Skip to main content
AAN.com

Abstract

Objective:

To clarify the relationship between depressive symptoms and the clinical and neuropathologic manifestations of dementia.

Methods:

In a clinical-pathologic cohort study, 1,764 older persons without cognitive impairment at enrollment completed annual clinical evaluations for a mean of 7.8 years. The evaluations included assessment of depressive symptoms (10-item Center for Epidemiological Studies Depression Scale) and cognitive function (battery of 17 performance tests). A total of 582 individuals died during follow-up and underwent a uniform neuropathologic examination to quantify β-amyloid plaques and tau tangle density in multiple brain regions and identify neocortical Lewy bodies, hippocampal sclerosis, and gross and microscopic cerebral infarcts.

Results:

Level of depressive symptoms slightly increased during follow-up. Incident mild cognitive impairment (52.2%) was associated with higher level of depressive symptoms before the diagnosis but not with change in symptoms after the diagnosis; incident dementia (17.9%) was associated with higher symptom level before dementia onset and with more rapid decline in symptoms after dementia onset. None of the neuropathologic markers was related to level of depressive symptoms or change in symptoms over time. In a mixed-effects model adjusted for the neuropathologic markers, higher level of depressive symptoms averaged over evaluations was associated with more rapid global cognitive decline, accounting for 4.4% of the variability in decline not attributable to the neuropathologic markers. Depressive symptoms did not modify the association of the neuropathologic markers with cognitive decline.

Conclusion:

In old age, depressive symptoms have an association with cognitive decline that is independent of the neuropathologic hallmarks of dementia.

Get full access to this article

View all available purchase options and get full access to this article.

Supplementary Material

File (figure_e-1.pdf)
File (table_e-1.doc)

