Subjective Cognitive Complaints, Personality and Brain Amyloid-beta in Cognitively Normal Older Adults

Abstract

Objectives Subjective cognitive complaints in otherwise normal aging are common but may be associated with preclinical Alzheimer Disease in some individuals. Little is known about who is mostly likely to show associations between cognitive complaints and preclinical Alzheimer pathology. We sought to 1) demonstrate associations between subjective complaints and brain amyloid-β in cognitively normal older adults; 2) to explore personality factors as potential moderators of this association. Design Cross-sectional observational study. Setting Clinical neuroimaging research center. Participants Community volunteer sample of 92 healthy older adults, screened for normal cognition with comprehensive neuropsychological evaluation. Measurements Subjective cognitive self-report measures included the Memory Functioning Questionnaire, Cognitive Failures Questionnaire, and the Subjective Cognitive Complaint Scale. Personality was measured with the NEO Five Factor Inventory. Brain amyloid-β deposition was assessed with Pittsburgh compound B (PiB)-PET imaging. Results One of three cognitive complaint measures, the Memory Functioning Questionnaire, was associated with global PiB retention (standardized beta =−.230, p=.046, adjusting for age, sex and depressive symptoms). Neuroticism moderated this association such that only high neuroticism individuals showed the predicted pattern of high complaint – high amyloid-β association. Conclusions Evidence for association between subjective cognition and brain amyloid-β deposition in healthy older adults is demonstrable but measure-specific. Neuroticism may moderate the MFQ – amyloid-β association such that it is observed in the context of higher trait neuroticism. Subjective cognitive complaints and neuroticism may reflect a common susceptibility toward psychological distress and negative affect, which are in turn risk factors for cognitive decline in aging and incident Alzheimer Disease.

Implementation of subjective cognitive decline criteria in research studies

“…It is not uncommon to observe anxiety and depresive symptoms among SCD particpants. In fact, self reported measures of SCD correlate more with personality traits than with AD biomarkers, being the opposite with proxy-related questionnaires (61, 90). Neverthelees, patients at early stages of AD also present emotional, psychological and mild behavioral disturances (113).…”

“…These studies, however, should make their aims clear and distinguish their approach from the study of SCD in preclinical AD. The majority of SCD studies will focus on early AD identification and prediction of cognitive decline and dementia or will aim to identify subjects in the preclinical stage of AD for intervention trials (2, 8, 16, 26, 61). These studies will treat a major psychiatric diagnosis as an exclusion criterion.…”

“…Affective symptoms may be accelerating factors for cognitive decline at the late stage of preclinical AD or may even be considered part of the late preclinical AD syndrome together with subtle cognitive dysfunction and SCD (on some occasions being the explanation for SCD) (68, 69). In this regard, personality traits, which are related to increased levels of stress, anxiety and depression have frequently been found to be associated with SCD (61, 70). While factors such as openness, conscientiousness, and self-esteem, correlate with low SCD scores, in particular neuroticism has been associated with high SCD reporting (71–73).…”

“…Recently, it was demonstrated that particular worries about memory decline in MCI predicts biomarker evidence for AD in CSF (77). In cognitively healthy individuals, an association of the SCD report with amyloid deposition has been observed in those individuals, who report high on neuroticism (61). Overall, the interaction of SCD, neuroticism, AD pathology and risk of dementia seems complex.…”

Hippocampal hypometabolism in older adults with memory complaints and increased amyloid burden

“…Whereas most studies have reported an association between SMCs and Ab, [3][4][5][6] others could not demonstrate this relationship. 7 Previous studies with fluorodeoxyglucose (FDG)-PET, a biomarker supposed to reflect neuronal integrity, 8 have demonstrated hypometabolism when comparing cognitively normal (CN) individuals with and without SMCs, but the results have been inconsistent as to which brain regions show hypometabolism, e.g., the precuneus, 9 parietotemporal and parahippocampal gyrus, 10 or periventricular region.…”