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Researchers looking for the genetic causes of Alzheimer's have identified five more genes related to the condition, making now seven genes known to be connected with the brain-wasting disease.
Publishing their work in the journal Nature Genetics on 3 April, the researchers at the John J. Hussman Institute for Human Genomics at the University of Miami report that if medications or lifestyle changes could change the activity of these five newly discovered genes, up to 60 per cent of late-onset Alzheimer's disease might be prevented.

Alzheimer's researchers have long known that having both of two possible genes for dementia usually triggers the disease before the age of 65. These genes have to be inherited from both parents. Because only about 1 in 1000 people who has Alzheimer's has both of these genes from both parents, researchers thought that most cases of the disease did not have an important genetic component. This research, looking at genetic data from 70,000 people, identified five other genes that seem to be related to Alzheimer's at different stages of the disease, explaining about 60 per cent of the 999 out of 1,000 cases not explained by earlier research.

Alzheimer's disease is the most common cause of dementia in persons over 65 years of age. It affects memory, and also the ability to make meaningful decisions. In later stages, people who suffer Alzheimer's may lose their ability to distinguish night and day, up and down, left and right, and lose coordination and mobility. Even worse, brief improvements in mobility without corresponding improvements in memory and "executive function," the ability to make good decisions, can result in falls and other kinds of accidents. A partially successful treatment can be worse than no treatment at all.

The physiological process that causes Alzheimer's involves the loss of neurons and neuron connections in the cerebral cortex, the part of the brain most associated with conscious activity. These neurons are finally removed by the immune system, but before their destruction by white blood cells, they are distorted by the accumulation of proteins that "tangle" and distort neurons and the way they connect to other neurons throughout the brain.

Before the formation of tangled proteins, however, there are also abnormalities in the brain uses cholesterol—which constitutes a very large percentage of all brain tissue. And before there are abnormalities in the ways the brain uses cholesterol, there are abnormalities in the the cycles of using and recharging antioxidants.

Scientists believe that intervening at any step might help stop the progression of Alzheimer's. Early intervention, of course, is preferable.

Other researchers have found, for instance, that as simple an intervention as avoiding overeating, and giving the brain at least 12 hours of "rest" from the free radical generating effects of eating carbohydrates, every day, drastically reduces the number of new cases of Alzheimer's disease. Whem the brain burns glucose for its fuel, it makes free radicals. If it is not "fed" quite as often as three square meals every day, it makes fewer free radicals. There is less damage to cholesterol, and the processes that lead to Alzheimer's take longer to get started, or maybe don't start at all.

This "treatment" costs nothing and even helps people maintain normal weight. But it only prevents the activation of one of the first genes in the Alzheimer's sequence. Short-term (12- to 18-hour) fasting later in the progression of the disease not only does not help, it hurts.

The scientists at the Alzheimer Disease Genetics Consortium who did this research believe that any medications developed on the basis of their research are probably at least 15 years away. If you don't have Alzheimer's already, however, simply giving your brain a break from the constant free radical generation after every meal may greatly increase your chances of avoiding the disease.

  • Luchsinger JA, Small S, Biessels GJ. Should we target insulin resistance to prevent dementia due to Alzheimer disease? Arch Neurol. 2011 Jan, 68(1):17-8
  • Naj AC, Jun G, Beecham GW, Wang LS, Vardarajan BN, Buros J, Gallins PJ, Buxbaum JD, et al. Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease. Nat Genet. 2011 Apr 3. [Epub ahead of print]