Five million Americans suffer from Alzheimer’s disease, but scientists still have more questions about it than answers. Arguments abound over whether the hallmark protein clusters that accumulate in the brain are a cause or an effect of the illness, and current treatments do not address the main problem that causes impaired thinking: broken synapses, the junctions that allow neurons to communicate with one another. Researchers are now zeroing in on a promising missing link: mitochondria, the cell components responsible for energy regulation. In October researchers at Columbia University reported that young mice predisposed to acquiring Alzheimer’s accumulate protein clusters in synaptic mitochondria and that these clusters directly impair synapse function.
The link between mitochondria and Alzheimer’s is not exactly new. In the 1990s studies suggested that in the diseased brains of people and mice, mitochondria do not produce and distribute energy normally. And as early as 1994 researchers at the University of Kentucky showed that amyloid-beta protein fragments, the type found in Alzheimer’s, interfere with mitochondrial function. But no one knew how, exactly, mitochondria were linked to synaptic problems, if at all.
To find out, Shirley ShiDu Yan and her colleagues at the Columbia University Medical Center genetically engineered mice to overproduce a compound that leads to the formation of amyloid-beta clusters. When the mice were at various ages, the researchers isolated mitochondria from their synapses and from other brain regions. When the mice were just four months old—well before they showed symptoms of the disease—their synaptic mitochondria had accumulated approximately five times more amyloid protein than nonsynaptic mitochondria had. The affected mitochondria could no longer provide the synapses with enough energy, which ultimately prevented the synapses from functioning—providing the first direct link between cellular injury caused by amyloid protein and the characteristic breakdown of neuronal communication that occurs in Alzheimer’s patients.
The findings could provide new treatment possibilities. In earlier research Yan reported that cyclosporin D, a drug used to treat patients with organ transplants and autoimmune diseases, prevents amyloid-beta proteins from injuring mitochondria. Although the drug has serious side effects, Yan hopes that she can develop a similar but safer compound that prevents synaptic problems early on. Scientists need to “stop the disease early, before neurons have already died,” she says.
This article was originally published with the title A Case of Low Energy.
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4 Comments
Add CommentMitochondrial problems are implicated in a lot of diseases. Without a proper power supply your cells have all sorts of problems. It's really damage the the mitochondrial DNA itself that causes the trouble. So far, the best solution I've heard of for this problem is "MitoSENS" (google it) It's a strategy that shields mitochondrial DNA in a rather unique way. If it works, it could affect a variety of diseases.
Reply | Report Abuse | Link to thisSleep breathing disorders like obstructive sleep apnea and for that matter, any condition that leads to sleep intermittent hypoxemia including involuntary sleep movement disorders ( nocturnal myoclonus ), should be included in this scheme. Sleep intermittent hypoxemia with cortical irritability leads to slow wave sleep eradication (NREM) leading as well to a dysfunctional HPA axis modulation. Compunding further the matter with possibly an added factor, is a Disynchrony of the circadian rhythm. Chronobiology.
Reply | Report Abuse | Link to thisThe resulting panorama is early senescence with all of the common underlying irreversible medical conditions.
Your MitoSENS idea is only in its infancy and quite bluntly, I don't like the idea of anyone radically altering my DNA without a complete picture of what it would do to all of me rather than just 1 cell. I prefer to have people with some idea of what the consequences of their actions are before I let them mess with my brain.
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