, distribution, and impact of mild cognitive impairment in Latin America, China, and India: a 10/66 population‐based study. PLoS Med. 2012;9:e1001170. doi: 10.1371/JOURNAL.PMED.1001170 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11. Ray Dorsey E, Elbaz A, Nichols E, et al. Global, regional, and national burden of Parkinson's disease, 1990‐2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2018;17:939‐953. doi: 10.1016/S1474-4422(18)30295-3 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12. von Elm E, Altman DG, Egger M, Pocock SJ, Gøtzsche PC, Vandenbroucke JP. The strengthening the reporting of observational studies in epidemiology (STROBE) statement: guidelines for reporting observational studies. J Clin Epidemiol. 2008;61:344‐349. doi: 10.1016/J.JCLINEPI.2007.11.008 [DOI] [PubMed] [Google Scholar]
- 13. Prina AM, Acosta D, Acosta I, et al. Cohort profile: the 10/66 study. Int J Epidemiol. 2017;46:406. doi: 10.1093/IJE/DYW056 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14. Prince M, Ferri CP, Acosta D, et al. The protocols for the 10/66 dementia research group population‐based research programme. BMC Public Health. 2007;7:165. doi: 10.1186/1471-2458-7-165 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15. Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico‐pathological study of 100 cases. J Neurol Neurosurg Psychiatry. 1992;55:181. doi: 10.1136/JNNP.55.3.181 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16. di Biase L, Pecoraro PM, Di Lazzaro V. Validating the Accuracy of Parkinson's Disease Clinical Diagnosis: A UK Brain Bank Case-Control Study. Ann Neurol. 2025;97(6):1110‐1121. doi: 10.1002/ana.27190 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17. Llibre Guerra JJ, Weiss J, Li J, et al. Assessing the 10/66 dementia classification algorithm for international comparative analyses with the U.S. Am J Epidemiol. 2024:kwae470. doi: 10.1093/AJE/KWAE470 [DOI] [PubMed] [Google Scholar]
- 18. Prince MJ, De Rodriguez JL, Noriega L, et al. The 10/66 dementia research group's fully operationalised DSM‐IV dementia computerized diagnostic algorithm, compared with the 10/66 dementia algorithm and a clinician diagnosis: a population validation study. BMC Public Health. 2008;8:219. doi: 10.1186/1471-2458-8-219 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19. Gmitrowicz A, Kucharska A. Developmental disorders in the fourth edition of the American classification: Diagnostic and Statistical Manual of Mental Disorders (DSM‐IV Options Book). Psychiatr Pol. 1994;28(5):509‐521. [PubMed] [Google Scholar]
- 20. Fine JP, Gray RJ. A proportional hazards model for the subdistribution of a competing risk. J Am Stat Assoc. 1999;94:496. doi: 10.2307/2670170 [DOI] [Google Scholar]
- 21. Broeders M, De Bie RMA, Velseboer DC, Speelman JD, Muslimovic D, Schmand B. Evolution of mild cognitive impairment in Parkinson disease. Neurology. 2013;81:346‐352. doi: 10.1212/WNL.0B013E31829C5C86 [DOI] [PubMed] [Google Scholar]
- 22. Hoogland J, Boel JA, de Bie RMA, et al. Mild cognitive impairment as a risk factor for Parkinson's disease dementia. Mov Disord. 2017;32:1056‐1065. doi: 10.1002/MDS.27002 [DOI] [PubMed] [Google Scholar]
- 23. Baiano C, Barone P, Trojano L, Santangelo G. Prevalence and clinical aspects of mild cognitive impairment in Parkinson's disease: a meta‐analysis. Mov Disord. 2020;35:45‐54. doi: 10.1002/MDS.27902 [DOI] [PubMed] [Google Scholar]
