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Mitochondria Link Alzheimer's Disease, Down Syndrome
28 February 2002 (All day)
Alzheimer's disease almost always afflicts people older than 60, but in people with Down syndrome, Alzheimer's often strikes before age 40. Now, a team of researchers reports that breakdowns in brain cells' energy-generating mitochondria contribute to the early onset of Alzheimer's in Down syndrome patients and may spur Alzheimer's in old age as well.
Researchers suspect that people with Down syndrome are more susceptible to Alzheimer's disease because their extra copy of chromosome 21 causes them to build more of some proteins whose genes sit on that chromosome. One such gene codes for amyloid precursor protein (APP). A set of enzymes trims APP into another protein, called A?42, that is the main component of the senile plaques that characterize Alzheimer's disease. But there might be other links between the two diseases as well. For instance, Down syndrome patients have defective mitochondria, organelles that also lose efficiency as people age. Some studies have linked malfunctioning mitochondria to brain cells' inability to properly process APP, suggesting a connection to Alzheimer's.
To test how mitochondrial defects might lead to signs of Alzheimer's disease, a team led by Jorge Busciglio of the University of Connecticut, Farmington, and Bruce Yankner of Harvard Medical School in Boston examined brain cells from aborted fetuses with Down syndrome. Compared with normal cells, the Down cells accumulated more A?42 and shuttled less APP out of the cell. The team found the same pattern when they poisoned the mitochondria of normal cells--evidence, they say, that defective mitochondria allow A?42 and APP to build up inside the Down cells. What's more, the secreted form of APP is known to protect neurons from various toxins, including A?42. Reporting their results in the 28 February issue of Neuron, the researchers argue that Alzheimer's disease can result from a deadly cycle in which an excess of APP impairs mitochondria, which causes cells to secrete less of the protective form of APP, making them vulnerable to damage from A?42 accumulation.
"It's a beautifully done paper," says neuroscientist M. Flint Beal of Cornell University Medical College in New York City. "I was always a little bit skeptical [of the hypothesis that mitochondria and APP interact in a toxic feedback loop], but I'm becoming more of a believer."