Related Experiment Video
Updated: Jun 8, 2026

Assessment of Spontaneous Alternation, Novel Object Recognition and Limb Clasping in Transgenic Mouse Models of Amyloid-β and Tau Neuropathology
Published on: May 28, 2017
Intraindividual cognitive variability predicts amyloid beta, tau PET, and dementia conversion in Down syndrome: a
Luciana Mascarenhas Fonseca1,2, Eardi Lila3, Ali Shojaie3
1The Krieger Klein Alzheimer's Research Center, Rutgers Health, New Brunswick, New Jersey, USA.
Introduction:
Adults with Down syndrome (DS) are at risk for Alzheimer's disease (AD), yet identifying the preclinical phase remains challenging. Intraindividual cognitive variability (IICV) may be a sensitive marker of early AD-related changes but remains understudied in DS.
Methods:
Adults from the Alzheimer's Biomarker Consortium-DS (ABC-DS) study (N = 460, mean age 43.3 years; 45.7% female) were included. Generalized linear models examined whether baseline IICV predicted incident mild cognitive impairment (MCI)/dementia, cognitive decline, and amyloid and tau positron emission tomography outcomes, adjusting for demographics, intellectual disability, apolipoprotein E ε4, site, assessment interval, and mean cognitive performance, with Bonferroni correction.
Results:
Greater IICV predicted incident MCI/dementia (odds ratio = 4.63 to 5.13, p < 0.05), greater amyloid burden, early tau accumulation, and higher tau across Braak stages, independent of mean cognition. Exploratory analyses suggested sex-specific interactions with tau outcomes.
Discussion:
IICV is a sensitive marker of dementia risk and cognitive resilience in DS, with potential utility for secondary prevention and trial enrichment.
Related Concept Videos
Alzheimer Disease l: Introduction
Alzheimer's Disease: Overview
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Dementia l: Introduction
Cognitive Development During Adulthood
Dementia
The progression of dementia is generally gradual.
Alzheimer Disease ll: Pathophysiology
