icture and the identical nature of the histopatholgy, distinctions between AD and senile dementia were arbitrary and no longer useful (Pitt, 12). Thus when it was understood that AD and senile dementia are similar, it was clear that AD is a common illness.In the mid-1970's two important contributions were made. First, Butler in his 1975 book Why survive? Being old in America criticized the widespread notion that senility was a normal part of aging. Butler argued that, senility, was a result of brain disease or depression and was potentially treatable. The extension of this view was that senility was abnormal, and that its usual causes were diseases, not just aging (Pitt, 1987). Second, three different labs (Bowen et al, 1976; Davies & Maloney, 1976; and Perry et al, reported low levels of choline acetyltransferase, the marker enzyme for acetylcholine 1977) (ACh), in the brains of patients who died from AD. ACh deficiency has since been the target of most therapeutic efforts in AD (see treatment).Throughout the 1980's and 1990's two trends emerged. First, with regards to diagnosis, criteria have been made stricter. Classification systems like the Diagnostic and Statistical Manual have evolved towards a more precise and comprehensive definition of dementia. Moreover, neuoroimaging techniques are becoming more and more standard, allowing in some cases for a more accurate diagnosis. Second, the past fifteen years have witnessed a substantial growth in genetically based research. For instance one of the genes involved in AD, the amyloid precursor protein (APP), has been localized to a specific segment of chromosome 21 (see risk factors).EpidemiologyDementia is known as the quiet epidemic, but it affects a significant proportion of our population. In 1989 the Canadian consensus conference on the assessment of dementia reported that Canada had about 250,000 cases of dementia (which at the time comprised about 1% of the populatio...
