Cited by 24Dementia and Cognitive Impairment ResearchPharmaceutical Practices and Patient OutcomesTreatment of Major Depression

The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index; 19 of the 30 sources its claims cite were checked for support.

Antidepressant use in relation to dementia risk, cognitive decline, and brain atrophy

Open access

Abstract

INTRODUCTION: We aimed to assess the effect of antidepressant use on dementia risk, cognitive decline, and brain atrophy. METHODS: In this prospective cohort study, we included 5511 dementia‐free participants (Mini‐Mental State Examination [MMSE] > 25) of the Rotterdam study (57.5% women, mean age 70.6 years). Antidepressant use was extracted from pharmacy records from 1991 until baseline (2002–2008). Incident dementia was monitored from baseline until 2018, with repeated cognitive assessment and magnetic resonance imaging (MRI) every 4 years. RESULTS: Compared to never use, any antidepressant use was not associated with dementia risk (hazard ratio [HR] 1.14, 95% confidence interval [CI] 0.92–1.41), or with accelerated cognitive decline or atrophy of white and gray matter. Compared to never use, dementia risk was somewhat higher with tricyclic antidepressants (HR 1.36, 95% CI 1.01–1.83) than with selective serotonin reuptake inhibitors (HR 1.12, 95% CI 0.81–1.54), but without dose–response relationships, accelerated cognitive decline, or atrophy in either group. DISCUSSION: Antidepressant medication in adults without indication of cognitive impairment was not consistently associated with long‐term adverse cognitive effects. Highlights: Antidepressant medications are frequently prescribed, especially among older adults. In this study, antidepressant use was not associated with long‐term dementia risk. Antidepressant use was not associated with cognitive decline or brain atrophy. Our results support safe prescription in an older, cognitively healthy population.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

In a prospective Rotterdam Study cohort of 5511 dementia-free older adults, antidepressant use was not consistently associated with long-term dementia risk, cognitive decline, or brain atrophy. Tricyclic antidepressant use showed a modest dementia risk association, but without dose-response or corroborating cognitive, imaging, or instrumental-variable evidence.

Key findings

  • Among 5511 participants (57.5% women, mean age 70.6 years), 923 (16.7%) had ever used antidepressants; 639 (11.6%) developed dementia over mean 10.2 years. Any antidepressant use versus never use was not significantly associated with dementia risk (HR 1.14, 95% CI 0.92–1.41), with no dose-response relationship.
  • Tricyclic antidepressant use was associated with higher dementia risk (HR 1.36, 95% CI 1.01–1.83), while SSRI use was not (HR 1.12, 95% CI 0.81–1.54); neither showed dose-response relationships. Current use HR was 1.38 (95% CI 0.99–1.93) and past use HR was 1.05 (95% CI 0.82–1.34).
  • Antidepressant use was not associated with global cognitive decline (mean difference in g-factor per year β 0.003, 95% CI −0.003 to 0.010) or with change in total brain, gray matter, white matter, hippocampus, amygdala, or thalamus volumes.
  • In instrumental variable analyses using CYP2D6 genotype among amitriptyline and paroxetine users, higher risk score was not associated with increased dementia risk (amitriptyline HR 0.90, 95% CI 0.80–1.01; paroxetine HR 0.94, 95% CI 0.81–1.09).

Methods

  • Prospective population-based cohort study within the Rotterdam Study; included 5511 dementia-free participants (MMSE >25) aged ≥60 years at baseline (2002–2008), with pharmacy records from 1991 onward, incident dementia follow-up until 2018, and repeated cognitive assessment and MRI every 4 years.
  • Exposure was any antidepressant prescription between pharmacy record inception and baseline; analyses compared ever versus never use, former versus current use, duration, cumulative defined daily dose, and tricyclic antidepressants versus SSRIs. Outcomes were all-cause dementia (Cox models), global cognition (linear mixed models), brain volumes (linear mixed models), and instrumental variable analysis using a CYP2D6 genetic risk score.
  • Models adjusted for age, sex, and education (Model 1), and additionally for smoking, alcohol, BMI, eGFR, CES-D score, benzodiazepine and antipsychotic use, and comorbidities (Model 2); missing covariates were imputed.

