A report in The Economist looks at a recent study which may explain the cause of autism:
One suggestion that does pop up from time to time is that the process which leads to autism involves faulty mitochondria. The mitochondria are a cell’s powerpacks. They disassemble sugar molecules and turn the energy thus liberated into a form that biochemical machinery can use. Mitochondrial faults could be caused by broken genes, by environmental effects, or by a combination of the two.
Nerve cells have a huge demand for energy, so a failure of the mitochondria would certainly affect them. The question is, could it cause autism? To try to find out Cecilia Giulivi of the University of California, Davis, and her colleagues studied the mitochondria of ten children, aged between two and five years, who had been diagnosed with autism. They have just published their results in the Journal of the American Medical Association.
[. . .]
The children in question were randomly selected from a previous study on autism. They were matched with ten children of similar ages and ethnic backgrounds who were developing normally. Dr Giulivi found that mitochondria from children with autism consumed far less oxygen than those from the control group. That is a sign of lower activity. One important set of enzymes — NADH oxidases — used, on average, only a third as much oxygen in autistic children as they did in non-autists, and eight of the autistic children had significantly lower NADH-oxidase activity than is normal.
The mitochondria of the autistic children also leaked damaging oxygen-rich chemicals such as hydrogen peroxide. These are a normal by-product of mitochondrial activity, but are usually mopped up by special enzymes before they can escape and cause harm — for instance, by damaging a cell’s DNA. The level of hydrogen peroxide in the cells of autistic children was twice that found in non-autists. Such high levels suggest the brains of autistic children are exposed to a lot of oxidative stress, something that would probably cause cumulative damage.
While such a mechanism may allow better treatments to be developed, it also implies that those who already suffer from autism may not benefit as much (or at all) from such treatments, as the cellular damage will be a much tougher challenge to reverse.
On the other hand, if the pattern can be detected early enough, it may allow treatment well in advance of serious damage.
