EGB761 ameliorates chronic cerebral hypoperfusion-induced cognitive dysfunction and synaptic plasticity impairment

Area of Science:

• Neuroscience
• Pharmacology
• Biochemistry

Background:

• Chronic cerebral hypoperfusion (CCH) is linked to cognitive dysfunction, but mechanisms remain unclear.
• Ginkgo biloba extract (EGB761) is a phytomedicine with known neuroprotective properties, used for cognitive disorders.
• The efficacy of EGB761 in improving cognitive function specifically after CCH requires further investigation.

Purpose of the Study:

• To investigate the effects of EGB761 on CCH-induced cognitive dysfunction.
• To elucidate the underlying mechanisms of EGB761's therapeutic actions in CCH models.

Main Methods:

• Behavioral tests to assess cognitive function.
• Electrophysiology to evaluate neural activity and synaptic function.
• Neurobiochemical and immunohistochemical analyses to examine molecular and structural changes.

Main Results:

• EGB761 ameliorated spatial cognitive deficits induced by CCH.
• Treatment improved long-term potentiation, synaptic transmission, and neural signal synchronization.
• EGB761 reversed CCH-induced inhibition of neural activity, dendritic spine degeneration, and prevented synaptic protein downregulation, while inhibiting axon demyelination and restoring mTOR signaling.

Conclusions:

• EGB761 treatment post-CCH enhances spatial cognitive function.
• Mechanisms involve ameliorating synaptic plasticity impairment, synapse degeneration, and axon demyelination.
• Rectification of mTOR signaling pathway inhibition is crucial for EGB761's therapeutic effects.