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It restores long-term potentiation in brain slices from tau-overexpressing mice, indicating potential for cognitive recovery. 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While extensively studied in oncology, geldanamycin has demonstrated neuroprotective effects in models of Parkinson’s disease. It reduces alpha-synuclein toxicity in dopaminergic neurons and destabilizes mutant p53, a protein linked to neuronal apoptosis. Geldanamycin also inhibits c-Jun N-terminal kinase (JNK) signaling and suppresses hypoxia-induced stress responses, both of which are implicated in neurodegeneration. By modulating protein folding, stress signaling, and autophagy, geldanamycin offers a mechanistic framework for targeting neurodegenerative pathways. 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