Limitations

  • Stated: exclusion of participants with MMSE <26 at baseline may introduce selection bias by disregarding pre-baseline antidepressant effects and excluding lower-educated participants.
  • Stated: attrition for repeated cognitive assessment and MRI was 27% and 35%, respectively, potentially attenuating associations; the CYP2D6 genetic risk score could not include gene deletions or duplications, possibly causing misclassification; and results in a predominantly White population may not generalize to non-White populations.
  • Evident from text: the observational cohort design cannot fully exclude residual confounding or reverse causation, although the authors attempted to mitigate these via exclusion, stratification, and instrumental variable analysis.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1002/alz.13807

Cites

49 of 49 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

19 of 30 cited sources checked · 8 supported · 1 flagged · accuracy not yet measured

  • Premisecitation
    § 1 INTRODUCTION · p. 2

    Few published studies have examined the effect of antidepressant use on cognitive decline.

    “but few published studies have examined the effect of antidepressant use on cognitive decline, 11,16”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [11] 11. Leng Y, Diem SJ, Stone KL, Yaffe K. Antidepressant use and cognitive outcomes in very old women. J Gerontol . 2018;73(10):1390-1395. source

      The Abstract describes a growing number of studies on the cognitive effects of antidepressants and cites several that examined cognitive decline. It says few studies examined the effects of *different classes* of antidepressants, a narrower gap than the citing sentence describes. The source therefore supports limited research on that specific question, but not the unqualified claim that few studies examined antidepressant use and cognitive decline. (LLM, conf=0.78)

      Experimental — accuracy not yet measured
    • cites [16] 16. Saczynski JS, Rosen AB, McCammon RJ, et al. Antidepressant use and cognitive decline: the health and retirement study. Am J Med . 2015;128(7):739-746. source

      The Discussion says that many clinical trials, mostly small, have assessed antidepressant treatment and cognitive decline. It limits the scarcity of published work to population-based studies, a qualification absent from the citing sentence. (LLM, conf=0.86)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
  • Premisecitation
    § 2.6 Genotyping · p. 3

    The cytochrome P450 (CYP)2D6 genotype is involved in the metabolization of amitriptyline and paroxetine.

    “Based on the established involvement of the cytochrome P450 (CYP)2D6 genotype in the metabolization of amitriptyline and paroxetine, 34”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [34] 34. Milosavljevic F, Bukvic N, Pavlovic Z, et al. Association of CYP2C19 and CYP2D6 poor and intermediate metabolizer status with antidepressant and antipsychotic exposure: a systematic review and metaanalysis. JAMApsychiatry . 2021;78(3):270-280. source
  • Premisecitation
    § 1 INTRODUCTION · p. 2

    Depression is a well-established risk factor of dementia.

    “Depression is a wellestablished risk factor of dementia, 20”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [20] 20. Byers AL, Yaffe K. Depression and risk of developing dementia. NatRev Neurol . 2011;7(6):323-331. source

      The Abstract reports a consistent association between earlier-life depression and increased dementia risk. But the Treatment and management implications section says research has not resolved whether depression is a risk factor or a prodromal symptom, so calling it a well-established risk factor overstates the review's conclusion. Page numbers are not available in our copy. (LLM, conf=0.90)

      Experimental — accuracy not yet measured
  • Premisecitation
    § 1 INTRODUCTION · p. 2

    To the authors' knowledge, only one study has examined the long-term effects of antidepressant use on brain atrophy.

    “and to our knowledge only one study examined the long-term effects of antidepressant use on brain atrophy. 22”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [22] 22. Frödl T, Jäger M, Smajstrlova I, et al. Effect of hippocampal and amygdala volumes on clinical outcomes in major depression: a 3-year prospective magnetic resonance imaging study. J Psychiatry Neurosci . 2008;33(5):423-430. source
  • Premisecitation
    § 1 INTRODUCTION · p. 2

    Long-term effects of antidepressants remain uncertain because short-term follow-up in clinical trials generally precludes investigation of chronic use and long-term adverse outcomes.

