Urolithin A for Alzheimer's Disease
Also known as: UA, Mitopure
Impaired mitophagy contributes to accumulation of damaged mitochondria in AD neurons, and urolithin A restores this quality control process.
Mechanism of Action
UA activates PINK1/Parkin-dependent mitophagy to clear damaged mitochondria in AD neurons. It reduces amyloid-beta and tau pathology in preclinical AD models, likely through improved mitochondrial quality and reduced ROS production from dysfunctional mitochondria.
General mechanism: Gut microbiome metabolite from ellagitannins. PINK1/Parkin mitophagy activator, AMPK activator, mTORC1 inhibitor.
Current Evidence
Preclinical AD models show cognitive improvement and reduced pathology with UA. The ATLAS trial and other human studies demonstrate safety and mitochondrial biomarker improvement.
Clinical Status: Phase II for aging. Preclinical for AD. Available as supplement.
Safety Profile
Very safe. Naturally derived from pomegranate/ellagitannin metabolism. Well-tolerated in clinical trials.
Key Research Questions
- Does UA-induced mitophagy reduce AD pathology in humans?
- Can UA prevent AD in people with impaired gut microbiome conversion of ellagitannins?