REFERENCES

1.
Wilson RS, Barnes LL, Mendes de Leon CF, et al. Depressive symptoms, cognitive decline, and risk of AD in older persons. Neurology 2002;59:364–370.
2.
Köhler S, van Boxtel MPJ, van Os J, et al. Depressive symptoms and cognitive decline in community-dwelling older adults. J Am Geriatr Soc 2010;58:873–879.
3.
Barnes DE, Alexopoulos GS, Lopez OL, Williamson JD, Yaffe K. Depressive symptoms, vascular disease, and mild cognitive impairment: findings from the Cardiovascular Health Study. Arch Gen Psychiatry 2006;63:273–279.
4.
Geda YE, Knopman DS, Mrazek DA, Jicha GA, Smith GE, Negash S. Depression, apolipoprotein E genotype, and the incidence of mild cognitive impairment: a prospective cohort study. Arch Neurol 2006;63:435–440.
5.
Saczynski JS, Beiser A, Seshadri S, Auerbach S, Wolf PA, Au R. Depressive symptoms and risk of dementia: the Framingham Heart Study. Neurology 2010;75:35–41.
6.
Barnes DE, Yaffe K, Byers AL, McCormick M, Schafer C, Whitmer RA. Midlife vs late-life depressive symptoms and risk of dementia. Arch Gen Psychiatry 2012;69:493–498.
7.
Panza F, Frisardi V, Capurso C, et al. Late-life depression, mild cognitive impairment, and dementia: possible continuum? Am J Geriatr Psychiatry 2010;18:98–116.
8.
Bennett DA, Schneider JA, Arvanitakis Z, Wilson RS. Overview and findings from the Religious Orders Study. Curr Alzheimer Res 2012;9:628–645.
9.
Bennett DA, Schneider JA, Buchman AS, Barnes LL, Boyle PA, Wilson RS. Overview and findings from the Rush Memory and Aging Project. Curr Alzheimer Res 2012;9:646–663.
10.
Kohout FJ, Berkman LF, Evans DA, Cornoni-Huntley J. Two shorter forms of the CES-D depression symptoms index. J Aging Health 1993;5:79–193.
11.
Radloff LS. The CES-D scale: a self-report depression scale for research in the general population. Appl Psychol Meas 1977;1:385–401.
12.
Wilson RS, Bienias JL, Mendes de Leon CF, Evans DA, Bennett DA. Negative affect and mortality in older persons. Am J Epidemiol 2003;158:827–835.
13.
Amieva H, Goff ML, Millett X, et al. Prodromal Alzheimer's disease: successive emergence of the clinical symptoms. Ann Neurol 2008;64:492–498.
14.
Wilson RS, Hoganson GM, Rajan KB, Barnes LL, Mendes de Leon CF, Evans DA. Temporal course of depressive symptoms during the development of Alzheimer's disease. Neurology 2010;75:21–26.
15.
Wilson RS, Beckett LA, Barnes LL, et al. Individual differences in rates of change in cognitive abilities of older persons. Psychol Aging 2002;17:179–193.
16.
Wilson RS, Barnes LL, Bennett DA. Assessment of lifetime participation in cognitively stimulating activities. J Clin Exp Neuropsychol 2003;25:634–642.
17.
Wilson RS, Barnes LL, Krueger KR, Hoganson G, Bienias JL, Bennett DA. Early and late life cognitive activity and cognitive systems in old age. J Int Neuropsychol Soc 2005;11:400–407.
18.
McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan E. Clinical diagnosis of Alzheimer's disease: report of the NINCDS/ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's disease. Neurology 1984;34:939–944.
19.
Bennett DA, Wilson RS, Schneider JA, et al. Natural history of mild cognitive impairment in older persons. Neurology 2002;59:198–205.
20.
Schneider JA, Li JL, Li Y, Wilson RS, Kordower JH, Bennett DA. Neurofibrillary tangles in the substantia nigra are related to gait impairment in older persons. Ann Neurol 2006;59:166–173.
21.
Bennett DA, Schneider JA, Arvanitakis Z, et al. Neuropathology of older persons without cognitive impairment from two community-based studies. Neurology 2006;66:1837–1844.
22.
Arvanitakis Z, Leurgans SE, Barnes LL, Bennett DA, Schneider JA. Microinfarct pathology, dementia, and cognitive systems. Stroke 2011;42:722–727.
23.
Bennett DA, Schneider JA, Wilson RS, Bienias JL, Arnold SE. Neurofibrillary tangles mediate the association of amyloid with clinical AD and level of cognitive function. Arch Neurol 2004;61:378–384.
24.
Wilson RS, Yu L, Schneider JA, Arnold SE, Buchman AS, Bennett DA. Lewy bodies and olfactory dysfunction in old age. Chem Senses 2011;36:367–373.
25.
McKeith IG, Galasko D, Kosaka K, et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the Consortium on DLB International Workshop. Neurology 1996;47:1113–1124.
26.
Min Y, Agresti A. Random effect models for repeated measures of zero-inflated count data. Stat Model 2005;5:1–19.
27.
Capuano AW, Dawson JD. The trend odds model for ordinal data. Stat Med 2013;32:2250–2261.
28.
Diggle PJ, Liang KY, Zeger SL. Analysis of Longitudinal Data. New York: Oxford University Press; 2002.
29.
Wilson RS, Leurgans SE, Boyle PA, Bennett DA. Cognitive decline in prodromal Alzheimer disease and mild cognitive impairment. Arch Neurol 2011;68:351–356.
30.
Koolschijn PCMP, van Haren NEM, Lensvelt-Mulders GJLM, Hulshoff Pol HE, Kahn RS. Brain volume abnormalities in major depressive disorder: a meta-analysis of magnetic resonance imaging studies. Hum Brain Mapp 2009;30:3719–3735.
31.
Dotson VM, Davatzikos C, Kraut MA, Resnick SM. Depressive symptoms and brain volumes in older adults: a longitudinal magnetic resonance imaging study. J Psychiatry Neurosci 2009;34:367–375.
32.
Sexton CE, Mackay CE, Ebmeier KP. A systematic review of diffusion tensor imaging studies in affective disorders. Biol Psychiatry 2009;66:814–823.
33.
Sexton CE, Allan CL, Masurier ML, et al. Magnetic resonance imaging in late-life depression: multimodal examination of network disruption. Arch Gen Psychiatry 2012;69:680–689.
34.
Wilson RS, Nag S, Boyle PA, et al. Brainstem aminergic nuclei and late-life depressive symptoms. JAMA Psychiatry 2013;70:1320–1328.
35.
Soetanto A, Wilson RS, Talbot K, et al. Anxiety and depression are associated with MAP2 and synaptopodin immunolabeled dendrite and spine densities in hippocampal CA3 of older humans. Arch Gen Psychiatry 2010;67:448–457.
36.
Holtzer R, Scarmeas N, Wegesin DJ, et al. Depressive symptoms in Alzheimer's disease: natural course and temporal relation to function and cognitive status. J Am Geriatr Soc 2005;53:2083–2089.
37.
Panza F, D'Introno A, Colacicco AM, et al. Temporal relationship between depressive symptoms and cognitive impairment: the Italian Longitudinal Study of Aging. J Alzheimers Dis 2009;17:899–911.
38.
Gale CR, Allerhand M, Deary IJ; HALCyon Study Team. Is there a bidirectional relationship between depressive symptoms and cognitive ability in older people? A prospective study using the English Longitudinal Study of Ageing. Psychol Med 2012;42:2057–2069.
39.
Jajodia A, Borders A. Memory predicts changes in depressive symptoms in older adults: a bidirectional longitudinal analysis. J Gerontol B Psychol Sci Soc Sci 2011;66:571–581.
40.
van den Kommer TN, Comijs HC, Aartsen MJ, Huisman M, Deeg DJH, Beekman ATF. Depression and cognition: how do they interrelate in old age? Am J Geriatr Psychiatry 2013;21:398–410.
Letters to the Editor
16 October 2014
Prevention of cognitive decline in old age by antidepressant treatment?
Hagen Kunte, Neurologist and Psychiatrist
Golo Kronenberg, Berlin, Germany; Rainer Hellweg, Berlin, Germany

The topical clinical-pathologic study by Wilson et al. provided exciting new evidence that depressive symptoms in old age have an association with cognitive decline independent of the neuropathologic hallmarks of dementia. [1] It is increasingly apparent that late-life depression is associated with an increase in risk of developing all-cause dementia. [2] However, several qualifications may be necessary.