    “Despite the frequent prescription of antidepressants, their long-term effects remain uncertain, as short-term follow-up in clinical trials generally precludes the investigation of chronic use and longterm adverse outcomes. 8”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [8] 8. Wang C, Gao S, Hendrie HC, et al. Antidepressant use in the elderly is associated with an increased risk of dementia. Alzheimer Dis Assoc Disord . 2016;30(2):99-104. source

      The Introduction says antidepressant trials involving older adults often last only weeks or months, and that little is known about long-term outcomes of use in elderly people with intact cognition. This supports the concern about short trials, but the cited paper frames the uncertainty around older adults and dementia risk, rather than long-term adverse outcomes across all antidepressant users. (LLM, conf=0.83)

      Experimental — accuracy not yet measured
  • It may state two separate claims as one. 17
  • The quote only partly states this claim. 1
  • Probably not a substantial claim. 17
  • It may state two separate claims as one.

    Findingown data
    § Abstract · p. 1

    Neither tricyclic antidepressant nor selective serotonin reuptake inhibitor use was associated with brain atrophy.

    “but without dose-response relationships, accelerated cognitive decline, or atrophy in either group.”
    Quote in the paperSubstantial claim
  • The quote only partly states this claim.

    Findingown data
    § 3.1 Incident dementia · p. 5

    Results for clinical AD only were comparable to all-cause dementia results (HR 1.05, 95% CI 0.82-1.35).

    “Results were comparableforclinical AD only (HR 1.05, 95% CI 0.821.35).”
    Quote in the paperNot a substantial claim
  • It may state two separate claims as one.

    Findingown data
    § 3.2 Cognition · p. 6

    Use of a combination of antidepressants was not associated with increased dementia risk, and no dose-response relationships were observed.

    “Use of a combination of antidepressants was not associated with increased dementia risk, and no dose-response relationships were observed (Table S2).”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Findingown data
    § Abstract · p. 1

    Neither tricyclic antidepressant nor selective serotonin reuptake inhibitor use was associated with accelerated cognitive decline.

    “but without dose-response relationships, accelerated cognitive decline, or atrophy in either group.”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Findingown data
    § 3.2 Cognition · p. 5

    Antidepressant use had no effect on long-term performance on the letter-digit substitution task, the Stroop test, the word fluency test, and the 15-word learning test (delayed recall).

    “For the separate cognitive tests, we did not observe an effect of antidepressant use on long-term performance on the letter-digit substitution task, the Stroop test (time adjusted for errors on trial 3), the word fluency test, and the 15-word learning test (delayed recall).”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Findingown data
    § Abstract · p. 1

    Neither tricyclic antidepressant nor selective serotonin reuptake inhibitor use showed a dose-response relationship with dementia risk.

    “but without dose-response relationships, accelerated cognitive decline, or atrophy in either group.”
    • Also stated in: § RESEARCHINCONTEXT · p. 2 · plain
      “This effect was independent of dose or duration of use.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given
    § 2.2 Use of antidepressant medication · p. 2

    Registry data were complete for all participants.

    “Registry data were complete for all participants.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim.

    Study design and conductreasoning
    § 2.2 Use of antidepressant medication · p. 2

    To limit reversed causation, antidepressant use was defined as prescription of any antidepressant during the exposure period between inception of pharmacy records (1991) and study baseline (2002-2008).

    “To limit reversed causation (i.e., the use of antidepressants for depression due to prodromal dementia), antidepressant use was defined as prescription of any antidepressant during the exposure period, which is between inception of pharmacy records (1991) and study baseline (2002-2008).”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. It may state two separate claims as one.

