What is it about?

We identified the gene, BRD2, as a cause of a specific form of human epilepsy. A standard way of proving one has identified the correct gene locus is to create a mouse model by changing the gene in mice and determining if the disease is reproduced in the mice. We successfully produced a seizure-susceptible mouse but we also noticed that those mice with the genetic change that produced the seizure-susceptibility also not only lived significantly longer than littermates without the change but also had fewer pathologies typically seen in older mice, pathologies such as cancer and kidney disease, and increased healthy behavior such as fertility and grooming.

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Why is it important?

This serendipitous observation suggests that an emphasis on metabolism-related genes in longevity, which is prominent in the literature, may be missing much of the background for increasing life- and health-span.


We did not start out seeking a longevity gene but only pursued this work when we noticed that the experimental knock-out mice, which we previously showed were seizure-susceptible, lived significantly longer than their wild-type littermates. Making such a serendipitous discovery is particularly satisfying, especially when it leads to an area of research that is completely foreign to one's scientific background. It renews the feeling of the adventure of discovery and forces one into new scientific territory, which is, in its way, also a return to a youthful perspective for the scientists.

David A Greenberg
Ohio State University Medical Center

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This page is a summary of: Brd2 haploinsufficiency extends lifespan and healthspan in C57B6/J mice, PLoS ONE, June 2020, PLOS,
DOI: 10.1371/journal.pone.0234910.
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