In the newly published study linked to below from the journal Geroscience, researchers Josué Ballesteros-Álvarez et al, found that Urolithin A can reduce amyloid beta levels and improve cognition in a rodent Alzheimer’s model. But they also tested the compound’s effects on lifespan in normal mice, finding that it substantially increased lifespan. They found that, “UA, likely via its actions as a autophagy inducer, is capable of removing Aβ from neurons and its dietary administration prevents the onset of cognitive deficits associated with pathological Aβ deposition in the 3xTg-AD mouse model as well as extending lifespan in normal aging mice.” […]
[W]e investigated whether long-term intermittent administration of the compound would be able to enhance lifespan in normal aging mice. For this purpose, we fed UA on alternate weeks (1 week on, 1 week off) to a cohort of male C57BL/6 mice starting at 3 months of age. We found that dietary supplementation of UA significantly increased survival. The median lifespan at 80th percentile mortality was extended 18.75% from the UA feeding start point. (emphasis added)
Ballesteros-Álvarez J, Nguyen W, Sivapatham R, Rane A, Andersen JK. Urolithin A reduces amyloid-beta load and improves cognitive deficits uncorrelated with plaque burden in a mouse model of Alzheimer’s disease. Geroscience. 2022 Dec 28. doi: 10.1007/s11357-022-00708-y. Epub ahead of print. PMID: 36576642.
At last!. This is to truly underline the fact this study is the first to my eyes with no competing interests for being funded total or partially by company Amazentis, Mitopure’s brand (urolithin A compound) owner.
“Results: Berberine dramatically alleviated hypertrophy of H9C2 cell line and significantly ameliorated mitochondrial function by rectifying the imbalance of fusion and fission in mitochondrial dynamics. Furthermore, berberine further promoted mitogenesis and cleared the damaged mitochondria via mitophagy. In addition, berberine also restored autophagic flux in high glucose-induced cardiomyocyte injury via AMPK signaling pathway activation.”
Timeline.com claims Urolithin-A is not present in any food item : the precursor is, but only a certain (unknown) gut bacteria is able to convert it to Urolithin-A and some people must be completely lacking in that gut bacteria since they never test positive for Urolithin-A in their blood.
Update : Sorry I missed your other link which identifies that gut bacteria.
Even Streptococcus thermophilus FUA 329 seems to work.
Only a limited number of studies have been conducted on the microbial species capable of transforming ellagic acid into urolithins. Ellagibacter isourolithifaciens DSM104140T (E. isourolithifaciens DSM104140T) and Gordonibacter urolithinfaciens DSM 27213T (G. urolithinfaciens DSM 27213T) were confirmed to convert ellagic acid to isourolithin A and urolithin C. Only a single strain of Bifidobacterium pseudocatenulatum INIA P815 (B. pseudocatenulatum INIA P815) could produce urolithin A.