yroid disease in women. However, their findings have not been replicated. Interestingly, there is some evidence to suggest that smoking can have a protective effect from AD. For instance, Duijn and Hofman (1991) [as cited by Graves & Kukull, 1994] have found a negative correlation between smoking and AD in a study involving 198 individuals.NeuropathologyFor each dementing disease a specific neuropathological pattern is observed. However, due to the limited scope of this essay the discussion will be limited to the most important dementing disease, AD.Gross FeaturesSeveral changes are observed at the gross neuropathological level in AD (Mirra & Gearing, 1994). Cortical atrophy is generally observed in the frontal, temporal, and parietal cortex. Sectioning of the brain reveals variable enlargement of the lateral and third ventricles. Disproportionate enlargement of the temporal horn of the lateral ventricle is commonly encountered, with concomitant atrophy of the entorhinal cortex, amygdala, and hippocampus.Microscopic FeaturesAt the microscopic level the two most distinguishing neuropathological features are senile plaques (SP) and Neurofibrillary tangles (NFT).There are two types of SP, neuritic and diffuse, both plaques share antigenic determinants with the Beta amyloid 4 protein. Neuritic plaques can be distinguished by their abnormally thickened neurites ( i.e., axons or dendrites) arranged around a central core of amyloid (Mirra & Gearing, 1994). By contrast the diffuse plaques lack the thickened neurites and the amyloid core seen in the neuritic plaques (Mirra & Gearing, 1994). Plaques of both types are found in varying degrees in the neocortex, entorhinal cortex, hippocampus, and in the amygdala. SP also occur in the brains of healthy people. It is only when they exceed a certain critical number that AD emerges.NFT are intraneuronal structures which occupy the cell body of the neuron. Usually NFT coexist with SP in ...
