Journal
BASIC AND CLINICAL NEUROSCIENCE
Volume 7, Issue 2, Pages 97-106Publisher
IRAN UNIV MEDICAL SCIENCES
DOI: 10.15412/J.BCN.03070203
Keywords
Alzheimer disease; Beta-amyloid; Long-term potentiation; Neuronal apoptosis; Rat
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Funding
- Ahvaz Physiology Research Center [APRC-73]
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Introduction: To study the effect of gallic acid (GA) on hippocampal long-term potentiation (LTP) and histological changes in animal model of Alzheimer disease (AD) induced by beta-amyloid (A beta). Methods: Sixty-four adult male Wistar rats (300 +/- 20 g) were divided into 8 groups: 1) Control (Cont); 2) AD; 3) Sham; 4-7) AD+GA (50, 100, and 200 mg/kg for 10 days, orally) or vehicle, 8) Cont+GA100, A beta (1 mu g/mu L in each site) was infused into hippocampus bilaterally. Changes of amplitude and slope of LTP induced in hippocampal dentate gyrus (DG) were evaluated by high frequency stimulation (HFS) of perforant path (PP). Results: Data showed that LTP amplitude and area under curve significantly impaired in AD rats (P<0.001), while significantly improved in AD rats treated with GA (P<0.05, P<0.01). Conclusion: Current findings suggest that GA reduces neural damage and brain amyloid neuropathology and improves cognitive function via free radicals scavenging and inhibiting oligomerization of A beta but with no effect on healthy rats.
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