Metformin promotes broad neuroprotection and proteostatic resilience via rngo/DDI2 stabilisation

Alzheimer’s disease (AD) is one of the most common age-related causes of death, with limited effective disease-modifying treatments. Although metformin shows promise as a disease-modifying agent for AD, its molecular mechanism—specifically how it confers neuroprotection despite potentially increasing amyloid-beta (Ab) load—remains obscure.