Article
Activated microglia mediate synapse loss and short-term memory deficits in a mouse model of transthyretin-related oculoleptomeningeal amyloidosis.
Cell death & disease - 5 Sept 2013
Azevedo E P, Ledo J H, Barbosa G, Sobrinho M, Diniz L, Fonseca A C C, Gomes F, Romão L, Lima F R S, Palhano F L, Ferreira S T, Foguel D
Abstract excerpt
Oculoleptomeningeal amyloidosis (OA) is a fatal and untreatable hereditary disease characterized by the accumulation of transthyretin (TTR) amyloid within the central nervous system. The mechanisms underlying the pathogenesis of OA, and in particular how amyloid triggers neuronal damage, are still unknown. Here, we show that amyloid fibrils formed by a mutant form of TTR, A25T, activate microglia, leading to the...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.