Abstract
The entry of molecular genetics into the field of Alzheimer's disease in the last few years has led to the usual plethora of data that results when any new methodology is applied to an old problem. The information has been of both a positive and negative type. On the positive side, the genes for two components of the Alzheimer amyloid deposits (the β–protein and the protease inhibitor α1–antichymotrypsin) have been identified, one previously unsuspected, and at least some families harboring the inherited form of Alzheimer's disease have been shown to carry their autosomal dominant mutation on chromosome 21. On the negative side, the early hoped–for explanation of familial Alzheimer's disease as a mutation in the β–protein or a triplication of the β–protein gene turned out not to be forthcoming, and the potential heterogeneity of familial Alzheimer's disease indicated by some studies means we still have much genetic work to do. The molecular genetic studies have also provided potential insights into the biochemistry of amyloid formation and into the normal function of the β–protein precursor.
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Abraham, C., Potter, H. Alzheimer's Disease: Recent Advances in Understanding the Brain Amyloid Deposits. Nat Biotechnol 7, 147–153 (1989). https://doi.org/10.1038/nbt0289-147
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DOI: https://doi.org/10.1038/nbt0289-147
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