Most likely, only a small fraction of this self-selected sample would fulfill DSM-IV criteria for a major depressive episode. It would be valuable to ascertain if patients with clinically significant depression at baseline, or during follow-up, differed from the rest regarding neuropathologic markers. In this context, it is worth mentioning that the presence of comorbid depression in Alzheimer dementia (AD) has been demonstrated to correspond to increases in AD-related neuropathologic changes beyond age, gender, level of education, and cognitive status. [3] Moreover, lifetime history of depression in AD patients has shown association with higher levels of plaque and tangle formation in hippocampus. [4]

The authors did not provide information on the use of psychotropic agents (antidepressants or lithium) in this sample. Conceivably, antidepressants or mood stabilizers may not only counteract depression, but also exert neuroprotective and neurotrophic actions extending beyond mood effects. [5]

1. Wilson RS, Capuano AW, Boyle PA, et al. Clinical-pathologic study of depressive symptoms and cognitive decline in old age. Neurology Epub 2014 July 30. 2. Diniz BS, Butters MA, Albert SM, et al. Late-life depression and risk of vascular dementia and Alzheimer's disease: systematic review and meta-analysis of community-based cohort studies. Br J Psychiatry 2013;202:329-335.

3. Rapp MA, Schnaider-Beeri M, Purohit DP, et al. Increased neurofibrillary tangles in patients with Alzheimer disease with comorbid depression. Am J Geriatr Psychiatry 2008;16:168-174.

4. Rapp MA, Schnaider-Beeri M, Grossman HT, et al. Increased hippocampal plaques and tangles in patients with Alzheimer disease with a lifetime history of major depression. Arch Gen Psychiatry 2006; 63:161-167.

5. Cirrito JR, Disabato BM, Restivo JL, et al. Serotonin signaling is associated with lower amyloid-? levels and plaques in transgenic mice and humans. Proc Natl Acad Sci U S A;108:14968-14973.

For disclosures, contact the editorial office at [email protected].

16 October 2014
Re:Prevention of cognitive decline in old age by antidepressant treatment?
Robert S. Wilson, Professor

We thank Drs. Kunte, Kronenberg, and Hellweg for their comments in which several important points were raised about our study. [1] We agree that the levels of depressive symptoms in the cohort were mostly mild (ie., 54.6% with none, 30.7% with 1 or 2, and 14.7% with 3 or more). This makes it all the more striking that variability within this relatively narrow range of depression severity accounted for nearly 5% of the variance in rates of cognitive decline (after adjustment for demographic and postmortem pathologic variables). If the cohort contained a higher proportion of participants with severe depression (defined psychometrically or diagnostically), the association of depression with cognitive decline would likely have been stronger. We agree that our findings do not rule out the possibility that depression only influences the accumulation of dementia related pathologies when it is severe. We plan to investigate this possibility in the future. We also agree that antidepressants may have a neuroprotective effect, but we have not yet seen evidence suggestive of this.

1. Wilson RS, Capuano AW, Boyle PA, et al. Clinical-pathologic study of depressive symptoms and cognitive decline in old age. Neurology Epub 2014 July 30. 2. Diniz BS, Butters MA, Albert SM, et al. Late-life depression and risk of vascular dementia and Alzheimer's disease: systematic review and meta-analysis of community-based cohort studies. Br J Psychiatry 2013;202:329-335.

For disclosures, contact the editorial office at [email protected].

8 September 2014
Depressive symptoms and cognitive decline in aging: is sleep a possible modulator?
Andre C. Boin
Camila Hirotsu, Sao Paulo, Brazil, Monica Levy Andersen, Sao Paulo, Brazil and Sergio Tufik, Sao Paulo, Brazil

We applaud Wilson et al. on their longitudinal research showing a novel model for cognitive decline in which depressive symptoms may play an essential role. [1] We would like to suggest the importance of sleep as a factor that also contributes in this depression-cognitive relationship.

Sleep could be an important confounding factor for cognitive evaluation in elderly population, since evidence has shown that both acute and chronic sleep deprivation may lead to deterioration in cognitive performance. [2] Moreover, sleep architecture changes across aging: sleep efficiency, percentage of slow wave sleep, and REM sleep decrease gradually. [3] Aging itself increases the risk of some sleep disorders, such as insomnia, which, in turn, is related to both depression and cognition. [4]

Recently a study showed that sleep plays an important role in the clearance of brain beta-amyloid protein, [5] and the possibility that such impairment across a lifespan closely relates to cognitive decline. Thus, the assessment of sleep would be essential in this research. Sleep evaluation is important in further protocol design since it may modulate the neuropathological manifestations of dementia.

