Neurology Central

Alzheimer’s and AMD: could elovanoids be a new therapeutic target?

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A research team led by Nicolas Bazan, Louisiana State University (LA, USA) have found a new mechanism by which elovanoids might protect retinal and brain cells against neurodegenerative diseases such as Alzheimer’s and age-related macular degeneration (AMD). The molecules could be used as a new therapeutic approach for Alzheimer’s and AMD. The results have been published online in the Proceedings of the National Academy of Sciences.

“It is the first report that elovanoids are potential senolytic therapies because they target and dramatically arrest gene expression engaged in cell disturbances, including senescence gene programs and retina cell death in conditions that recapitulate retinal degenerative diseases,” commented Bazan. “Since the retina is key in age-related macular degeneration and is an integral part of the nervous system, the reported discoveries are also applicable to Alzheimer’s disease and other neurodegenerative conditions.”

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When humans age, cells gradually become senescent and therefore lose the ability to divide and renew. Later in life these dysfunctional cells and build up in tissues, which attract inflammatory cells. Amyloid beta can accumulate in retinal and brain tissues and chronic inflammation can lead to brain and photoreceptor cell death, leading to the development of neurodegenerative diseases.

“We demonstrate in the paper that the elovanoids block these events and foster the survival and function of these cells,” explained Bazan.

The research team used models of Alzheimer’s disease and AMD and found that elovanoids reduced the build-up of the senescent cells. The molecules work by targeting a senescent protein, senescent genes, and the expression of senescence-related genes in retinal epithelial cells. It was also found that elovanoids restore the structure and integrity of the retinal epithelial and photoreceptor cells after being damaged by amyloid beta.

Bazan stated that “further research is needed, particularly by using these models to define the intimacy of the gene transcription of senescence and the epigenomic implications of these findings.” And that his lab is “poised to define further novel unifying regulatory mechanisms that sustain health span during aging and neurodegenerative diseases.”

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Source: Bazan N, Do K, Bokkyoo J et al. Data from: elovanoids counteract oligomeric β-Amyloid-induced gene expression and protect photoreceptors. Dryad, Dataset, doi:10.5061/dryad.59zw3r233 (2019); www.eurekalert.org/pub_releases/2019-11/lsuh-lhr110719.php[/userpro_private]

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