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Amyloid plaque can build up in body organs other than the brain. The resulting diseases — AL amyloidosis, ATTR amyloidosis and more — cause much suffering.
One class of drugs has already found success in treating the painful, disorienting and common attacks. Excitement is building about a slew of additional drug targets.
Polygenic risk scores — a patient’s chance, based on tiny DNA variants, of developing cardiovascular disease, breast cancer and more — are coming to clinics. But there are kinks to iron out and accuracy remains an issue.
As cells divide, they must copy all of their chromosomes once and only once, or chaos would ensue. How do they do it? Key controls happen well before replication even starts.
To understand the origins of multicelled life, researchers are studying a motley assortment of simpler animal relatives. The commonalities they’re unearthing offer a trove of clues about our mutual past.
More than 70 years ago, mathematician Alan Turing proposed a mechanism that explained how patterns could emerge from bland uniformity. Scientists are still using his model — and adding new twists — to gain a deeper understanding of animal markings.
Picture your body: It’s a collection of cells carrying thousands of DNA errors accrued over a lifetime — many harmless, some bad, and at least a few that may be good for you.
With the first medical therapy approved and systems like CRISPR-Cas showing up in complex cells, there’s a lot going on in the genome editing field. Here’s our primer.
Our genomes are peppered with DNA segments called retrotransposons that can move from place to place. When unleashed, some can kill nerves and promote inflammation — a discovery that may inspire treatments for neurodegeneration.
Scientists are finding that microscopic membranous bubbles called extracellular vesicles transmit messages from cells and do big jobs in many areas of biology — plus they might be useful for therapies.
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