ArticleNeurochemical research2022
The Anti-Parkinson Potential of Gingko biloba-Supplement Mitigates Cortico-Cerebellar Degeneration and Neuropathobiological Alterations via Inflammatory and Apoptotic Mediators in Mice.
Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- TCMNet: an AI-driven strategy for optimizing traditional Chinese medicine.Chinese medicine · 2026Article
- Ginkgo biloba L. leaf extract (EGb 761) alleviates reserpine-induced depression-like symptoms in aged rats by enhancing serotonin/norepinephrine levels and reducing oxidative/nitrosative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Ginkgolide B as a biopsychosocial treatment salvages repeated restraint stress-induced amygdalar anomalies in mice.IBRO neuroscience reports · 2025Article
- Whole Plant Extracts for Neurocognitive Disorders: A Narrative Review of Neuropsychological and Preclinical Studies.Nutrients · 2024Review
- Anti-Aging of the Nervous System and Related Neurodegenerative Diseases With Chinese Herbal Medicine.American journal of Alzheimer's disease and other dementiasReview
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
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Abstract
Activation of nuclear factor erythroid 2 related factor 2 (Nrf2) associated with the suppression of various oxido-inflammatory pathways and the controller of several gene expressions involving "antioxidant response elements" (AREs) in their promoters to mediate and restores homeostatic functions is now considered as one of the main switch regulating the immune response, and it is also now involved in inflammatory cascade in PD. Whether therapeutic approach using Ginkgo biloba would have significant protective effects against cortico-cerebellar dopaminergic degeneration in rotenone-induced mice remains unknown. In this present study, we studied the therapeutic effects of Ginkgo biloba-supplement (Gb-S) administration in cortico-cerebellar dopaminergic degeneration. The results revealed that treatment with Gb-S suppresses cognitive decline and neuromuscular incompetence in the mice, abated tyrosine hydroxylase depletion and synucleinopathy development in the cortico-cerebellar neurons of the mice before and after rotenone induction. However, our data further shows increase Nrf2 immunoexpression with decrease oxido-nitrergic and neuroinflammatory release, increase cholinergic enzyme activity and downregulated executioner caspase-3 that may mediate cortico-cerebellar apoptosis. Also, the loss of cortico-cerebellar neurons was attenuated, marked by increase in dendritic spine length and width with numerous viable neurons. Overall findings suggest that Gb-S could be a potential pharmacotherapeutic candidate providing a strong protection for cortico-cerebellar neurocellular substances and against Parkinsonism-like non-motor and motor symptoms.
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