Word: amyloid
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Dates: during 2000-2009
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...researchers, working separately, homed in on three genes linked to the late-onset form of the disease, the type that hits people in their 60s or later and accounts for 90% of Alzheimer's cases in the U.S. Two of the genes are known to interact with the amyloid-protein plaques that build up in the brain of Alzheimer's patients and eventually cause nerve-cell death and cognitive problems. The third affects the junction of nerve cells, where various neurochemicals work to relay signals from one nerve cell to another. It's not clear yet exactly how the genes...
...separate area of research, Xie at Massachusetts General tested another anesthetic, isoflurane, on a culture of human brain cells. (Isoflurane had already been shown to cause cognitive impairment in rats.) He saw a vicious cycle of apoptosis and the accumulation of beta-amyloid protein - the sticky plaques that build up in Alzheimer's patients' brains - among the cells. But in this case, it may have been an excess of calcium that led to cell death. Xie and his colleagues have since found that the Alzheimer's drug memantine, which works by reducing calcium levels inside cells, can slow the rate...
...these genes, two - clusterin and CR1 - are known to interact with the amyloid protein that builds up in the brain of Alzheimer's patients and eventually causes nerve cell death and cognitive problems. Clusterin may be involved in helping to clear away the amyloid that forms in the brain; but another variant of the gene may also allow amyloid to form fibrils, the sticky protein arms that further anchor amyloid plaques to nerve cells, much like a spider web ensnares prey. In late-onset Alzheimer's, it's possible that the body cannot balance these two functions of clusterin...
...other gene, CR1, codes for an immune system protein and may be involved in the body's ability to recognize the accumulating plaques of amyloid as foreign. If that's true, says Amouyel, then new treatments based on this approach might be possible. "Maybe there is some metabolic pathway that we can use to stimulate the immune system to work on CR1 to improve the clearance of amyloid," he says. "There may be new pharmacological targets, and this finding opens up ideas...
...discovery of PICALM came as a bit of a surprise. That gene's activity affects the junction between nerve cells, where various neurochemicals work to relay signals from one nerve cell to another. While most of the research attention in Alzheimer's has been on the build up of amyloid protein and tau tangles that strangle nerve function, the identification of PICALM suggests that some part of the disease may have to do with a breakdown in nerve-cell communication at the junctures. "If you had given people a list of genes and said which ones were involved in late...