Neuroprotective role of Asiatic acid in aluminium chloride induced rat model of Alzheimer's disease

Mashoque Ahmad Rather, Arokiasamy Justin Thenmozhi, Thamilarasan Manivasagam, Mathiyazahan Dhivya Bharathi, Musthafa Mohamed Essa, Gilles J. Guillemin

Research output: Contribution to journalArticlepeer-review

80 Citations (Scopus)

Abstract

Alzheimer's disease (AD) is the most common form of dementia, characterized by memory loss, cognitive impairment and personality disorders accompanied by diffuse structural abnormalities in the brain of elderly people. The current investigation explored the neuroprotective potential of asiatic acid (AA), a natural triterpene of Centella asiatica on aluminium chloride (AlCl3) induced rat model of AD. Oral administration of AlCl3 (100 mg/kg b.w.) for 42 days significantly elevated the levels of Al, activity of acetyl cholinesterase and expressions of amyloid precursor protein, amyloid beta1-42, beta and gamma secretases, glial fibrillary acidic protein, ionized calcium binding adaptor molecule 1, interleukins -1β, 6, 4, 2, tumor necrosis factor alpha, inducible nitric oxide synthase, nuclear factor- k beta and cyclooxygenase-2 in the hippocampus and cortex  compared to the control group. Our observations suggested that AA treatment mitigated AlCl3 induced AD associated pathologies, which might be due to its multiple pharmacological actions. Further studies are necessary in order to explore the link between AlCl3-mediated oxidative stress and associated apoptosis to establish its neuroprotective role in AD.

Original languageEnglish
Pages (from-to)262-275
Number of pages14
JournalFrontiers in bioscience (Scholar edition)
Volume10
DOIs
Publication statusPublished - 1 Jan 2018

Keywords

  • Alzheimer’s disease
  • Asiatic Acid
  • Memory Deficits
  • Amyloid Pathology
  • Inflammation

Fingerprint

Dive into the research topics of 'Neuroprotective role of Asiatic acid in aluminium chloride induced rat model of Alzheimer's disease'. Together they form a unique fingerprint.

Cite this