Study summary · research use only
BAM15 Relieves Neurodegeneration in Aged Caenorhabditis elegans and Extends Lifespan
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study using the nematode Caenorhabditis elegans, researchers investigated whether BAM15, a mitochondrial membrane protonophore uncoupler, could reduce neuronal defects during aging, using green fluorescence protein-tagged mechanosensory neurons along with touch and chemotaxis assays. Wild-type animals treated with 50 µM BAM15 or 10 µM DNP showed reduced mechanosensory neuronal defects during aging, correlating with maintained touch responses and short-term memory. The uncoupler mutant ucp-4 responded similarly to wild-type animals treated with 50 µM BAM15 and 10 µM DNP compared to DMSO control. The authors describe 50 µM BAM15 as alleviating neurodegeneration phenotypically and functionally in aging C. elegans, potentially through mitochondrial uncoupling, and report that 50 µM BAM15 extended the mean lifespan in both wild-type and ucp-4 mutant animals.
Abstract
BAM15 was recently screened as a protonophore uncoupler specifically for the mitochondrial membrane but not the plasma membrane. It is equally as potent as FCCP, but less toxic. Previously, mitochondrial uncoupling via DNP alleviates neurodegeneration in the nematode Caenorhabditis elegans during aging. Therefore, we investigated whether BAM15 uncouplers could phenotypically and functionally reduce neuronal defects in aged nematodes. We observed green fluorescence protein-tagged mechanosensory neurons and performed touch and chemotaxis assays during aging. Wild-type animals treated with both 50 µM BAM15 and 10 µM DNP showed reduced mechanosensory neuronal defects during aging, which correlates with the maintenance of touch responses and short-term memory during aging. Uncoupler mutant ucp-4 also responded the same way as the wild-type, reducing neurodegeneration in 50 µM BAM15 and 10 µM DNP-treated animals compared to the DMSO control. These results suggest that 50 µM BAM15 alleviates neurodegeneration phenotypically and functionally in C. elegans during aging, potentially through mitochondrial uncoupling. In accordance with the preserved neuronal shape and function in aged C. elegans, 50 µM BAM15 extended the mean lifespan of both wild-type and ucp-4 mutants.
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