Standardized Extract of Ginkgo biloba L. Reverses Memory Impairment in Older Female Mice with Basal Forebrain Cholinergic Dysfunction.

Authors

Beatriz G Muratori, Carlos R Caetano, Irina Emanuela T da Veiga, Andressa G Soliani, Sofia M S E Silva, Juliana P Gava, Lucinéia F Ceridório, Luciano Caselli, Rodrigo P Ureshino, Carla M Prado, Suzete Maria Cerutti

Published in

Neurochemical research. Volume 51. Issue 4. Jul 14, 2026. Epub Jul 14, 2026.

Abstract

Aging induces neurochemical changes, particularly in the dentate gyrus (DG), that impair memory. In late-onset Alzheimer's disease (LOAD), neuronal loss in regions like the entorhinal cortex (EC) and hippocampus proper (HP), along with amyloid-β (Aβ) plaques, tau tangles, and reduced cholinergic signaling, accelerates cognitive decline. Building on our group's previous findings of cognitive benefits and neuroprotection from Ginkgo biloba L. leaf extract (EGb), and considering the limited success of current therapies, EGb has emerged as a promising multi-target strategy for reversing memory impairments. This study evaluates the effects of chronic EGb treatment on memory, anxiety-like behaviors, and motor activity in older female wild-type and VAChT knockdown KD^HET and KD^HOM mice, which show 45% and 65% reductions in VAChT expression, respectively. We assessed the impact of EGb on Aβ_1-42 peptide and phosphorylated tau (pTauT231) by quantifying Aβ IR⁺ and pTau IR⁺ cells in the dCA1, dCA3, and dDG, via immunohistochemistry. Results showed that aging led to short- and long-term memory deficits, which were exacerbated in the VAChT KD^HOM mice. However, EGb treatment reversed these deficits in a dose-dependent manner by modulating Aβ and pTau-IR⁺ cells in the dCA1, and dDG regions. In vitro, EGb significantly inhibited Aβ aggregation through interactions with Aβ and the POPC monolayer. These findings suggest that EGb may provide a promising therapeutic strategy for AD, improving cognition and offering neuroprotection by targeting key neuropathological features like Aβ plaques and phosphorylated tau.

PMID:
42443567
Bibliographic data and abstract were imported from PubMed on 14 Jul 2026.

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