Road to Alzheimer's disease: The Pathomechanism underlying

R. Anand*, Alka Kaushal, Willayat Yousuf Wani, Kiran Dip Gill

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

13 Scopus citations

Abstract

Alzheimer's disease (AD), the most common cause of dementia, results from the interplay of various deregulated mechanisms triggering a complex pathophysiology. The neurons suffer from and slowly succumb to multiple irreversible damages, resulting in cell death and thus memory deficits that characterize AD. In spite of our vast knowledge, it is still unclear as to when the disease process starts and how long the perturbations continue before the disease manifests. Recent studies provide sufficient evidence to prove amyloid β (Aβ) as the primary cause initiating secondary events, but Aβ is also known to be produced under normal conditions and to possess physiological roles, hence, the questions that remain are: What are the factors that lead to abnormal Aβ production? When does Aβ turn into a pathological molecule? What is the chain of events that follows Aβ? The answers are still under debate, and further insight may help us in creating better diagnostic and therapeutic options in AD. The present article attempts to review the current literature regarding AD pathophysiology and proposes a pathophysiologic cascade in AD.

Original languageEnglish (US)
Pages (from-to)55-71
Number of pages17
JournalPathobiology
Volume79
Issue number2
DOIs
StatePublished - Feb 2012

Keywords

  • Alzheimer's disease
  • Amyloid
  • Dementia
  • Neurofibrillary tangles
  • Oxidative stress
  • Senile plaques
  • Tau protein

ASJC Scopus subject areas

  • Molecular Biology
  • Pathology and Forensic Medicine
  • Cell Biology

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