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Alzheimer’s disease is thought to be connected with neurons in the memory center of the brain that are choked as a result of the buildup of two types of proteins: tau protein, which turns destructive when aberrant forms of the  protein form fibrous tangles, and amyloid beta, which produces an amyloid plaque.

The NYU Medical Center researchers focused their attention on the tau protein, which is important in a healthy brain to transport chemicals within neurons. The main problem was that, unlike amyloid beta protein, which is extracellular and more easily treated by chemicals, the tau protein confines itself to the inside of brain cells—making it difficult for medication to reach it. The other problem was to find a way to effect only the abnormal tau protein which cause the fibrous tangles to form.

The researchers developed a vaccine of antibodies using fragments of abnormal tau protein. Normally, the blood brain barrier blockades antibodies from getting to the brain in large quantities, but in Alzheimer’s patients there is a breakdown of the blood brain barrier that allows more antibodies to pass through to the brain. Once the vaccine antibodies passes through the blood brain barrier they readily bind with the unhealthy fibrous tangles formed by the aberrant tau protein, while ignoring the healthy form of the protein.

The study used mice which were genetically engineered to produce abnormal tau proteins early in life. There are plans to conduct follow-up studies using mice which slowly develop tangles and cognitive impairments.

What the researchers feel is important about their findings is that their approach allows specific targeting of the problematic protein. Although their treatment may not be a cure, it will help in delaying the onset of advanced Alzheimer’s disease.

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