Increased functional connectivity of the precuneus in individuals with a family history of Alzheimer’s disease

Abstract

Background First‐degree relatives of individuals with late‐onset Alzheimer’s Disease (AD) have increased risk for AD, with children of affected parents at an especially high risk. We sought to test how structural or functional abnormalities in the default mode network (DMN) during the brain’s “resting state” characterized individuals at risk for AD. Method We used MRI and fMRI to study cognitively healthy individuals (n=28) with and without AD family history (FH+ and FH‐, respecitvely), those with amnestic mild cognitive impairment (aMCI; n=31) and early‐stage AD (n=25). We tested connectivity within the DMN, as well as measures of volume and thickness within both the medial temporal cortex and in selected seed regions. Our primary hypothesis was that there would be a linear decline within the risk groups on all measures of AD risk (FH‐>FH+>aMCI>AD). Result As expected, we identified significantly decreased medial temporal cortex volumes in the aMCI and AD groups compared to both nondemented groups. We also observed patterns of connectivity across risk groups that suggest a nonlinear relationship of change, such that the FH+ group showed increased connectivity compared to the FH‐ and AD groups. This pattern emerged primarily in connectivity between the precuneus and frontal regions. Conclusion We present distinct structural and functional brain imaging profiles for two AD‐risk groups; cognitively healthy, FH+ individuals, and individuals with aMCI. These results add to a growing literature that suggests compensatory brain function in otherwise cognitively healthy individuals with a family history of AD.

Mapping the Interplay of Atrial Fibrillation, Brain Structure and Cognitive Dysfunction

“…The anterior cingulate, medial temporal lobe and precuneus have a particular role in Alzheimer's and vascular dementia, directly influencing associations with cognitive symptoms. [57][58][59][60] It is plausible that pathology in these areas might accelerate cognitive decline and the onset of dementia in individuals with AF. As there is an observable disparity between cortical patterns of macro-and microstructural changes, we propose that these differences could represent varying local stages of tissue changes all tethered to a shared disease mechanism.…”