LAMP2A gene therapy mitigates Parkinson's disease-related pathology in nonhuman primates.

Boosting LAMP2A expression in nonhuman primates protects nigral dopaminergic neurons from LB-extract–induced αSyn neurodegeneration and delays pathology-related αSyn species formation and release.

• Why it matters: CMA, controlled by LAMP2A, is linked to αSyn clearance and is a direct target of αSyn-related neurotoxicity, but translational evidence in primates is limited.
• What they did: Nonhuman primates received injections of Parkinson’s disease patient-derived Lewy body extract, then LAMP2A expression was increased to test effects on αSyn pathology and function.
• The result: LAMP2A enhancement delayed αSyn pathology progression and produced beneficial effects on motor behavior and cognitive functions, supporting CMA enhancement as a therapeutic strategy for αSynucleinopathies.

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