p-Coumaric acid mitigates passive avoidance memory and hippocampal synaptic plasticity impairments in aluminum chloride-induced Alzheimer's disease rat model

• Published in: Journal of functional foods Vol. 94; p. 105117
• Main Authors: Rashno, Masome, Gholipour, Parsa, Salehi, Iraj, Komaki, Alireza, Rashidi, Khodabakhsh, Esmaeil Khoshnam, Seyed, Ghaderi, Shahab
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.07.2022; Elsevier
• Subjects: Aluminum chloride; Alzheimer’s disease; Long-term potentiation; p-Coumaric acid; Passive avoidance memory; Rat; p-Coumaric acid; Passive avoidance memory; Alzheimer’s disease; Rat; Aluminum chloride; Long-term potentiation
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2022.105117

[Display omitted] •p-CA alleviated AlCl3-induced passive avoidance memory deficit in rats.•p-CA improved hippocampal synaptic plasticity impairment in AlCl3-exposed rats.•p-CA lowered accumulation of Aβ plaque in the hippocampal neurons of AlCl3-treated rats. The present study was designed to determine the effects of p-coumaric acid (p-CA), a phenolic compound, on passive avoidance memory function and hippocampal long-term potentiation (LTP) in an Alzheimer's disease (AD) rat model induced by aluminum chloride (AlCl3). p-CA (100 mg/kg; P.O.) was administered concomitantly with AlCl3 (100 mg/kg; P.O.) for 42 consecutive days. Results of this study revealed an attenuation of memory capacity, which was accompanied by a reduction in both components of LTP (field excitatory postsynaptic potentials slope and population spike amplitude) and an increase in amyloid-beta (Aβ) plaques production in the AlCl3-exposed rats. Intriguingly, treatment with p-CA improved passive avoidance memory dysfunction, ameliorated hippocampal LTP impairment, and hindered Aβ plaque accumulation in the hippocampal dentate gyrus of AlCl3-treated rats. This data provides evidence that p-CA improves AlCl3-induced passive avoidance memory decline, which may be partly related to amelioration of synaptic dysfunction and suppression of Aβ plaque formation.