Tau Accumulation and Network Breakdown in Alzheimer's Disease.

Tau Accumulation and Network Breakdown in Alzheimer's Disease. Adv Exp Med Biol. 2019;1184:231-240 Authors: Watanabe H, Bagarinao E, Yokoi T, Yamaguchi H, Ishigaki S, Mausuda M, Katsuno M, Sobue G Abstract Misfolded and aggregated tau and amyloid β (Aβ) proteins are the pathological hallmarks of Alzheimer's disease (AD). These aberrant proteins lose their physiological roles, acquire neurotoxicity, and propagate across neural systems. Despite the growing understanding of the molecular pathophysiology, the relationship among molecular alterations, pathological changes, and dementia onset and progression remain to be elucidated. Connectivity is an exclusive characteristic of the brain, and the integrity and segregation of the functional and anatomical networks are crucial for normal functioning. Interestingly, a lot of magnetic resonance imaging (MRI) studies have demonstrated successive structural and functional disconnection among brain regions supporting the idea that AD is a disconnection syndrome. Recent several studies using the combination of cutting-edge Aβ and tau PET tracers integrated by data-driven statistical methods, resting-state functional MRI, and diffusion tensor imaging have shed light on the spatial distribution pattern of tau retention as well the relationship between tau retention and functional/structural network disruption in AD. Regional retention of tau PET traces is associated with gray matter changes, str...
Source: Advances in Experimental Medicine and Biology - Category: Research Tags: Adv Exp Med Biol Source Type: research