1. Wilson RS, Capuano AW, Boyle PA, et al. Clinical-pathologic study of depressive symptoms and cognitive decline in old age. Neurology 2014;83:702-709.

2. Lo JC, Groeger JA, Santhi N, et al. Effects of partial and acute total sleep deprivation on performance across cognitive domains, individuals and circadian phase. PLoS One 2012;7:e45987.

3. Ohayon MM, Carskadon MA, Guilleminault C, Vitiello MV. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan. Sleep 2004;27:1255-1273

4. Koffel EA, Koffel JB, Gehrman PR. A meta-analysis of group cognitive behavioral therapy for insomnia. Sleep Med Rev Epub 2014 May 14.

5. Xie L, Kang H, Xu Q, et al. Sleep drives metabolite clearance from the adult brain. Science 2013;342:373-377.

For disclosures, contact the editorial office at [email protected].

26 August 2014
Re:Prevention of cognitive decline in old age by antidepressant treatment?
Donald R. Royall, Professor of Psychiatry

Wilson et al. recently reported in Neurology that depressive symptoms in old age affect cognition independently of neurodegenerative lesions. We concur. In a similarly large, longitudinal population-based cohort, the Honolulu-Asia Aging Study (HAAS), we found that baseline depressive symptoms were associated with the longitudinal rate of change in cognition over 10 years. This effect was independent of neurodegenerative [i.e., neuritic plaque (NP), diffuse plaque, neurofibrillary tangles and cortical Lewy Bodies] and ischemic lesions, and that the effect of depressive symptoms on cognition was comparable in strength to that of NP. [1]

Since then, we have defined dementing processes by a latent phenotype extracted from Spearman's general intelligence factor "g". Our phenotype (named "d" for "dementia") is strongly associated with clinical dementia [2] and can be specifically associated with the Default Mode Network (DMN). [3] d scores predict dementia across a wide range of conditions. [4] Interestingly, a d ortholog targeting "the cognitive correlates of depressive symptoms" also maps to the DMN and correlates r = 0.93 with d. [5] This finding leads to an interpretation which Wilson et al. did not discuss in their paper: Depressive symptoms may appear to hasten conversion to dementia because depression is itself a dementing illness (not a "pseudodementia") that must be considered independently of neurodegenerative lesion-related cognitive declines. Perhaps incident dementia could be treated with off-label antidepressants?

1. Royall DR, Palmer RF. Alzheimer pathology does not mediate the association between depressive symptoms and subsequent cognitive decline. Alzheimer's Disease & Dementia, 2013; 9:318-325.

2. Royall DR, Palmer RF, O'Bryant SE. Validation of a latent variable representing the dementing process. Journal of Alzheimer's Disease 2012;30:639-649.

3. Royall DR, Palmer RF, Vidoni ED, Honea RA. The Default Mode Network may be the key substrate of depression-related cognitive changes. Journal of Alzheimer's Disease, 2013;34:547-560.

4. Gavett BE, Vudy V, Jeffrey M, John SE, Gurnani A, Adams J. The ? latent dementia phenotype in the NACC UDS: Cross-validation and extension. Neuropsychology, in press.

5. Royall DR, Palmer RF, Vidoni ED, Honea RA, Burns JM. The Default Mode Network and related right hemisphere structures may be the key substrates of dementia. Journal of Alzheimer's Disease, 2012;32:467-478

For disclosures, contact the editorial office at [email protected].

Information & Authors

Information

Published In

Neurology®
Volume 83Number 8August 19, 2014
Pages: 702-709
PubMed: 25080520

Publication History

Received: February 6, 2014
Accepted: May 17, 2014
Published online: July 30, 2014
Published in print: August 19, 2014

Permissions

Request permissions for this article.

