Skip to main navigation Skip to search Skip to main content

Deciphering New Drug Targets in Alzheimer’s Disease

  • Nitin Verma
  • , Komal Thapa
  • , Neha Kanojia
  • , Gagandeep Kaur
  • , Parul Sood
  • , Kamal Dua
  • Chitkara University
  • University of Technology Sydney

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Alzheimer’s disease (AD) currently has no known treatments that can reverse the disease or cure it. Numerous pharmacological targets have already been identified for potential involvement to enhance efforts to find treatments for AD. There are roughly three basic therapeutic approaches for treating AD. The first strategy focuses on preventing the production and aggregation of Aβ oligomers as well as hyperphosphorylated tau tangles, which are the two main pathological characteristics of AD, and either causes their clearance. The second tactic controls neurotransmitter signalling. The clinically authorized therapies for the symptomatic relief of AD, including N-methyl-D-aspartate receptor inhibitors and cholinesterase inhibitors, make up this method. There are also mentioned other targets that try to stabilize cell signalling by altering neurotransmitters and their receptors. The third strategy includes a number of “sensitive targets” that indirectly affect the build-up of Aβ as well as tau. These targets are proteins whose activity is modified as a consequence of an accumulation in the brain cells or a direct Aβ-target interaction. This book chapter focuses on highlighting existing and novel emerging drug targets for AD.

Original languageEnglish
Title of host publicationDeciphering Drug Targets for Alzheimer’s Disease
PublisherSpringer Nature
Pages1-18
Number of pages18
ISBN (Electronic)9789819926572
ISBN (Print)9789819926565
DOIs
StatePublished - 1 Jan 2023
Externally publishedYes

Keywords

  • Alzheimer’s disease
  • Aβ oligomers
  • Drug targets
  • Therapeutics

Fingerprint

Dive into the research topics of 'Deciphering New Drug Targets in Alzheimer’s Disease'. Together they form a unique fingerprint.

Cite this