- 24. Weil RS, Costantini AA, Schrag AE. Mild cognitive impairment in Parkinson's disease—what is it?. Curr Neurol Neurosci Rep. 2018;18:1‐11. doi: 10.1007/S11910-018-0823-9/TABLES/1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25. Pedersen KF, Larsen JP, Tysnes OB, Alves G. Prognosis of mild cognitive impairment in early Parkinson disease: the Norwegian ParkWest study. JAMA Neurol. 2013;70:580‐586. doi: 10.1001/JAMANEUROL.2013.2110 [DOI] [PubMed] [Google Scholar]
- 26. Brucki SMD. Epidemiology of mild cognitive impairment in Brazil. Dement Neuropsychol. 2013;7:363. doi: 10.1590/S1980-57642013DN74000002 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27. Godinho C, Camozzato AL, Onyszko D, Chaves ML. Estimation of the risk of conversion of mild cognitive impairment of Alzheimer type to Alzheimer's disease in a south Brazilian population‐based elderly cohort: the PALA study. Int Psychogeriatr. 2012;24:674‐681. doi: 10.1017/S1041610211002043 [DOI] [PubMed] [Google Scholar]
- 28. Nitrini R, Bottino CMC, Albala C, et al. Prevalence of dementia in Latin America: a collaborative study of population‐based cohorts. Int Psychogeriatr. 2009;21:622. doi: 10.1017/S1041610209009430 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29. Bertola L, Suemoto CK, Aliberti MJR, et al. Prevalence of dementia and cognitive impairment no dementia in a large and diverse nationally representative sample: the ELSI‐Brazil study. J Gerontol A. 2023;78:1060‐1068. doi: 10.1093/GERONA/GLAD025 [DOI] [PubMed] [Google Scholar]
- 30. Martinez‐Martin P, Chaudhuri KR, Rojo‐Abuin JM, et al. Assessing the non‐motor symptoms of Parkinson's disease: mDS‐UPDRS and NMS scale. Eur J Neurol. 2015;22:37‐43. doi: 10.1111/ENE.12165 [DOI] [PubMed] [Google Scholar]
- 31. DeCarli C. Mild cognitive impairment: prevalence, prognosis, aetiology, and treatment. Lancet Neurol. 2003;2:15‐21. doi: 10.1016/S1474-4422(03)00262-X [DOI] [PubMed] [Google Scholar]
- 32. Wilson RS, Beckett LA, Bennett DA, Albert MS, Evans DA. Change in cognitive function in older persons from a community population: relation to age and Alzheimer disease. Arch Neurol. 1999;56:1274‐1279. doi: 10.1001/ARCHNEUR.56.10.1274 [DOI] [PubMed] [Google Scholar]
- 33. Graham JE, Rockwood K, Beattie BL, et al. Prevalence and severity of cognitive impairment with and without dementia in an elderly population. Lancet. 1997;349:1793‐1796. doi: 10.1016/S0140-6736(97)01007-6 [DOI] [PubMed] [Google Scholar]
- 34. Saredakis D, Collins‐Praino LE, Gutteridge DS, Stephan BCM, Keage HAD. Conversion to MCI and dementia in Parkinson's disease: a systematic review and meta‐analysis. Parkinsonism Relat Disord. 2019;65:20‐31. doi: 10.1016/J.PARKRELDIS.2019.04.020 [DOI] [PubMed] [Google Scholar]
- 35. Price JL, Morris JC. Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease. Ann Neurol. 1999;45(3):358‐368. doi: [DOI] [PubMed] [Google Scholar]
- 36. Morris JC. Is Alzheimer's disease inevitable with age?: Lessons from clinicopathologic studies of healthy aging and very mild Alzheimer's disease. J Clin Invest. 1999;104:1171‐1173. doi: 10.1172/JCI8560 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37. Morris JC, Storandt M, Miller JP, et al. Mild cognitive impairment represents early‐stage Alzheimer disease. Arch Neurol. 2001;58:397‐405. doi: 10.1001/ARCHNEUR.58.3.397 [DOI] [PubMed] [Google Scholar]
