Volume 13, Issue 1 (February 2026)
Avicenna J Neuro Psycho Physiology 2026, 13(1): 0-0 |
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Ethics code: IR.UMSHA.REC.1394.397
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Sattari S, Vaezi G, Komaki A, Shahidi S, Hajati V. Neuroprotective Effects of Alpha-Tocopherol against Amyloid-β-Induced Hippocampal Synaptic Dysfunction, and Oxidative Stress in a Rat Model of Alzheimer’s Disease: Behavioral, Electrophysiological, and Biochemical Insights. Avicenna J Neuro Psycho Physiology 2026; 13 (1)
URL: http://ajnpp.umsha.ac.ir/article-1-570-en.html
URL: http://ajnpp.umsha.ac.ir/article-1-570-en.html
1- Department of Biology, Da.C., Islamic Azad University, Damghan, Iran.
2- Department of Biology, Da.C., Islamic Azad University, Damghan, Iran. ,gh.vaezi@yahoo.com
3- Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
4- Neurophysiology Research Center, Institute of Neuroscience and Mental Health, Hamadan University of Medical Sciences, Hamadan, Iran.
2- Department of Biology, Da.C., Islamic Azad University, Damghan, Iran. ,
3- Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
4- Neurophysiology Research Center, Institute of Neuroscience and Mental Health, Hamadan University of Medical Sciences, Hamadan, Iran.
Abstract: (16 Views)
Alzheimer’s disease (AD) remains a major health challenge, with current treatments offering limited efficacy. Its pathologies are cognitive decline, synaptic deterioration, and heightened oxidative stress—factors that are both interconnected and amenable to targeted intervention. While antioxidant strategies have shown promise, the neuroprotective potential of vitamin E (alpha-tocopherol) against amyloid-beta (Aβ)-induced neurotoxicity requires further elucidation. The present study pioneers a comprehensive evaluation of alpha-tocopherol’s ability to mitigate cognitive deficits, synaptic impairments, and oxidative damage in an innovative rat model of AD induced by Aβ.
Fifty adult male Wistar rats were assigned to control, sham, AD, vitamin E, and combined AD + vitamin E groups, with assessed through behavioral paradigms (novel object recognition, Morris water maze, and passive avoidance tests) alongside electrophysiological measures of hippocampal synaptic plasticity and, biochemical analyses, including malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant capacity (TOC), and glutathione peroxidase (GPx).
The results indicated that treatment with vitamin E significantly increased the discrimination index (P<0.001), step-through latency (P<0.001), time in the target quadrant (P<0.001), excitatory postsynaptic potential (P<0.05) and the amplitude of population spikes (P<0.05), TAC (P<0.001) and GPx (P<0.001) relative to the AD group.
It can be concluded that vitamin E decreased oxidative stress, preserved synaptic integrity, and cognitive function in Aβ-induced AD.
Fifty adult male Wistar rats were assigned to control, sham, AD, vitamin E, and combined AD + vitamin E groups, with assessed through behavioral paradigms (novel object recognition, Morris water maze, and passive avoidance tests) alongside electrophysiological measures of hippocampal synaptic plasticity and, biochemical analyses, including malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant capacity (TOC), and glutathione peroxidase (GPx).
The results indicated that treatment with vitamin E significantly increased the discrimination index (P<0.001), step-through latency (P<0.001), time in the target quadrant (P<0.001), excitatory postsynaptic potential (P<0.05) and the amplitude of population spikes (P<0.05), TAC (P<0.001) and GPx (P<0.001) relative to the AD group.
It can be concluded that vitamin E decreased oxidative stress, preserved synaptic integrity, and cognitive function in Aβ-induced AD.
Keywords: Alpha-tocopherol, Amyloid-β, Cognition, Hippocampus, Oxidative stress, Synaptic plasticity
Article Type: Research Article |
Subject:
Learning and Memory, Dementia, Alzheimer
Received: 2026/06/3 | Accepted: 2026/06/29 | Published: 2026/03/23
Received: 2026/06/3 | Accepted: 2026/06/29 | Published: 2026/03/23
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