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Baker warns that he has no idea if the same approach would work with other strains of lab mice that mimic the symptoms of Alzheimer's disease in different ways – let alone if it works in people. Alzheimer's researchers have an atrocious history of translating the promising results of rodent studies into actual treatments. After decades of false starts and failed clinical trials, they are naturally wary.
Nevertheless, most of these earlier trials involved drugs designed to get rid of a different protein that is thought to be at the heart of Alzheimer's, beta-amyloid. The concept of the pursuit of senescent cells is new. "If these cells play an important role in people with neurodegenerative disease, the implications for treatment could be very important," says Li-Huei Tsai of MIT, who was not part of the new study.
This is because there are several "senolytic" medications that can eliminate senescent cells, and some of them have already been approved for the treatment of cancers. "If they've been effective in preventing or slowing down neurodegeneration, that would be a major step forward, especially in light of the ongoing failures of amyloid-based clinical trials," says Tsai.
Most people think that Alzheimer's disease is part of aging
Despite these failures, or maybe because among them, the National Institutes of Health has dramatically increased its spending on Alzheimer's research, tripling its annual three-year budget to $ 1.9 billion. This financial explosion was partly intended to encourage new researchers to tackle the Alzheimer's puzzle – and in Baker's case, it certainly worked.
His team, including Tyler Bussian and Asef Aziz, worked with a mouse strain that accumulates tau tangles in their neurons at six months of age. At eight months, their neurons began to die, their brains began to contract, and their memories began to weaken. But Bussian and Aziz have found that all these problems are preceded by the accumulation of senescent cells and can be avoided by removing these cells at an early stage.
They did this in two ways: first, by genetically manipulating mouse bodies to destroy their own senescent cells when they receive a particular chemical; and secondly, using a senolytic drug called navitoclax that kills these cells directly. Both approaches have been successful in preventing tau entanglements.
Navitoclax was originally developed as an anti-cancer drug, and it is one of many anti-tumor drugs that could also be used as senolysis. To kill tumors, these drugs must be administered in high doses, so that no tumor cells can escape. But when one kills senescent cells, total annihilation is not necessary, and it might be possible to get by with much lower doses. A company called Unity Biotechnology is developing several senolytic drugs and Baker is a co-inventor of some of their patent applications.
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