Amyloid beta modulators and neuroprotection in Alzheimer's disease: a critical appraisal.

ABSTRACT: Multiple cellular changes have been identified as being involved in Alzheimer's disease (AD) pathogenesis, including mitochondrial damage, synaptic loss, amyloid beta (A?) production and/or accumulation, inflammatory responses, and phosphorylated tau formation and/or accumulation. Studies have established that A?-induced synaptic dysfunction is dependent on abnormal amyloid precursor protein (APP) processing caused by ?- and ?-secretases, resulting in the generation of A?. The A? formed as a result of abnormal APP processing induces phosphorylated tau and activates glycogen synthase kinase-3? (GSK3?) and cyclin-dependent kinase-5 (CDK5). Here, we review the latest research on the development of A? modulators for neuroprotection in AD. We also review the use of molecular inhibitors as therapeutic targets in AD.

SUBMITTER: Kuruva CS 

PROVIDER: S-EPMC5344027 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature