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

Chandra Sekhar Kuruva, P (Hemachandra) Reddy

Research output: Contribution to journalReview article

26 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)223-233
Number of pages11
JournalDrug Discovery Today
Volume22
Issue number2
DOIs
StatePublished - Feb 1 2017
Externally publishedYes

ASJC Scopus subject areas

  • Pharmacology
  • Drug Discovery

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