ePoster

STANDARDIZED <EM>GINKGO BILOBA</EM> EXTRACT ATTENUATES MEMORY DEFICITS IN A STREPTOZOTOCIN-INDUCED ALZHEIMER’S–LIKE NEURODEGENERATION MODEL

Jacqueline G.P. Abrunheiroand 3 co-authors

Federal University of Sao Paulo

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-253

Presentation

Date TBA

Board: PS01-07AM-253

Poster preview

STANDARDIZED <EM>GINKGO BILOBA</EM> EXTRACT ATTENUATES MEMORY DEFICITS IN A STREPTOZOTOCIN-INDUCED ALZHEIMER’S–LIKE NEURODEGENERATION MODEL poster preview

Event Information

Poster Board

PS01-07AM-253

Abstract

Alzheimer’s disease (AD) is the leading cause of dementia and is characterized by progressive cognitive decline, particularly affecting memory formation and retrieval. Late-onset AD (LOAD), accounting for approximately 95% of cases, has a multifactorial etiology, with population ageing and insulin resistance as major risk factors. Given the limited efficacy of current pharmacological treatments in halting or reversing disease progression, the investigation of novel therapeutic approaches is warranted. Previous studies from our group have demonstrated that flavonoid-rich compounds, such as the standardized Ginkgo biloba extract (EGb), exert beneficial effects on memory processes. This study aimed to evaluate the effects of chronic EGb treatment at doses (0.25, 0.5, and 1.0 g/kg), compared with control treatments (donepezil, 5 mg/kg, or 0.9% saline), administered from days 3 to 17, on object recognition memory (ORM; day 16) and object location memory (OLM; day 17) in male Wistar rats (3–4 months old). Animals were subjected to intracerebroventricular injections of streptozotocin (STZ-icv, 3 mg/kg) or vehicle on day 1, a well-established neurodegenerative model that reproduces key features of LOAD. Approved by the Institutional Animal Care and Use Committee (no. 7325190220). Behavioural results demonstrated that EGb at doses of 0.25 and 0.5 g/kg reversed STZ-induced memory deficits, indicating a dose-dependent protective effect. Ongoing molecular and cellular analyses of hippocampal and prefrontal cortical regions are expected to further elucidate the mechanisms underlying EGb-mediated cognitive improvement. Together, these findings support the potential of EGb as a neuroprotective strategy in experimental models of LOAD.

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