    Study design and conductnone given
    § 2.8 Statistical analyses · p. 4

    All analyses were adjusted for age, sex, and education (Model 1), and additionally for smoking, alcohol, BMI, eGFR, CES-D score, benzodiazepine use, antipsychotic use, and prevalence of diabetes, hypertension, stroke, parkinsonism, atrial fibrillation, congestive heart failure, coronary heart disease, cancer, and COPD (Model 2).

    “All analyses were adjusted for age, sex, and education (Model 1), and additionally for smoking habits, alcohol use, BMI, eGFR, CES-D score, benzodiazepine use, antipsychotic use, and prevalence of diabetes, hypertension, stroke, parkinsonism, atrial fibrillation, congestive heart failure, coronary heart disease, cancer, and chronic obstructive pulmonary disease (Model 2).”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given
    § 2.4 Cognitive assessment · p. 3

    Missing data on individual cognitive tests were imputed using single imputation based on age, sex, education, MMSE score, and other available cognitive tests.

    “In the event that data on the individual cognitive tests were missing, these data were imputed using single imputation, based on age, sex, education, MMSE score, and other available cognitive tests.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim.

    Study design and conductnone given
    § 2.5 MRI protocol and image processing · p. 3

    All MRI segmentations were visually inspected and manually corrected when necessary.

    “All segmentations were visually inspected and manually corrected when necessary.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim.

    Study design and conductreasoning
    § 4 DISCUSSION · p. 8

    We attempted to minimize reversed causation by stratifying by (history and severity of) depression and excluding participants with cognitive impairment at baseline.

    “We attempted to minimize reversed causation by stratifying by (history and severity of) depression and excluding participants with cognitive impairment at baseline.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. It may state two separate claims as one.

    Study design and conductown data
    § 2.4 Cognitive assessment · p. 3

    A standardized compound score (g-factor) was calculated using the first factor of a principal component analysis including each cognitive test, and it explained 49.5% of the variance in cognitive scores.

    “To obtain a measure of global cognitive functioning, a standardized compound score (g-factor) was calculated using the first factor of a principal component analysis, including each of the aforementioned cognitive tests, which explained 49.5% of the variance in cognitive scores.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim.

    Study design and conductreasoning
    § 2.8 Statistical analyses · p. 4

    To assess confounding by indication, analyses were stratified by history of depression and severity of depressive symptoms according to CES-D score (cutoff ≥16).

    “To assess confounding by indication, we further stratified analyses by history of depression and severity of depressive symptoms according to CES-D score (cutoff: ≥ 16).”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Interpretationreasoning
    § 4 DISCUSSION · p. 6

    Because depression is a risk factor for dementia, antidepressants prescribed for depression might show an association with increased dementia risk even in the absence of a causal relationship (i.e., confounding-by-indication).

    “In addition, because depression is a risk factor for dementia, antidepressants prescribed for depression might show an association with increased dementia risk even in the absence of a causal relationship (i.e., confounding-by-indication).”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Depression is a risk factor for dementia.
  • Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.

    Study design and conductown data
    § 2.8 Statistical analyses · p. 4

    Missing covariate data (maximum 10%) was imputed using 10-fold multiple imputation, with all covariates included as predictors, and the distribution of variables was similar in imputed and nonimputed datasets.

    “Missing covariate data (maximum 10%) was imputed using 10-fold multiple imputation; all covariates were included as predictors in the model. Distribution of variables was similar in the imputed and nonimputed datasets.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim.

    Study design and conductown data
    § 2.8 Statistical analyses · p. 4

    An instrumental variable analysis was performed to strengthen the causal inference of associations with dementia risk.

    “Finally, we performed an instrumental variable analysis to strengthen the causal inference of associations with dementia risk.”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Study design and conductown data
    § 3.3 Imaging-derived brain volume · p. 6

    Participants without MRI were more often women, older, and less educated; had on average more depressive symptoms and a higher BMI; were more often diagnosed with hypertension, diabetes, stroke, CHD, CHF, AF, cancer, and COPD; were less often smokers and consuming alcohol; and had lower eGFRs than those with available MRI.

