root of the problem? mutations in mitochondrial DNA can trigger late-onset Alzheimer's disease.
The most common form of Alzheimer's disease is not hereditary, and little is known about its causes. Now researchers have found a handful of genetic mutations that occur more frequently in patients with the disease. The results reinforce earlier suggestions that Alzheimer's is caused in part by deficits in energy cell power plants.
The researchers found some of the genes involved in familial Alzheimer's disease, accounting for about 10% of cases and usually strikes people in their 60s, but they have had little success finding genetic glitches associated with the most common form of late-onset. Some evidence indicated an ongoing accumulation of mutations in the DNA in mitochondria, the cells inside the energy-producing organelles. For example, Douglas Wallace, now at the University of California, Irvine, and colleagues found that a small percentage of patients with Alzheimer carried a specific mutation in their mitochondrial DNA. But it simply could not explain the large number of late-onset victims. So they kept looking.
After reviewing each mitochondrial gene that encodes a protein, without success, Wallace's team decided to test the changes in a short DNA region that regulates the expression of mitochondrial genes and helps copy mitochondrial DNA when cells divide. By comparing the DNA of the brains of 23 Alzheimer's patients brains against 40 healthy age-matched, the team found a mutation that occurred exclusively in the brain of Alzheimer's - 65% of diseased brains contained this mutation the reports online this week in the team Proceedings of the national Academy of sciences . Other mutations were also more common in patients with Alzheimer's. In addition, the team found that the brains of people who died of Alzheimer's disease before 80 years harbored few mutations in many cells, whereas those who died later brought a greater variety of mutations in less cells. This suggests that the mutations that occur early in life and accumulate in brain cells may increase the risk of disease.
The mutant mitochondrial DNA the team found "are worth," says Rudolph Tanzi neurogeneticist of Harvard Medical School in Boston. But, although the data are consistent with other evidence linking mitochondria to Alzheimer's disease, he warned that the sample size of the study is so small that the results should be considered preliminary.
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