A bat the size of a mouse lives 50 years and almost never gets cancer

A bat that weighs roughly as much as a house mouse has turned up alive 50 years after it was first tagged, and scientists now think its genes hold clues to why it barely ages and almost never develops cancer. The animal, a Brandt’s myotis, anchors a new genetic study of eight bat species that found a direct link between long lifespans and unusually strong cancer-fighting immune activity. Researchers say the pattern echoes what has been seen in elephants, another famously long-lived and cancer-resistant animal, and could eventually point toward new ways to protect aging human cells.

A Brandt’s Myotis Recaptured Five Decades Later

The record-setting animal belongs to Myotis brandtii, a species that can weigh less than an ounce yet survive for roughly 50 years in the wild, a lifespan wildly out of proportion to its size. One individual banded in Europe was recaptured five decades later, a data point that has fascinated biologists studying why body size and lifespan are so often mismatched among mammals. A UC Berkeley postdoctoral researcher, Juan Manuel Vazquez, began chasing that mismatch after finding little published genomic data on bats during his graduate studies, eventually leading teams of undergraduates across the western United States to net bats over streams and rivers at night, take small tissue samples, and release the animals unharmed.

Eight Myotis Genomes Point to an Immune Connection

The resulting research, published in the journal Nature, presents the first comparative analysis of eight genomes from the genus Myotis, which includes about 139 of the roughly 1,511 known bat species. The comparison revealed that species with longer lifespans consistently carried higher levels of genes associated with fighting cancer, and that genes linked to aging overlapped heavily with genes involved in defending against infection. That overlap suggests the two processes, immune defense and longevity, may be far more intertwined than scientists previously assumed, since a genetic tweak that helps a bat fend off a virus might also help it resist the cellular damage that accumulates with age.

When Damaged Cells Choose to Die Instead of Repair

To test that idea directly, Vazquez grew cell cultures from wing-biopsy samples, ultimately assembling cultures representing 259 individual bats across 32 species, and exposed them to a toxic chemical designed to simulate severe cellular damage. The little brown bat, Myotis lucifugus, the longest-lived species in the sample, responded in a way the team did not expect: instead of activating genes that repair damaged DNA, its cells ramped up genes that trigger programmed cell death, effectively sacrificing the damaged cell rather than trying to save it. According to the original Berkeley research summary, that same “kill the cell if it can’t be saved” strategy has previously been documented in elephants, another species that rarely develops cancer despite carrying vastly more cells, and vastly more opportunities for a cell to turn cancerous, than smaller mammals.

Why Bat Immunity Cuts Both Ways

The study also found that Myotis bats carry an unusually large set of genes producing proteins that interact with DNA viruses such as herpesviruses, a pattern distinct from humans and other primates, which tend to have more genes tuned to RNA viruses like those behind COVID-19 and HIV. Researchers argue that mismatch helps explain why viruses that jump from bats to people, including relatives of the coronavirus that causes COVID-19, can prove so dangerous once they cross into a species whose immune system evolved along a different track. The paper’s authors, whose work was funded by the National Institutes of Health and the National Science Foundation according to the journal record, say that same high-alert immune system that lets bats coexist with dangerous pathogens may be a byproduct of their nightly flights, which researchers have compared to running the metabolic equivalent of an ultramarathon.

Vazquez and his collaborator Elise Lauterbur, who worked on the project first at the University of Arizona and now at the University of Vermont, found that genes tied to bat longevity overlapped with genes tied to viral interactions far more often than random chance would predict. That overlap suggests bats may have evolved a shared genetic toolkit that simultaneously extends lifespan and manages chronic viral exposure, rather than two separate systems that happen to coexist. Researchers caution that humans and bats are, in Vazquez’s words, “badly suited to each other” immunologically, which is part of why direct contact with wild bat populations carries a two-way infection risk that field researchers take seriously.

What Bats Could Teach Human Medicine

Bats first appear in the fossil record roughly 60 million years ago and today make up about one-fifth of all mammal species, occupying nearly every terrestrial habitat except Antarctica. Within that diversity, closely related species can have dramatically different lifespans: Brandt’s myotis lives roughly seven times longer than the black myotis of Central and South America, a gap researchers have compared to a hypothetical where Neanderthals outlived modern humans by a factor of nine. Peter Sudmant, a Berkeley associate professor who studies the genetics of aging, said the goal now is to understand how the interplay between DNA damage and immune response could be harnessed for human health, while Vazquez continues the cell-culture work in a new faculty role at Pennsylvania State University. Neither researcher has proposed a treatment derived from the findings; the work remains basic science aimed at mapping the biological mechanisms rather than a therapy ready for testing.

This article was created with the assistance of AI and reviewed by an editor.

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