Ginkgo Biloba Extract Protects Brain Cells from Damage in Alzheimer's Disease

Jim Crocker
7th August, 2024

Ginkgo Biloba Extract Protects Brain Cells from Damage in Alzheimer's Disease

Image Source: Natural Science News, 2024

Key Findings

  • The study from Shanghai University of Traditional Chinese Medicine found that Ginkgo biloba extracts (GBE) can reduce oxidative stress in an Alzheimer's disease (AD) rat model
  • GBE administration decreased harmful hydrogen peroxide levels and increased antioxidant enzyme activities in the brain, helping to protect neurons
  • GBE also regulated proteins involved in cell death, reducing DNA damage and potentially slowing AD progression
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. Recent research from Shanghai University of Traditional Chinese Medicine has explored the potential benefits of Ginkgo biloba extracts (GBE) in mitigating some of the detrimental effects associated with AD[1]. This study is particularly significant as it seeks to uncover the mechanisms by which GBE can protect neurons from oxidative stress, a pivotal factor in AD progression. Oxidative stress refers to the damage caused by free radicals, which are unstable molecules that can harm cells. In the context of AD, oxidative stress leads to lipid peroxidation (LPO), damaging cell membranes and contributing to neuronal dysfunction[2]. Previous studies have shown that oxidative stress precedes amyloid-beta (Aβ) deposition, a hallmark of AD, suggesting that targeting oxidative damage could be a viable therapeutic strategy[2][3]. The study by Shanghai University researchers used an AD-like rat model, where amyloid beta 25-35 (Aβ25-35) was injected into the hippocampal CA1 region of the brain. This model mimics the oxidative stress and neuronal damage observed in human AD. The rats were then administered either 7.5 g/L or 15 g/L GBE50 solution orally. The researchers assessed learning and memory abilities, mitochondrial H2O2 levels (a marker of oxidative stress), and the activity of several related enzymes. One of the key findings was that GBE50 administration resulted in a decrease in H2O2 levels and monoamine oxidase (MAO) activity in the hippocampus of AD rats. MAO is an enzyme that breaks down neurotransmitters and produces hydrogen peroxide as a byproduct, contributing to oxidative stress. Conversely, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), both of which are antioxidant enzymes, were increased. This indicates that GBE50 helps to balance oxidative stress by enhancing the brain's antioxidant defenses. Additionally, the study examined the effects of GBE50 on apoptosis-related proteins. Apoptosis is the process of programmed cell death, and its dysregulation is a feature of AD. The researchers found that GBE50 enhanced the expression of Bcl-2, a protein that prevents apoptosis, and inhibited the release of cytochrome C (Cyto C) from mitochondria, which is a key step in the apoptotic pathway. Furthermore, GBE50 suppressed the levels of caspase-3, an enzyme that plays a critical role in the execution phase of apoptosis, without affecting cleaved caspase-3. The study also looked at DNA damage by measuring levels of 8-hydroxydeoxyguanosine (8-OHdG), a marker of oxidative DNA damage. GBE50 administration was found to lower the generation of 8-OHdG, indicating a protective effect against DNA oxidative stress. Interestingly, the expression of caspase-activated DNase (CAD), which is involved in DNA fragmentation during apoptosis, was not influenced by GBE50, suggesting that the extract specifically targets oxidative stress pathways rather than general apoptotic mechanisms. These findings align with earlier studies that emphasize the role of oxidative stress in AD pathogenesis. For instance, it has been documented that oxidative damage occurs before amyloid plaque formation in AD models, highlighting the potential of antioxidant therapies in early intervention[2][3]. Moreover, the study's use of Aβ25-35 to induce oxidative stress and cellular dysfunction is consistent with previous research showing that this peptide fragment can cause multiple disturbances to cellular integrity[4]. In conclusion, the study from Shanghai University of Traditional Chinese Medicine provides compelling evidence that Ginkgo biloba extracts can mitigate oxidative stress and protect against neuronal damage in an AD-like rat model. By regulating oxidative stress-related enzymes and apoptotic proteins, GBE50 offers a promising therapeutic approach to delay or prevent the progression of Alzheimer's disease. These findings not only build upon previous research but also open new avenues for developing antioxidant-based treatments for neurodegenerative disorders.

MedicineHealthBiochem

References

Main Study

1) Ginkgo biloba extract inhibits hippocampal neuronal injury caused by mitochondrial oxidative stress in a rat model of Alzheimer's disease.

Published 6th August, 2024

https://doi.org/10.1371/journal.pone.0307735

Related Studies

2) Increased lipid peroxidation precedes amyloid plaque formation in an animal model of Alzheimer amyloidosis.

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience, Issue: Vol 21, Issue 12, Jun 2001

3) Oxidative stress in Alzheimer disease: a possibility for prevention.

https://doi.org/10.1016/j.neuropharm.2010.04.005

4) Subcellular and metabolic examination of amyloid-beta peptides in Alzheimer disease pathogenesis: evidence for Abeta(25-35).

https://doi.org/10.1016/j.expneurol.2009.09.005


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