Title:Neurodegenerative Pathways in Alzheimer’s Disease: A Review
Volume: 19
Issue: 5
Author(s): Anu Kunnath Ramachandran, Subham Das, Alex Joseph*, Gurupur Gautham Shenoy, Angel Treasa Alex and Jayesh Mudgal
Affiliation:
- Department of Pharmaceutical Chemistry, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal, Karnataka-576104,India
Keywords:
Alzheimer's disease, neurodegenerative pathways, novel drug targets, acetylcholinesterase, glycogen synthase kinase,
notch signaling, apolipoprotein E.
Abstract: Alzheimer’s disease (AD) is a complex neurodegenerative disease that leads to insidious
deterioration of brain functions and is considered the sixth leading cause of death in the world.
Alzheimer’s patients suffer from memory loss, cognitive deficit and behavioral changes; thus, they
eventually follow a low-quality life. AD is considered as a multifactorial disorder involving different
neuropathological mechanisms. Recent research has identified more than 20 pathological factors
that are promoting disease progression. Three significant hypotheses are said to be the root
cause of disease pathology, which include acetylcholine deficit, the formation of amyloid-beta senile
plaques and tau protein hyperphosphorylation. Apart from these crucial factors, pathological
factors such as apolipoprotein E (APOE), glycogen synthase kinase 3β, notch signaling pathway,
Wnt signaling pathway, etc., are considered to play a role in the advancement of AD and therefore
could be used as targets for drug discovery and development. As of today, there is no complete
cure or effective disease altering therapies for AD. The current therapy is assuring only symptomatic
relief from the disease, and progressive loss of efficacy for these symptomatic treatments warrants
the discovery of newer drugs by exploring these novel drug targets. A comprehensive understanding
of these therapeutic targets and their neuropathological role in AD is necessary to identify
novel molecules for the treatment of AD rationally.