    “Participants without MRI were more often women, older, and less educated; had on average more depressive symptoms and a higher BMI; were more often diagnosed with hypertension, diabetes, stroke, coronary heart disease (CHD), congestive heart failure (CHF), atrial fibrillation (AF), cancer, and chronic obstructive pulmonary disease (COPD),werelessoftensmokersandconsumingalcohol,andhadlower eGFRs”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim.

    Study design and conductnone given
    § 2.3 Dementia screening and surveillance · p. 3

    All cases suspicious for dementia were reviewed by a consensus panel including a consultant neurologist, which applied standard DSM-IV criteria for dementia to come to a final diagnosis.

    “All cases that were suspicious for dementia were reviewed by a consensus panel, including a consultant neurologist, which applied standard criteria for dementia (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition [DSM-IV]) to come to a final diagnosis.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim.

    Study design and conductnone given
    § 2.3 Dementia screening and surveillance · p. 3

    Follow-up for dementia until January 1, 2018, was complete for 96.8% of the potential person-years.

    “Follow-up for dementia until January 1, 2018, was complete for 96.8% of the potential person-years.”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Interpretationown data
    § 4 DISCUSSION · p. 6

    In this study, antidepressant use was not related to an increased dementia risk, cognitive decline, or brain atrophy in older individuals without indication of cognitive impairment.

    “In this study, antidepressant use was not related to an increased dementia risk, cognitive decline, or brain atrophy in older individuals without indication of cognitive impairment.”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Interpretationown data
    § 4 DISCUSSION · p. 8

    The absence of any protective effect on dementia risk, brain MRI, and in instrumental variable analyses, and the absence of dose-response and duration-response relationships between antidepressant use and cognitive decline do not support a protective effect of antidepressant use on cognition.

    “however, the absence of any protective effect on dementia risk, brain MRI, and in instrumental variable analyses, and the absence of dose-response and duration-response relationships between antidepressant use and cognitive decline do not support a protective effect of antidepressant use on cognition.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductnone given
    § 4 DISCUSSION · p. 8

    We were unable to include the presence of gene deletions or duplications in the CYP2D6 genotype in the genetic risk score, which may introduce a degree of misclassification.

    “Third, we were unable to include the presence of gene deletions or duplications in the CYP2D6 genotype in the genetic risk score, which may introduce a degree of misclassification.”
    Quote in the paperNot a substantial claim
  • It may state two separate claims as one.

    Study design and conductreasoning
    § 4 DISCUSSION · p. 8

    The exclusion of participants with MMSE < 26 at baseline prevented reversed causation but may have introduced selection bias by disregarding the effects of antidepressant use prior to baseline and excluding participants with lower education.

    “First, the exclusion of participants with MMSE &lt; 26 at baseline prevented reversed causation (i.e., the use of antidepressants due to depression in the prodromal phase of dementia) but may have introduced selection bias by disregarding the effects of antidepressant use prior to baseline and excluding participants with lower education.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductreasoning
    § 4 DISCUSSION · p. 8

    Because individuals with severe mental health disorders and cognitive impairment might be more likely to drop out, this may have attenuated the association with cognitive decline and brain volume.

    “Because individuals with severe mental health disorders and cognitive impairment might be more likely to drop out, this may have attenuated the association with cognitive decline and brain volume.”
    Quote in the paperNot a substantial claim
  • It may state two separate claims as one.

    Interpretationown data
    § 4 DISCUSSION · p. 8

    In conclusion, in this population-based study, antidepressant use was not associated with long-term adverse effects on dementia risk, cognitive decline, or brain atrophy in older individuals without clear signs of cognitive impairment.

    “In conclusion, in this population-based study, antidepressant use was not associated with long-term adverse effects on dementia risk, cognitive decline, or brain atrophy in older individuals without clear signs of cognitive impairment.”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Study design and conductown data
    § 4 DISCUSSION · p. 8

    Although attrition for dementia follow-up was only 3.2%, a higher share of participants did not undergo repeated cognitive assessment or brain MRI (27% and 35%, respectively).

