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Published on: July 4, 2018
BAM15 Relieves Neurodegeneration in Aged Caenorhabditis elegans and Extends Lifespan
Injeong Cho1, Hyun-Ok Song2, Ha Eun Ji1
1Department of Biology Education, College of Education, Chosun University, Gwangju 61452, Republic of Korea.
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.
Insights
BAM15, a less toxic mitochondrial uncoupler, reduces neurodegeneration and neuronal defects in aged Caenorhabditis elegans. This compound also extends the mean lifespan of these nematodes.
Area of Science:
- Neuroscience
- Gerontology
- Biochemistry
Background:
- Mitochondrial uncouplers, like DNP, can alleviate neurodegeneration.
- BAM15 is a potent yet less toxic mitochondrial uncoupler compared to FCCP.
- Investigating BAM15's effects on age-related neuronal decline is warranted.
Purpose of the Study:
- To determine if BAM15 can reduce neurodegeneration and neuronal dysfunction in aged nematodes.
- To assess the functional and phenotypic impact of BAM15 on aging C. elegans.
Main Methods:
- Utilized green fluorescence protein-tagged mechanosensory neurons in C. elegans.
- Performed touch and chemotaxis assays to evaluate neuronal function during aging.
- Compared the effects of BAM15 and DNP in wild-type and ucp-4 mutant nematodes.
Main Results:
- BAM15 treatment reduced mechanosensory neuronal defects in aged wild-type and ucp-4 mutant C. elegans.
- Neuronal function, including touch responses and short-term memory, was maintained in BAM15-treated animals.
- BAM15 extended the mean lifespan of both wild-type and ucp-4 mutant nematodes.
Conclusions:
- BAM15 alleviates age-related neurodegeneration and functional decline in C. elegans.
- The neuroprotective effects of BAM15 may be mediated through mitochondrial uncoupling.
- BAM15 demonstrates potential as a therapeutic agent for age-related neurological disorders.
