Researchers are rethinking causes of Alzheimer's disease...moving from amyloid to myelin targets

For decades, many Alzheimer's researchers have targeted the peptide amyloid beta as the toxic culprit that forms sticky plaque in the brains of Alzheimer's patients. But some researchers are now wondering if this is the wrong target. What if the disease starts much earlier, fed by a natural process? George Bartzokis, UCLA professor of psychiatry, said a better working hypothesis of Alzheimer's cause is the "myelin model," a model of the human brain that could lead to new and better therapeutic approaches, according to a UCLA news release. Myelin, the fatty sheath that coats our nerve axons, allows for efficient conduction of nerve impulses and is the key to the fast processing speeds that support our higher cognitive functions, the report says. It also helps to encode our memories.But because the human brain is myelinatd throughout our lives, it is also more vulnerable to damage. In the myelin model of Alzheimer's disease, the normal, routine maintenance and repair of myelin throughout life initiates the mechanisms that produce degenerative diseases like Alzheimer's. Bartzokis believes the amyloid beta may actually develop (and build up in the brain) as a result of the natural process of the repair and maintenance of myelin. He believes that the breakdown that leads to AD and other age-related brain diseases, such as Parkinson's may begin much earlier, before the formation of the protein deposits that are used to define these diseases. This new approach to studying Alzheimer's may eventually produce treatments that actually prevent AD, rather than treating the symptoms, offering new hope for the next generation that faces these brain-wasting diseases.