Acta Neuropathologica, Journal Year: 2014, Volume and Issue: 129(2), P. 207 - 220

Published: Dec. 9, 2014

Neurofibrillary tangles and amyloid plaques constitute the hallmark brain lesions of Alzheimer’s disease (AD) patients. Tangles are composed fibrillar aggregates microtubule-associated protein tau, comprise forms a proteolytic cleavage product, amyloid-β (Aβ). Although end-stage in AD, small oligomers Aβ tau now receiving increased attention as they shown to correlate best with neurotoxicity. One key question debate, however, is which these pathologies appears first hence upstream pathocascade. Studies suggest that there an intense crosstalk between two molecules and, based on work animal models, increasing evidence Aβ, at least part, exerts its toxicity via Src kinase Fyn playing crucial role this process. In other experimental paradigms, have been found exert both separate synergistic modes toxicity. The challenge, integrate different scenarios into coherent picture. Furthermore, ability therapeutic interventions targeting just one molecules, successfully neutralize other, needs be ascertained improve current strategies, such immunotherapy, for treatment AD. article not intended provide comprehensive review currently pursued we will discuss what has achieved by immunotherapy particular, how inherent limitations approach can possibly overcome novel strategies involve single-chain antibodies.

Language: Английский