학술논문

Regional amyloid accumulation and cognitive decline in initially amyloid-negative adults
Document Type
article
Source
Neurology. 91(19)
Subject
Alzheimer's Disease
Aging
Neurodegenerative
Dementia
Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD)
Acquired Cognitive Impairment
Clinical Research
Brain Disorders
Prevention
Neurosciences
Neurological
Adult
Aged
Aged
80 and over
Amyloid beta-Peptides
Brain
Cognitive Dysfunction
Female
Humans
Longitudinal Studies
Male
Memory
Episodic
Middle Aged
Clinical Sciences
Cognitive Sciences
Neurology & Neurosurgery
Language
Abstract
ObjectiveTo assess whether global or regional changes in amyloid burden over 4 years predict early declines in episodic memory in initially amyloid-negative adults.MethodsOne hundred twenty-six initially amyloid-negative, cognitively normal participants (age 30-89 years) were included from the Dallas Lifespan Brain Study who completed florbetapir PET and a cognitive battery at baseline and 4-year follow-up. Standardized uptake value ratio (SUVR) change was computed across 8 bilateral regions of interest. Using general linear models, we examined the relationship between change in global and regional SUVR and change in episodic memory, controlling for baseline SUVR, baseline memory, age, sex, education, and APOE status.ResultsIn initially amyloid-negative adults, we detected a regionally specific relationship between declining episodic memory and increasing amyloid accumulation across multiple posterior cortical regions. In addition, these amyloid-related changes in memory persisted when we focused on middle-aged adults only and after controlling for atrophy in global cortical, hippocampal, and Alzheimer disease signature cortical volume.ConclusionOur results indicate that assessing regional changes in amyloid, particularly in posterior cortical regions, can aid in the early detection of subclinical amyloid-related decline in episodic memory as early as middle age. Future research incorporating tau and other markers of neurodegeneration is needed to clarify the sequence of events that lead to this early, subclinical memory decline.