    “Second, although attrition for dementia follow-up was only 3.2%, a higher share of participants did not undergo repeated cognitive assessment or brain MRI (27% and 35%, respectively).”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim. It may state two separate claims as one.

    Study design and conductown data
    § 4 DISCUSSION · p. 8

    Our study was strengthened by its linkage with pharmacy records, which provided detailed information on use up to 15 years before baseline, the availability of genetic data as proxy for metabolic rate, and the 10-15 years follow-up on cognitive decline and brain atrophy.

    “Our study was strengthened by its linkage with pharmacy records, which provided detailed information on use up to 15 years before baseline, the availability of genetic data as proxy for metabolic rate, and the 10-15 years follow-up on cognitive decline and brain atrophy.”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Interpretationown data
    § 4 DISCUSSION · p. 8

    Risk estimates for dementia in our study were somewhat higher for TCA users, but a causal association was not supported by a dose-response relationship, and no associations were observed with subclinical outcomes or in instrumental variable analysis.

    “Risk estimates for dementia in our study were somewhat higher for TCA users, but a causal association was not supported by a dose-response relationship, and no associations were observed with subclinical outcomes or in instrumental variable analysis.”
    Quote in the paperSubstantial claim
  • It may state two separate claims as one.

    Study design and conductown data
    § 4 DISCUSSION · p. 8

    Results were obtained in a predominantly White population, and results may, therefore, be less generalizable to non-White populations.

    “Fourth, results were obtained in a predominantly White population, and results may, therefore, be less generalizable to non-White populations.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim. The paper’s conclusions may not depend on it.

    Study design and conductown data
    § 4 DISCUSSION · p. 8

    A post hoc power analysis showed that with our sample of 5511 participants, we had 80% power to detect a difference of 1.40 in the HR for dementia with any versus no use of antidepressants.

    “A post hoc power analysis showed that with our sample of 5511 participants, we had 80% power to detect a difference of 1.40 in the HR for dementia with any versus no use of antidepressants.”
    Quote in the paperNot a substantial claim
31 of 31
  • The paper relies on this without support.

    Depression is a risk factor for dementia.

    “because depression is a risk factor for dementia”
  • The paper relies on this without support.

    A higher CYP2D6 risk score reflects slower drug metabolism rate and is a valid proxy for metabolic rate.

    “A higher CYP2D6 risk score, reflecting slower drug metabolism rate”
2 of 2

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Repeat-assessment attrition percentages are reversed

    Minor

    The reported 66.0% with a repeated cognitive assessment implies 34.0% without one, not the 27% attributed to cognitive assessment in the limitations. The reported MRI repeat rate of 73.0% likewise implies 27.0% without one, rather than 35%.

1 of 1

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Metadata

Authors
vom Hofe, I., Stricker, B. H., Vernooij, M. W., Ikram, M. K., Ikram, M. A., & Wolters, F. J.
Affiliations
  • Department of Epidemiology Erasmus University Medical Center Rotterdam The Netherlands
  • Erasmus MC (NL)
Corresponding author
Wolters, Frank J.
Venue
Alzheimer's & Dementia
Publisher
Wiley
Published
2024-04
Volume
20
Issue
5
Pages
3378-3387
ISSN
  • 1552-5260 (ISSN-L)
  • 1552-5279
OpenAlex
W4394750643
Cited by
24
References
49
Citations by year
2026: 8 · 2025: 13 · 2024: 3
FWCI
5.68
Type
journal article
Language
en
Open access
Locations
  • Alzheimer s & Dementia (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (publishedVersion, cc-by)
Funders
  • European Commission
  • Alzheimer Nederland
  • Brain and Behavior Research Foundation
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Geriatrics and Gerontology › Pharmaceutical Practices and Patient Outcomes
  • Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
Keywords
antidepressant use, dementia risk
MeSH terms
Aged, Antidepressive Agents, Atrophy, Brain, Dementia, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Prospective Studies, Risk Factors, Cognitive Dysfunction

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