Disclosure

R. Wilson serves as a consulting editor for Aging, Neuropsychology, and Cognition, Psychology and Aging, and Neuropsychology; has served as a consultant for Pain Therapeutics, Inc.; and receives research support from NIH (P30AG010161 [coinvestigator], R01AG015819 [coinvestigator], R01AG017917 [coinvestigator], R01AG034374 [coinvestigator], R01AG039478 [coinvestigator], R01AG036042 [coinvestigator], R01AG036836 [coinvestigator], R01AG041797 [coinvestigator], R01AG042210 [coinvestigator], and R01NR013151 [coinvestigator]) and Alzheimer's Association (NIRGD-11-205469). A. Capuano receives research support from NIH (R01AG022018 [coinvestigator], R01AG017917 [coinvestigator], R01AG015819 [coinvestigator], P30AG010161 [coinvestigator], R01AG043379 [coinvestigator], R01HL096944 [coinvestigator], and R01AG040039 [coinvestigator]). P. Boyle receives research support from the NIH (R01AG034374 [principal investigator], R01AG034119 [coinvestigator], R01AG033678 [principal investigator], and R01AG040039 [coinvestigator]). G. Hoganson and L. Hizel report no disclosures. R. Shah receives research support from NIH (P30AG010161 [coinvestigator], P20MD006886 [coinvestigator], U01AG024904 [coinvestigator], U01AG029824 [coinvestigator], U01AG046152 [coinvestigator], U01AG010483 [coinvestigator], R01AG036042 [coinvestigator], and R01AG017917 [coinvestigator]), Merck & Company (clinical trial site principal investigator), Genentech, Inc. (clinical trial site principal investigator), Eli Lilly & Company (clinical trial site principal investigator), and Navidea Biopharmaceuticals (clinical trial site principal investigator). S. Nag receives research support from NIH (R01AG017917 [coinvestigator], P30AG010161 [coinvestigator], R01AG043379 [coinvestigator], R01NS078009 [coinvestigator], and R01NS082416 [coinvestigator]). J. Schneider receives research support from NIH (R01AG042210 [principal investigator], P30AG010161 [coinvestigator], R01HL096944 [coinvestigator], R01AG039478 [coinvestigator], R01AG017917 [coinvestigator], R01AG015819 [coinvestigator], R01AG022018 [coinvestigator], R01AG036042, [coinvestigator], R01AG040039 [coinvestigator], R01AG036836 [coinvestigator], R01AG034374 [coinvestigator], U01AG046152 [coinvestigator], R01AG043379 [coinvestigator], R01NS078009 [coinvestigator], R01AG043975 [coinvestigator], R01AG033678 [coinvestigator], and R21ES021290 [coinvestigator]). S. Arnold serves as an associate editor for Translational Neuroscience and Journal of Alzheimer's Disease, has been a consultant for Teva Pharmaceuticals, Inc., and receives research support from the NIH (R01AG039478 [principal investigator], P30AG10124 [clinical core principal investigator], R01DA025201 [coinvestigator], U01DK057135 [coinvestigator], U01AG024904 [site principal investigator]), the BrightFocus Foundation (principal investigator), the Marian S. Ware Charitable Giving Fund (project principal investigator), Johnson & Johnson (coinvestigator), Merck (clinical trial site principal investigator), Bristol-Myers Squibb (clinical trial site principal investigator), and Pain Therapeutics, Inc. (site principal investigator). D. Bennett serves on the editorial board of Neurology®; has served as a consultant to Schering-Plough Corp., Mediation, Inc., and the Gerson Lehrman Group; and receives research support from Danone Inc., the NIH (R01AG017917 [principal investigator], R01AG015819 [principal investigator], R01AG036042 [principal investigator], U01AG032984 [co-principal investigator, leader of epidemiologic cohort studies], R01HL096944 [coinvestigator], R01AG033678 [coinvestigator], R01AG034374 [coinvestigator], R01AG022018 [coinvestigator], R01AG034119 [coinvestigator], P30AG010161 [principal investigator—administrative core leader, Religious Orders Study core leader], U01AG046152 [coinvestigator], R01AG040039 [coinvestigator], R01AG039478 [coinvestigator], R01AG038651 [coinvestigator], R01AG036836 [coinvestigator], R01AG041797 [coinvestigator], R01AG042210 [coinvestigator], P20MD006886 [coinvestigator], R01NS078009 [coinvestigator], R01AG043617 [coinvestigator], R01AG043975 [coinvestigator], U18NS082140 [coinvestigator], and R01NS082416 [coinvestigator]), and the Illinois Department of Public Health. Go to Neurology.org for full disclosures.

Study Funding

This research was supported by the National Institute on Aging (R01AG17917, P30AG10161, R01AG15819, R01AG34374) and the Illinois Department of Public Health. The funding organizations had no role in the design or conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript.

