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May 30, 2026Complementary Medicine Research0 citations

Neuroprotective Effects of Ginkgo biloba Extract in Neurological Disorders: Integrating Anti-Inflammatory and Antioxidant Mechanisms

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KBKumar M. R. BhatMemorial University of NewfoundlandPLPrasanna LCNTNaveen Kumar Thonse

Key Points

  • The review aims to evaluate the neuroprotective effects of Ginkgo biloba extract in treating neurological disorders through its antioxidant and anti-inflammatory properties.
  • Synthesis of evidence from preclinical and clinical studies on Ginkgo biloba extract.
  • Assessment of antioxidant, anti-inflammatory, and mitochondrial-protective mechanisms.
  • Analysis of clinical trials reporting outcomes in cognition and function in dementia and Parkinsonism.
  • Preclinical models show significant improvements in cognition, motor function, and neuronal survival.
  • Clinical trials report variable outcomes: some indicate improved cognition in dementia, while others show no benefit over placebo.
  • Findings highlight the need for consistent extract standardization and treatment regimens to enhance clinical applicability.

Abstract

Background: Neurological disorders such as Alzheimer’s disease, Parkinson’s disease, epilepsy, and ischemic stroke are major causes of global disability and mortality. Neuroinflammation and oxidative stress play central roles in their pathogenesis. Ginkgo biloba extract (GBE), particularly the standardized formulation EGb 761, contains flavonoids and terpenoids that exert antioxidant, anti-inflammatory, and mitochondrial-protective effects. These pleiotropic actions position GBE as a promising candidate for neuroprotection. Summary: This narrative review synthesizes evidence from preclinical and clinical studies on the neuroprotective actions of GBE. Experimental data demonstrate that GBE attenuates oxidative stress by scavenging reactive oxygen species and enhancing endogenous antioxidant defenses, while simultaneously downregulating pro-inflammatory mediators through NF-κB inhibition and NLRP3 inflammasome suppression. Additional benefits include stabilization of mitochondrial function, modulation of neurotransmission, and prevention of apoptosis. Preclinical models consistently show improvements in cognition, motor function, and neuronal survival across diverse disease contexts. Clinical findings, however, are mixed: some randomized trials report improved cognition and functional outcomes in dementia and Parkinsonism, whereas others show no superiority over placebo. Variability in study design, extract standardization, and treatment regimens contribute to these discrepancies. Key Messages: GBE exerts multifaceted neuroprotective effects through combined antioxidant, anti-inflammatory, mitochondrial, and neurotransmitter-modulating actions. Preclinical evidence strongly supports its role in mitigating pathological processes underlying Alzheimer’s disease, Parkinson’s disease, epilepsy, and ischemic injury. But clinical outcomes remain inconsistent. GBE holds potential as a safe, multi-target adjunctive therapy for complex central nervous system disorders, but translation into consistent clinical practice requires further validation.

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Cite This Study

Bhat et al. (2026) studied this question.

synapsesocial.com/papers/6a1a818e0307b78509433616https://doi.org/10.1159/000552633
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