Older adults who ultimately develop dementia experience accelerated cognitive decline long before diagnosis. A similar acceleration in cognitive decline occurs in the years before death as well. To evaluate preclinical and terminal cognitive decline, past researchers have incorporated change points in their analyses of longitudinal data, identifying point estimates of how many years prior to diagnosis or death that decline begins to accelerate. The current systematic review aimed to summarize the published literature on preclinical and terminal change points in relation to mild cognitive impairment (MCI), dementia, and death, identifying the order in which cognitive and neurological outcomes decline and factors that modify the onset and rate of decline. A systematic search protocol yielded 35 studies, describing 16 longitudinal cohorts, modeling change points for cognitive and neurological outcomes preceding MCI, dementia, or death. Change points for cognitive abilities ranged from 3–7 years prior to MCI diagnosis, 1–11 years prior to dementia diagnosis, and 3–15 years before death. No sequence of decline was observed preceding MCI or death, but the following sequence was tentatively accepted for Alzheimer’s disease: verbal memory, visuospatial ability, executive functions and fluency, and last, verbal IQ. Some of the modifiers of the onset and rate of decline examined by previous researchers included gender, education, genetics, neuropathology, and personality. Change point analyses evidence accelerated decline preceding MCI, dementia, and death, but moderators of the onset and rate of decline remain ambiguous due to between-study modeling differences, and coordinated analyses may improve comparability across future studies. (PsycINFO Database Record (c) 2018 APA, all rights reserved)

Introduction: Although personality change is typically considered a symptom of dementia, some studies suggest that personality change may be an early indication of dementia. This project examines this possibility by examining trajectories of personality traits preceding dementia diagnosis in several longitudinal studies of aging.

Methods: Three independent series of latent growth curve models were fitted to data from the Origins of Variance in the Oldest-Old (OCTO-Twin), Longitudinal Aging Study Amsterdam (LASA) and Einstein Aging Study (EAS) to estimate trajectories of personality traits in individuals with incident dementia diagnosis (Total N = 295), in individuals with incident Mild Cognitive Impairment (N = 135), and in individuals who did not receive a diagnosis during follow-up periods (Total N = 2109).

Results: Controlling for sex, age, education, depressive symptoms, and the interaction between age and education, growth curve analyses consistently revealed significant linear increases in neuroticism preceding dementia diagnosis in both datasets and in individuals with MCI. Analyses examining individuals without a diagnosis revealed non-significant change in neuroticism overtime.

Discussion: Replication in several datasets provides compelling evidence that increases in neuroticism may be early indication of dementia, which can facilitate development of screening assessments and aid in early care strategies.

Objectives: To determine whether assessment-to-assessment fluctuations in episodic memory (EM) reflect fluctuations in olfaction over time.

Methods: Within-person coupled variation in EM and the Brief Smell Identification Test (BSIT) was examined in 565 participants aged 58–106 with autopsy data from the Rush Memory and Aging Project. A growth model for up to 15 years of EM data, with BSIT as time-varying covariate, was estimated accounting for main effects of sex, education, ε4 allele, and Alzheimer’s disease (AD) pathology, BSIT and time-varying BSIT, as well as the interaction between AD pathology and time-varying BSIT.

Results: Individuals with higher BSIT scores (b = .01, standard error [SE] = .004, p = .009) had slower declines in EM. High AD pathology (b = −.06, SE = .02, p = .001) was associated with more rapid declines in EM. The association between time-specific fluctuations in EM and BSIT differed by level of AD pathology (b = .08, SE = .034, p = .028), with a higher EM–BSIT association at higher levels of pathology. Discussion: BSIT and EM fluctuate together over measurement occasions, particularly for individuals with AD pathology. Repeated intraindividual measurements provide information that could lead to early detection and inexpensive monitoring of accumulating AD pathology.