Authors

Affiliations & Disclosures

Robert S. Wilson, PhD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
NONE
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
(1) Aging, Neuropsychology, and Cognition, Consulting Editor, 2004-present; (2) Psychology and Aging, Consulting Editor, 2007-present; (3) Neuropsychology, Consulting Editor, 2014-present.
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
(1) Pain Therapeutics, Inc.
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
NONE
Research Support, Government Entities:
1.
(1) NIH/NIA R01AG17917, Co-I, 2001-2014; (2) NIH/NIA P30AG10161, Co-I, 1991-2014; (3) NIH/NIA R01AG34374, Co-I, 2008-2014; (4) NIH/NIA R01AG15819, Co-I, 1998-2014.
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
Ana W. Capuano, PhD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
NONE
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
NONE
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
NONE
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
NONE
Research Support, Government Entities:
1.
NIH (R01AG022018 [co-investigator], R01AG017917 [co-investigator], R01AG015819 [co-investigator], P30AG010161 [co-investigator], R01AG043379 [co-investigator], R01HL096944 [co-investigator], and R01AG040039 [co-investigator]).
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
Patricia A. Boyle, PhD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
NONE
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
NONE
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
NONE
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
NONE
Research Support, Government Entities:
1.
(1) NIH/NIA R01AG034374, PI; (2) NIH/NIA R01AG033678, PI
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
George M. Hoganson, MD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
NONE
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
NONE
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
NONE
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
NONE
Research Support, Government Entities:
1.
NONE
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
Loren P. Hizel, BA
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
NONE
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
NONE
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
NONE
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
NONE
Research Support, Government Entities:
1.
(1) NIH/NIA, R01AG017917 & P30AG10161, research assistant, 2010-2012
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
Raj C. Shah, MD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
advisory board service for (1) Merck & Co., Inc. (2) Genentech, Inc.
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
(1) Journal of Alzheimer's Disease, Associate Editor, 2013
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
(1) Danone Trading B.V. (2) W. Health, L.P.
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
(1) Danone Research B.V. (2) Eli Lilly & Co., Inc. (3) Genentech, Inc. (4) Merck & Co., Inc. (5) Metabolic Solutions Development Company (6) Navidea Biopharmaceuticals (7) Takeda Development Center Americas, Inc.
Research Support, Government Entities:
1.
(1) NIH, P30 AG101061, Education and Information Transfer Core Leader and Clinical Core Coinvestigator, 2009-present (2) NIH, P20 MD006886, Leader, Education/Research Training Core & Co-investigator, Community Engagement/Outreach Core, 2012-present (3) NIH U01 AG010483, Site Investigator, 2004-present (4) NIH U01 AG029824, Site Principal Investigator, 2009-present (5) NIH, U01 AG046152, Coinvestigator, 2013-present (6) NIH U01, AG024904, Site Coinvestigator, 2004-2013, Site Principal Investigator 2013-present (7) NIH, RC2 AG03653501, Site Investigator, 2009-2012 (8) NIH R01 AG011101, Examining Geriatrician, 2002-2012 (9) NIH R01 NR009543, Coinvestigator, 2007-2013 (10) NIH, P01 AG009466, Coinvestigator, Administrative Core, 2004-2013 (11) Illinois Department of Public Health, Alzheimer�s Disease Assistance Center, Associate Director, 2012-present (12) PCORI, CDRN-1306-04737, Site Principal Investigator, 2014-present (13) Center for Medicare & Medicaid Services, FP050658, Site Principal Investigator, 2012-present (14) DOD, W81XWH-12-2-0012, Site Investigator, 2012-present
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
Sukriti Nag, MD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
NONE
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
NONE
Patents:
1.
NONE
Publishing Royalties:
1.
The blood-brain & Other neural barriers, Springer Science + Business Media,Humana Press, 2011 Nag S (Editor)
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
NONE
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
NONE
Research Support, Government Entities:
1.
NONE
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
Julie A. Schneider, MD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
1. served on scientific advisory board for GE Healthcare (2010) 2. served on scientific advisory board for Eli Lilly and Company (2011) 3. served on advisory board for Genetech (2013)
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
2005-current Journal Histochemistry and Cytochemistry (Monitoring editor) 2008-current International Journal of Clinical and Experimental Pathology (IJCEP, ISSN 1936-2625) (Editorial Board) 2010 Journal of Alzheimer's Disease (Associate Editor)
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
Neuropathology consultant, AVID radiopharmaceuticals 2009-12
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
AVID radiopharmaceutical phase III clinical trial Neuropathologist 2010-2011
Research Support, Government Entities:
1.
