PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
May 20, 2026Neurological Research0 citations

Evaluation of neuroprotective effects of Pyracantha crenulata (D. Don) M. Roem against aluminium chloride induced memory impairment of rats

View Full Paper
PSPayal SaxenaPKPreeti KothiyalPRParminder Ratan

Key Points

  • To evaluate the neuroprotective effects of Pyracantha crenulata against memory impairment induced by aluminium chloride in rats.
  • Rats were administered Pyracantha crenulata extract at doses of 250 and 500 mg/kg for 21 days.
  • Cognitive performance was assessed using the Morris Water Maze (MWM) and Elevated Plus Maze (EPM).
  • Biochemical parameters including oxidative stress markers (SOD), cholinesterase activity (AChE), and myeloperoxidase levels (MPO) were measured.
  • The higher dose of extract significantly improved spatial and long-term memory in a dose-dependent manner.
  • Modulation of biochemical parameters was noted, with suppressed levels of amyloid precursor protein and Tau.
  • Histopathological examination confirmed protective effects on the hippocampus and cerebral cortex.

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE: , traditionally used in Himalayan folk medicine, valued for enhancing vitality, mental clarity, and combating age-related cognitive decline due to its antioxidant constituents. AIM: )-induced Alzheimer's disease in rats. MATERIALS AND METHODS: extract (250 and 500 mg/kg) for 21 days. Cognitive and behavioural performance were assessed using the Morris Water Maze (MWM) and Elevated Plus Maze (EPM). Biochemical parameters, including oxidative stress markers (SOD), cholinesterase activity (AChE), and myeloperoxidase levels (MPO), were measured. Histopathological examination of the hippocampus and cerebral cortex was conducted. RESULTS: extract significantly enhanced spatial and long-term memory in a dose-dependent manner, with the higher dose producing the most pronounced improvement. CONCLUSION: , demonstrated through modulation of biochemical parameters and suppression of amyloid precursor protein and Tau, key pathological hallmarks of Alzheimer's disease, further validated by histopathological evidence.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Saxena et al. (2026) studied this question.

synapsesocial.com/papers/6a0d5114f03e14405aa9d620https://doi.org/10.1080/01616412.2026.2673060
Ask AI
Helpful
Bookmark
Share
View Full Paper

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Diastolic dysfunction in Alzheimer’s disease model mice is associated with Aβ-amyloid aggregate formation and mitochondrial dysfunction2024 · 19 citations
  2. 2Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease2019 · 1,990 citations
  3. 3Amelioration of Cognitive Deficit by Embelin in a Scopolamine-Induced Alzheimer’s Disease-Like Condition in a Rat Model2018 · 117 citations
  4. 4Extracellular vesicles as therapeutic modulators of neuroinflammation in Alzheimer’s disease: a focus on signaling mechanisms2025 · 21 citations
  5. 5Myeloperoxidase activity as a quantitative assessment of neutrophil infiltration into ischemie myocardium1985 · 998 citations