https://doi.org/10.1016/j.brainresbull.2021.02.024

Objectives: Alzheimer disease (AD) is a neurodegenerative disorderliness that involves deductible progressive cognition function caused by amyloid-beta (Aβ) peptide accumulation in the
interstitial space. The increase of Aβ stimulates all kinds of active oxygen and causes oxidative
stress and apoptosis. In this investigation, we researched the neuroprotective impacts of
vanillic acid (VA) on the Aβ-induced (Aβ1-40) long-term potentiation (LTP) of the hippocampus – a commonly probed synaptic plasticity model that happens at the same time as memory
and learning – in the AD rats.
Methods: Forty-five male Wistar rats were categorized into five groups (n = 8 rats/group,
200–220 g), and studied as control (standard diet), sham (vehicle), VA (50 mg/kg), Aβ and Aβ + VA
(50 mg/kg) groups. In vivo electrophysiological recordings were implemented after the stereotaxic surgery to gauge the excitatory postsynaptic potential (EPSP) slope and population spike
(PS) amplitude in the dentate gyrus of the hippocampus. By the stimulation at high-frequency of
the perforate pathway, long-term potentiation (LTP) was induced. To assess the plasma levels of
malondialdehyde (MDA) and total thiol group (TTG), blood samples were garnered.
Results: In the Aβ-injected rats, EPSP slope, and PS amplitude were significantly reduced
after the induction of LTP. Thus, the findings demonstrate that VA decreases the impacts of Aβ
on LTP; also, the treatments through VA neuroprotective against the negative effects of Aβ on
the synaptic plasticity of the hippocampus can decrease the MDA levels and also increase the
TTG levels significantly.
Discussion: Therefore, based on this experiment on male rats, VA has neuroprotective
effects and antioxidants benefits against the Aβ-mediated inhibition of long-term
potentiation