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

- Multiple cellular changes have been identified as being involved in AD pathogenesis.
- Studies concluded that abnormal APP processing causes Aβ-induced synaptic dysfunction.
- Aβ induces tau phosphorylation and activates GSK-3β and CDK-5, ultimately causes neuronal dysfunction.
- Aβ modulators are potential therapeutic drugs to treat patients with Alzheimer's disease.

Multiple cellular changes have been identified as being involved in Alzheimer's disease (AD) pathogenesis, including mitochondrial damage, synaptic loss, amyloid beta (Aβ) production and/or accumulation, inflammatory responses, and phosphorylated tau formation and/or accumulation. Studies have established that Aβ-induced synaptic dysfunction is dependent on abnormal amyloid precursor protein (APP) processing caused by β- and γ-secretases, resulting in the generation of Aβ. The Aβ formed as a result of abnormal APP processing induces phosphorylated tau and activates glycogen synthase kinase-3β (GSK3β) and cyclin-dependent kinase-5 (CDK5). Here, we review the latest research on the development of Aβ modulators for neuroprotection in AD. We also review the use of molecular inhibitors as therapeutic targets in AD.