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    ALZHEIMER'S RESEARCH
    Protein links

    The number of people with Alzheimer's disease is expected to triple in the next two decades. This sobering prediction continues to motivate efforts to identify the causes and risk factors associated with this devastating illness. Among the tools being used to study Alzheimer's are those made recently available by molecular genetics. These tools are helping in the study of neuritic (filament-containing) plaques that are a characteristic of the disease.

    Plaques are diagnostic

    Alzheimer's disease was first described by Dr. Alois Alzheimer in 1906. Using a microscope to study brain tissue from autopsies, Dr. Alzheimer observed the pathological changes that he said resembled tangles and plaques. In the years since Dr. Alzheimer's discovery, progress in understanding the disease has been slow but steady.

    Recently, the pace of progress has accelerated substantially. Recombinant DNA technology, developed in the 1970s, allows DNA from one organism to be "spliced" or recombined with that of another to form a new "piece" of DNA in the laboratory. In 1983, the creation of polymerase chain reaction (PCR) technology, a laboratory method by which a small fragment of human genetic material (DNA) can be quickly reproduced millions of times, was a another major advance in the genetic study of Alzheimer's, as well as many other neurodegenerative diseases.

    Researchers at Mayo Clinic are using these molecular genetic techniques to explore the causes of Alzheimer's disease. They're focusing attention on the amyloid peptide (part of a protein called amyloid beta) and on other proteins called presenilins (which are involved in metabolizing amyloid). Specifically, they've shown that simple genetic mutations in these proteins can lead to Alzheimer's disease by causing more of the amyloid peptide to be made by the brain.

    There are still many unanswered questions about how amyloid beta protein is deposited, and why the brain over-produces the protein or fails to rid itself of excess protein. Like fitting together the pieces of a puzzle, each answer increases understanding.

    Ongoing, collaborative research among several medical and academic centers has yielded findings that a specific form of amyloid beta protein (amyloid beta 42) is present in elevated levels in the blood of individuals whose chromosomes carry the genetic mutations characteristic of the early form of Alzheimer's.



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