抗中樞退行性疾病藥(參考版)
2025-01-05 02:17本頁(yè)面
【正文】 s and another $48 million if it succeeds in bringing to market a viable vaccine. That money, plus funding from other investors, will enable Acumen to devise three other ADDLbased strategies for preventing Alzheimer39。re wasting about 90 percent of the Alzheimer39。s opinion, is to remove the ADDLs or prevent them from forming. Attempts to eradicate amyloid plaques are misguided, he believes, and any attempt to intervene after neurons have started to die es too late to do much good. It39。s, whereas brains from normal patients were virtually free of ADDLs. What is more, they discovered that neurons of mice functioned normally once the ADDLs were removed. The obvious solution to treat Alzheimer39。 it diffuses throughout the brain instead of aggregating into fixed plaques。s often have relatively few plaques. Another proposed culprit is the presence of tangles of tau protein, which form inside neurons and coincide with the collapse of microtubules that support the cell body and transport nutrients. The tau tangles correlate much better with the disease but tend to appear later, suggesting that they are a consequence, not a cause. In 1994 Caleb E. Finch, a neurogerontologist at the University of Southern California, attempted to create amyloid plaque by mixing a solution of amyloid precursor protein fragments with clusterin, a substance produced at higher levels in the brains of people with Alzheimer39。s, which holds that fragments of amyloid precursor protein, produced by normal neurons, aggregate into sticky, insoluble plaques that damage neurons. The problem with this theory is that virtually every older person carries some amyloid plaque, but only a few develop Alzheimer39。s
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