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Every age-related neurodegenerative condition presents researchers with a vast and complex problem to solve; biochemistry is a real challenge, even in this age of rapidly advancing biotechnology, as illustrated by the vast sums required to build scientific infrastructure and win progress from the mysteries of the brain. Even seemingly simple questions remain unanswered, and there are never enough resources to explore every aspect of a biochemical process as well as we'd like.
Here are a couple of pieces illustrative of that state of research: so much to do, small but significant victories in the form of new knowledge, and the vast spaces yet to be explored.
Study Puts 1 Alzheimer's Theory in Doubt:
In prior studies, examination of the brain cells of people with Alzheimer's found some defects in an enzyme produced by the cytochrome c oxidase ( COX) gene, which is important for mitochondrial energy production.
In addition, so-called "free radicals," which cause oxidative stress, are produced in the cell's mitochondria, Moraes noted. "It was assumed that when you have a problem with the COX gene, you have more free radicals being formed," he said.
To see how the gene worked, Moraes's group removed the COX10 gene in mice engineered to develop Alzheimer's disease. "We expected to see that these animals would have more amyloid plaques," Moraes said. "But we got the opposite result," he said. The animals without the COX10 gene actually developed fewer brain plaques than those with the gene, Moraes said. "Those animals also had less free radicals," he said.
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"The results are consistent with other evidence that reducing free radicals can limit Alzheimer amyloid plaque pathology," Cole added. "Examples include reducing caloric intake or increasing antioxidant intake. So, even though clinical trials to treat Alzheimer's with [antioxidant] vitamin E have been disappointing, earlier and more effective reduction of free radical damage could mimic the success of this genetic approach and should still be pursued,"
Recovering Lost Memory
Fischer and his colleagues found that while environmental enrichment did not substantially replace the lost hippocampal neurons, it significantly increased the number of connections, or synapses, between the hippocampal neurons that remained. This increase in connectivity, apparently compensating somehow for the previous death of neurons, led the mice to recover the memories that had apparently disappeared with the loss of the neurons.
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Amazingly, the researchers identified a chemical that -- in mice -- mimicked the effect of environmental enrichment. They found that the environmental enrichment modifies the function of proteins that regulate the activity of genes; a substance that blocks an enzyme called HDAC (histone deacetylase) seemed to have a similar impact on the gene activity involved, and tests subsequently showed that this HDAC blocker could allow the recovery of lost memories.
If common forms of neurodegeneration can be repaired from the state of memory and function loss - if memories are stored in ways that persist through the early stages of Alzheimer's, for example - hundreds of millions more lives might be saved at the future cusp between merely advanced medicine and the ability to rejuvenate the aged.
The same would be true if everyone adopted the practice of calorie restriction, by the look of the human studies presently taking place, but I'm not holding my breath waiting for that to happen. Most folk would rather not think about the future, or trust themselves to advances in science; while those advances are certainly on the way, it doesn't seem wise to bet on their arrival soon enough to rescue you from any particular fate.
Technorati tags: medical research, neurodegeneration
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Posted by Reason
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