1R01AG042210 (Schneider) 07/1/12- 06/30/17 Epidemiologic Study of TDP-43 Pathology in Aging and Dementia Major goal is to determine whether age-related TDP-43 pathology represents a separate pathologic process associated with a dementia syndrome with a distinct cognitive phenotype and specific genetic risk factors that are separate from AD. Role: Principal investigator R01NS078009 (Buchman) 9/15/12-6/30/17 NINDS The Clinical Profile of Parkinson's Disease (PD) Pathology. The overall goal is to characterize the clinical profile of PD pathology in older persons without a diagnosis of PD. Role: co-investigator R01AG043379 (Buchman) 9/30/12-8/31/17 NIA Brain and Spinal Cord Microvascular Pathology in Late-Life Motor Impairment The overall goal is to test the hypothesis that specific microvascular pathologies in the brain and spinal cord contribute to late-life motor impairment. U01AG016976 (Kukull/Montine) 7/1/12-6/30/13 NIA (Pilot) Optimization of Neuropathologic Assessment of Alzheimer�s Disease; The overall goal is to optimize neuropathologic diagnosis of Alzheimer�s disease for uniformity and accurancy across centers Role: Site Principal Investigator P30 AG10161 (Bennett) 9/30/91-6/30/16 Rush Alzheimer's Disease Core Center Major goals to provide core infrastructure support for research regarding aging/dementia/AD. Role: Associate Director, Core Leader: Neuropathology Core R01 AG031553 (Morris) 3/15/08 � 2/28/13 Epidemiologic Study of Brain Vitamin E, Diet, and Age-Related Neurologic Diseases; Major goal is analyze Vitamin E in brain, CSF, serum, and diet and compare to neuropathology and dementia. Role: Co-Principal Investigator R01 AG17917 (Bennett) 9/30/01-6/30/13 Epidemiologic Study of Neural Reserve and Neurobiology of Aging; Major goals are to identify structural bases of reserve and examine mechanisms risk factors lead to age-related functional impairment. Role: Co-Investigator R01 AG15819 (7/1/98 � 6/30/13 Risk Factors, Pathology and Clinical Expressions of AD The major goals of this project are to examine the pathologic mechanisms through which risk factors lead to clinical AD. Role: Co-investigator P01 AG14449 (Mufson) 9/1/97 � 3/31/13 Neurobiology of Mild cognitive impairment in the Elderly; The major goals are to identify neurobiologic substrates of mild cognitive impairment. Role: Co-investigator (Neuropathologist) R01AG033678-01 (Boyle) 9/15/2009 - 6/30/14 Epidemiologic study of impaired decision making in preclinical Alzheimer�s disease. The overall goal of the proposed epidemiologic study is to examine the causes and consequences of impaired decision-making in old age. Role: Neuropathologist R01AG034374 (Boyle) 8/15/2009 -7/31/14 Characterizing the behavior profile of healthy cognitive aging. Goal is to use innovative statistical approaches to characterize the profile of healthy cognitive aging defined as age-related cognitive change not accounted for by the presence of common neuropathologies (i.e., Alzheimer's disease, cerebral infarcts, and the Lewy body diseases) or terminal decline. Role: Neuropathologist. P01 AG09466 (deToledo-Morrell) 4/1/1991-8/31/12 Anatomic, Physiologic, Cognitive Pathology of AD; major goals- to identify neurobiologic, radiologic, physiologic, cognitive markers with AD; Role: Co-Investigator; Neuropathologist, Administrative Core R01 AG36042 (Bennett) 9/15/09-8/31/14 Exploring the Role of the Brain Epigenome: Cognitive Decline and Life Experiences The goal of the study is to examine the relation of DNA methylation to cognitive decline and life experiences. Role: Neuropathologist R01 HL096944 (Levine) 9/1/09 � 6/30/13 Stroke and aPL: Community-Based Clinicopathologic Study The major goal of this project is to investigate the role and mechanisms of antiphospholipid antibodies (aPL) in the development of pathologically-proven ischemic brain infarction. Role: Neuropathologist R01AG040039 (Arvanitakis) 9/30/11-8/31/16 National Institute on Aging Vascular Cognitive and Motor Decline: Impact of aPL The major goal of this project is to investigate the role and mechanisms of antiphospholipid antibodies (aPL) in the development of cognitive and motor decline in aging. R01AG039478 (Arnold) 4/1/11-3/31/16 National Institute on Aging Targeted Proteomics of Resilient Cognition in Aging The major goal of the study is to identify candidate proteins and pathways that best confer cognitive resilience despite the accumulation of neurodegenerative disease pathology. Role: Neuropathologist R01AG036836 (DeJager) 9/15/11-8/31/15 National Institute on Aging Exploring the Role of the Brain Transcriptome in Cognitive Decline The major goal is to investigate the transcriptome of human brain tissue to identify molecular pathways that contribute to cognitive decline. Role: Neuropathologist
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
Steven E. Arnold, MD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
Teva
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
NONE
Editorial Boards:
1.
Journal of Alzheimer's Disease
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
NONE
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
Eli Lilly; Pfizer; Merck; Neuronetrix; Johnson & Johnson; Baxter; Tohyama
Research Support, Government Entities:
1.
NIH
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
Marian S. Ware Family Foundation Barra Foundation; BrightFocus Foundation
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE
David A. Bennett, MD
From the Rush Alzheimer's Disease Center (R.S.W., A.W.C., P.A.B., G.M.H., L.P.H., R.C.S., S.N., J.A.S., D.A.B.) and Departments of Behavioral Sciences (R.S.W., P.A.B.), Neurological Sciences (R.S.W., A.W.C., J.A.S., D.A.B.), Pathology (S.N., J.A.S.), and Family Medicine (R.C.S.), Rush University Medical Center, Chicago, IL; and Departments of Psychiatry and Neurology (S.E.A.), University of Pennsylvania, Philadelphia.
Disclosure
Scientific Advisory Boards:
1.
(1) Vigorous Minds, Scientific Advisory Board (2) Takeda Pharm - Adjudication committee AD4833/TOMM40_301 study
Gifts:
1.
NONE
Funding for Travel or Speaker Honoraria:
1.
Nutricia, paid for travel to scientific meeting
Editorial Boards:
1.
(1) Neurology, Editorial Board; (2) Current Alzheimer Research, Editorial Board; (3) Neuroepidemiology, Editorial Board
Patents:
1.
NONE
Publishing Royalties:
1.
NONE
Employment, Commercial Entity:
1.
NONE
Consultancies:
1.
(1) Nutricia, Inc., (2) Eli Lilly, Inc., (3) Enzymotec Ltd.,
Speakers' Bureaus:
1.
NONE
Other Activities:
1.
NONE
Clinical Procedures or Imaging Studies:
1.
NONE
Research Support, Commercial Entities:
1.
(1) Nutricia Inc., co-PI (2) Zinfandel, PI
Research Support, Government Entities:
1.
NIH: P30AG10161, PI; R01AG15819, PI; R01AG17917, PI; R01AG36042, PI; U01AG32984, Co-I; R01AG22018, Co-I; R01AG33678, Co-I; R01AG36836, Co-I; R01AG41797, Co-I; R01AG42210, Co-I; U01AG46152, MPI; and Illinois Department Public Health
Research Support, Academic Entities:
1.
NONE
Research Support, Foundations and Societies:
1.
NONE
Stock/stock Options/board of Directors Compensation:
1.
NONE
License Fee Payments, Technology or Inventions:
1.
NONE
Royalty Payments, Technology or Inventions:
1.
NONE
Stock/stock Options, Research Sponsor:
1.
NONE
Stock/stock Options, Medical Equipment & Materials:
1.
NONE
Legal Proceedings:
1.
NONE

