Volume 16, Issue 3 (May & June- In Press 2025)
BCN 2025, 16(3): 0-0 |
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Mansouri Z, Motamedi F, Khodagholi F, Zahmatkesh M. Histone Deacetylase Class IIb Inhibition Improves Amyloid-β-Induced Learning and Memory Deficits in Male Rats. BCN 2025; 16 (3)
URL: http://bcn.iums.ac.ir/article-1-2881-en.html
URL: http://bcn.iums.ac.ir/article-1-2881-en.html
1- Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
2- Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2- Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
Background and Objective: Alzheimer's disease (AD) is a neurodegenerative disease associated with progressive impairment of cognitive function. The primary pathological features of AD include aggregation of amyloid-β (Aβ) and hyperphosphorylation of the tau protein. Histone deacetylases (HDACs) play a crucial role in the pathophysiology of neurodegenerative diseases. This study aimed to investigate the potential neuroprotective effects of HDAC6 and HDAC10 inhibition in a rodent model of AD.
Methods: Learning and memory deficits were induced by bilateral intra-hippocampal Aβ injections in male Wistar rats. Tubacin (HDAC6 inhibitor) and bufexamac (HDAC6 and 10 inhibitors) were microinjected 30 minutes after Aβ injection. The possible molecular changes in the hippocampus following Aβ injection were also assessed by western blotting analysis of pCREB/CREB and Pp70/P70 ratios.
Results: Our results revealed that Bufexamac significantly recovered learning and memory impairments induced by Aβ in the Morris water maze (MWM) task. Tubacin improved memory decline without affecting learning. Bilateral intra-hippocampal injection of each of the HDAC inhibitors significantly increased the pCREB/CREB and Pp70/p70 ratios compared to the Aβ group, which was concurrent with behavioral alterations.
Conclusion: HDAC IIb treatment may be a promising strategy for improving learning and memory impairments in an animal model of AD, suggesting that HDAC targeting is a valuable strategy for further investigation.
Methods: Learning and memory deficits were induced by bilateral intra-hippocampal Aβ injections in male Wistar rats. Tubacin (HDAC6 inhibitor) and bufexamac (HDAC6 and 10 inhibitors) were microinjected 30 minutes after Aβ injection. The possible molecular changes in the hippocampus following Aβ injection were also assessed by western blotting analysis of pCREB/CREB and Pp70/P70 ratios.
Results: Our results revealed that Bufexamac significantly recovered learning and memory impairments induced by Aβ in the Morris water maze (MWM) task. Tubacin improved memory decline without affecting learning. Bilateral intra-hippocampal injection of each of the HDAC inhibitors significantly increased the pCREB/CREB and Pp70/p70 ratios compared to the Aβ group, which was concurrent with behavioral alterations.
Conclusion: HDAC IIb treatment may be a promising strategy for improving learning and memory impairments in an animal model of AD, suggesting that HDAC targeting is a valuable strategy for further investigation.
Keywords: Alzheimer's disease, Bufexamac, Cyclic adenosine monophosphate response element binding protein, Histone deacetylase enzymes, Ribosomal protein S6 kinase, Tubacin
Type of Study: Original |
Subject:
Cellular and molecular Neuroscience
Received: 2024/02/7 | Accepted: 2024/08/18 | Published: 2025/05/29
Received: 2024/02/7 | Accepted: 2024/08/18 | Published: 2025/05/29
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