Evidence map›Paper›PMID 40237934›Full record

ArticleNeurochemical research2025

Alpha-Pinene Ameliorates Memory Deficits in 3-Nitropropionic Acid-Induced Rat Model of Huntington's Disease.

Paria Hashemi, Mohammad Raman Moloudi, Helia Rahmani, Katayoun Hassanzadeh, Zakaria Vahabzadeh, Esmael Izadpanah

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Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Paria Hashemi *Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Mohammad Raman Moloudi *Neurosciences Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Helia RahmaniDepartment of Physiology and Pharmacology, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Katayoun HassanzadehDepartment of Physiology and Pharmacology, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Zakaria VahabzadehLiver and Digestive Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran. zakariav@gmail.com.
Esmael IzadpanahCellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran. eizadpanah2000@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Memory impairment is one of the cognitive symptoms in Huntington's disease (HD) which appears before motor dysfunction in patients. Various molecular mechanisms, including disruptions in neurotrophins levels, are involved in the occurrence of memory problems in HD. Alpha-pinene (APN), a member of the monoterpene family, exhibited beneficial effects in animal models of neurodegenerative disorders. As a result, this study assessed the impact of APN on memory in the 3-nitropropionic acid (3-NP) induced model of HD in rats. Male Wistar rats received saline, 3-NP to model HD, or APN (1, 5, or 10 mg/kg) plus 3-NP for 21 days to assess APN's effects. Working and spatial memory were examined by the Y-maze and Morris-water-maze (MWM) tests. The mRNA levels of neurotrophins and their receptors in the brain cortex and hippocampus of the rats were quantitatively assessed through Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR) analysis. The results showed that APN, at all three doses, significantly prevented the disease phenotype induced by 3-NP administration. In addition, APN treatment elevated the gene expression levels of BDNF, TrkA, TrkB, and CREB, while significantly decreasing P75 NTR showing a dose-dependent effect in the brain cortex and hippocampus, compared to the 3-NP group. These findings suggest that APN alleviates 3-NP-induced memory deficits by enhancing neurotrophins and their receptor levels in an animal model of HD.

Indexed as

Bicyclic MonoterpenesHuntington DiseaseMemory DisordersAnimalsBrain-Derived Neurotrophic FactorDisease Models, AnimalHippocampusMaleMaze LearningNitro CompoundsPropionatesRatsRats, Wistar3-nitropropionic acidalpha-pineneBicyclic MonoterpenesBrain-Derived Neurotrophic FactorNitro CompoundsPropionatesAlpha-pineneHuntington’s diseaseMemoryNeurotrophin

Identifiers

PMID40237934

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.