Notes

Correspondence to Dr. Wilson: [email protected]
Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

Author Contributions

Drafting/revising manuscript for content: Wilson, Capuano, Boyle, Hoganson, Hizel, Shah, Nag, Schneider, Arnold, Bennett. Study concept or design: Wilson, Capuano, Boyle, Hoganson, Hizel, Shah, Nag, Schneider, Arnold, Bennett. Analyses or interpretation of the data: Wilson, Capuano, Boyle, Shah, Nag, Schneider, Arnold, Bennett. Acquisition of data: Bennett, Nag, Schneider. Statistical analysis: Capuano. Study supervision or coordination: Bennett. Obtaining funding: Boyle, Bennett.

Metrics & Citations

Metrics

Citations

Download Citations

If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Select your manager software from the list below and click Download.

Cited By
  1. From theory to practice: translating the concept of cognitive resilience to novel therapeutic targets that maintain cognition in aging adults, Frontiers in Aging Neuroscience, 15, (2024).https://doi.org/10.3389/fnagi.2023.1303912
    Crossref
  2. Distinguishing features of depression in dementia from primary psychiatric disease, Discover Mental Health, 4, 1, (2024).https://doi.org/10.1007/s44192-023-00057-y
    Crossref
  3. Is later-life depression a risk factor for Alzheimer’s disease or a prodromal symptom: a study using post-mortem human brain tissue?, Alzheimer's Research & Therapy, 15, 1, (2023).https://doi.org/10.1186/s13195-023-01299-2
    Crossref
  4. Depressive Disorders, The American Psychiatric Association Publishing Textbook of Geriatric Psychiatry, (2023).https://doi.org/10.1176/appi.books.9781615375196.ds09
    Crossref
  5. Can Depressive Symptomatology at Diagnosis Predict Cognitive and Functional Decline Over 1 Year in Rural Canadian Patients With Dementia?, Alzheimer Disease & Associated Disorders, 37, 3, (179-183), (2023).https://doi.org/10.1097/WAD.0000000000000574
    Crossref
  6. Well-Being and Aging-Related Decline in Financial and Health Literacy in Advanced Age, The Journals of Gerontology: Series B, 78, 9, (1526-1532), (2023).https://doi.org/10.1093/geronb/gbad059
    Crossref
  7. The association of spousal depressive symptoms and cognitive function among older adults: mediation and moderated mediation analyses, Aging & Mental Health, 27, 11, (2162-2169), (2023).https://doi.org/10.1080/13607863.2023.2213665
    Crossref
  8. Depressive Symptoms Mediate Associations between Subjective Memory Complaints, Cognitive Ability, and Instrumental Activities of Daily Living, Physical & Occupational Therapy In Geriatrics, 41, 4, (556-575), (2023).https://doi.org/10.1080/02703181.2023.2198559
    Crossref
  9. Biological factors influencing depression in later life: role of aging processes and treatment implications, Translational Psychiatry, 13, 1, (2023).https://doi.org/10.1038/s41398-023-02464-9
    Crossref
  10. Selective serotonin reuptake inhibitor use, age-related neuropathology and cognition in late-life, Psychiatry Research, 328, (115471), (2023).https://doi.org/10.1016/j.psychres.2023.115471
    Crossref
  11. See more
Loading...

View Options

Get Access

Login options

Check if you have access through your login credentials or your institution to get full access on this article.

Personal login Institutional Login
Purchase Options

Purchase this article to get full access to it.

Purchase Access, $39 for 24hr of access

View options

Full Text

View Full Text

Full Text HTML

View Full Text HTML

Media

Figures

Other

Tables

Share

Share

Share article link

Share