Benjamin Thompson
speaker
746 appearances
10 recordings
1 series
first heard Jul 2026
last heard 2 Sep
Benjamin Thompson’s voice in public audio — every appearance, attributed to the second.
Trend
recordings per month · last 12 monthsRecordings per month over the last 12 months — 10 in all, peaking in Jul 2026 with 5.
Appearances
In the study, Schumacher's team suppressed the dream complex by inhibiting an enzyme that helps to build it.
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The enzyme called Dirk 1A is already a potential drug target.
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It is overexpressed in people with Down syndrome and is tied to cognitive impairments and neurodegeneration associated with the condition.
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Schumacher sees Dream as a game changer for the field because it seems to act as a master regulator of repair, affecting many systems.
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For the first time we could really boost the overall capacity to repair, he says.
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Robbins agrees that the finding is exciting, calling the study quote, beautiful work, end quote.
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But he says that there's a lot more research to do to work out whether the complex could be targeted and how best to do it.
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Studying other types of cell with different apparent levels of repair could inform future strategies.
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There is evidence, for example, that stem cells, which also need to maintain their genome across many divisions, have lower mutation rates than do other somatic cells.
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If stem cells are better at DNA repair, then partially reprogramming somatic cells into a stem like state could, among other advantages, improve their repair.
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Even among other somatic cells, there might be variations in DNA fixing habits and strategies.
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Vick's team has found that cells in the liver have relatively high numbers of mutations, and one hypothesis is that because the liver acts as a detoxifier, its cells are exposed to more DNA damaging agents than are those in other tissues.
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Liver cells commonly have more than two copies of chromosomes, a situation known as polyploidy.
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Maybe, Vig says, making these extra copies is a cheaper solution than trying to create better repair.
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A special case involves cancer cells, in which DNA repair is a double edged sword.
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Cancer cells rely heavily on good repair to divide so rapidly.
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But they can also take advantage of defective repair to evolve quickly, thus evading cancer targeting drugs.
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Rather than enhancing DNA repair, some existing and emerging treatments block specific DNA repair pathways to ultimately kill the cancer cells.
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Since cancer is a disease of aging, researchers hoping to prolong healthy life will need not only to treat cancer, but also to prevent it from forming in the first place, Spare says.
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It's tempting to think that boosting DNA repair might solve cancer and other aspects of aging at once, but there's not yet evidence that such a double blow is possible, says Spair.
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Showing 81–100 of 746 · page 5 of 38
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