- 38. Levy G, Tang MX, Cote LJ, et al. Do risk factors for Alzheimer's disease predict dementia in Parkinson's disease? An exploratory study. Mov Disord. 2002;17:250‐257. doi: 10.1002/MDS.10086 [DOI] [PubMed] [Google Scholar]
- 39. Aarsland D, Zaccai J, Brayne C. A systematic review of prevalence studies of dementia in Parkinson's disease. Mov Disord. 2005;20(10):1255‐1263. doi: 10.1002/MDS.20527 [DOI] [PubMed] [Google Scholar]
- 40. Prince M, Acosta D, Chiu H, Scazufca M, Varghese M, Group for the 10/66 DR . Dementia diagnosis in developing countries: a cross‐cultural validation study. Lancet. 2003;361:909‐917. [DOI] [PubMed] [Google Scholar]
- 41. Pasquini L, Llibre Guerra J, Prince M, Chua KC, Prina AM. Neurological signs as early determinants of dementia and predictors of mortality among older adults in Latin America: a 10/66 study using the NEUROEX assessment. BMC Neurol. 2018;18:1‐11. doi: 10.1186/S12883-018-1167-4/TABLES/5 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 42. Prince M, Acosta D, Ferri CP, et al. Dementia incidence and mortality in middle‐income countries, and associations with indicators of cognitive reserve: a 10/66 dementia research group population‐based cohort study. Lancet. 2012;380:50‐58. doi: 10.1016/S0140-6736(12)60399-7 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 43. Counsell C, Giuntoli C, Khan QI, Maple‐Grødem J, Macleod AD. The incidence, baseline predictors, and outcomes of dementia in an incident cohort of Parkinson's disease and controls. J Neurol. 2022;269:4288. doi: 10.1007/S00415-022-11058-2 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 44. Hughes TA, Ross HF, Musa S, et al. A 10‐year study of the incidence of and factors predicting dementia in Parkinson's disease. Neurology. 2000;54:1596‐1602. doi: 10.1212/WNL.54.8.1596 [DOI] [PubMed] [Google Scholar]
- 45. Chang TY, Yang CP, Chen YH, Lin CH, Chang MH. Age‐stratified risk of dementia in Parkinson's disease: a nationwide, population‐based, retrospective cohort study in Taiwan. Front Neurol. 2021;12:748096. doi: 10.3389/FNEUR.2021.748096/FULL [DOI] [PMC free article] [PubMed] [Google Scholar]
- 46. de Lau LM, Breteler MM. Epidemiology of Parkinson's disease. Lancet Neurol. 2006;5:525‐535. doi: 10.1016/S1474-4422(06)70471-9 [DOI] [PubMed] [Google Scholar]
- 47. Poewe W, Gauthier S, Aarsland D, et al. Diagnosis and management of Parkinson's disease dementia. Int J Clin Pract. 2008;62:1581. doi: 10.1111/J.1742-1241.2008.01869.X [DOI] [PMC free article] [PubMed] [Google Scholar]
- 48. Meireles J, Massano J. Cognitive impairment and dementia in Parkinson's disease: clinical features, diagnosis, and management. Front Neurol. 2012;3:88. doi: 10.3389/FNEUR.2012.00088 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 49. Wood KL, Myall DJ, Livingston L, et al. Different PD‐MCI criteria and risk of dementia in Parkinson's disease: 4‐year longitudinal study. NPJ Parkinsons Dis. 2016;2:1‐8. doi: 10.1038/npjparkd.2015.27 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 50. Dubois B, Burn D, Goetz C, et al. Diagnostic procedures for Parkinson's disease dementia: recommendations from the movement disorder society task force. Mov Disord. 2007;22:2314‐2324. doi: 10.1002/MDS.21844 [DOI] [PubMed] [Google Scholar]
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