New research has shown the effects of early amyloid-beta and tau protein accumulation on disrupted brain connectivity.
The study, published online in the journal Proceedings of the National Academy of Sciences, specify on how such disrupted connections could be evident before indications of cognitive impairment.
“It is hypothesized that amyloid-β and tau pathology in preclinical Alzheimer’s disease (AD) spread through functional networks, disrupting neural communication that results in cognitive dysfunction,” the study states.
“We used high-resolution (voxel-level) graph-based network analyses to test whether in vivo amyloid-β and tau burden was associated with the segregation and integration of brain functional connections, and episodic memory, in cognitively unimpaired Presenilin-1 E280A carriers who are expected to develop early-onset AD dementia in ∼13 y on average.”
What researchers concluded in their study: “These findings enlighten our understanding of how AD-related pathology distinctly alters the brain’s functional architecture in the preclinical stage, possibly contributing to pathology propagation and ultimately resulting in dementia.”
The study was published April 5, 2022.