Study partner-reported decline identifies cognitive decline and dementia risk
- PMID: 31721455
- PMCID: PMC6917311
- DOI: 10.1002/acn3.50938
Study partner-reported decline identifies cognitive decline and dementia risk
Abstract
Objective: Identifying individuals at risk for cognitive decline, Mild Cognitive Impairment (MCI), and dementia due to Alzheimer's disease (AD) is a critical need. Functional decline is associated with risk and can be efficiently assessed by participants and study partners (SPs). We tested the hypothesis that SP-reported functional decline is an independent predictor of dementia risk and cognitive decline.
Methods: In 1048 older adults in the Alzheimer's Disease Neuroimaging Initiative (ADNI), we measured associations between Everyday Cognition Scale scores (ECog, self- and SP-reported versions) and (1) baseline and longitudinal change in neuropsychological test (NPT scores) across multiple cognitive domains; (2) diagnostic conversion to MCI or dementia. Models included Mini Mental Status Exam (MMSE) score and ApoE ε4 genotype (APOE) as predictors. Model fits were compared with and without predictors of interest included.
Results: SP-reported ECog was the strongest predictor of cognitive decline across multiple domains, as well as diagnostic conversion. Self-reported ECog was associated with baseline NPT scores in some cognitive domains, and diagnostic conversion to MCI in participants with biomarker evidence for AD (elevated brain β-amyloid, Aβ). Models including SP-reported ECog were significantly stronger at predicting outcomes.
Conclusions: SP-reported functional decline is an independent indicator of cognitive decline and dementia risk, even when accounting for cognitive screening, genetic risk, demographics, and self-report decline. The results provide a rationale for greater utilization of SP-reported functional decline to identify those at risk for dementia due to AD and other causes.
© 2019 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.
Conflict of interest statement
RLN, JN, PSI, JN, and RSM have no potential conflicts of interest to disclose related to the work in this manuscript. MWW reports personal fees from Bioclinica, personal fees from Cerecin/Accera, personal fees from Genentech, grants and personal fees from NIH, personal fees from Indiana University, personal fees from CHU Toulouse, personal fees from St. George University, personal fees from Eli Lilly, personal fees from Roche, personal fees from Lynch Group GLC, personal fees from Dolby Family Ventures, personal fees from Nestec/Nestle, personal fees from Health & Wellness Partners for American Academy of Neurology Conference, personal fees from AC Immune, personal fees from Alzheimer's Association, personal fees from Merck, personal fees from Bionest Partners, personal fees from Alzheon, Inc., personal fees from University of Tokyo, personal fees from Australian Catholic University, personal fees from University of Melbourne, personal fees from National Cntr for Geriatrics & Gerontology (Japan), grants from Department of Defense (DOD), grants from Johnson & Johnson (J&J), grants from Connie & Kevin Shanahan, grants from General Electric Research Labs (GE), grants from PCORI, grants from California Dept. of Public Health, grants from VUmc Vanderbilt University Medical Center, grants from University of Michigan, grants from Ray & Dagmar Dolby Fund, grants from Biogen, grants from Hillblom Foundation, grants from Stroke Foundation, grants from Siemens, grants from Veterans Administration. All relationships stated above are outside the submitted work.
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