the neocortex, but they may be absent there in up to 30% of AD patients (Mirra & Gearing, 1994). However, NFT are consistently found in the entorhinal cortex, hippocampus, amygdala, nucleus basalis of Meynert, and dorsal raphe nucleus (Mirra & Gearing, 1994). It is thought that the major antigenic component in NFT is the protein tau.Neuronal LossNeuronal loss is directly related to the degree of synaptic density, which has been found to be crucial in determining the severity of cognitive decline. It is greatest in the temporal lobes, but is also significant in the frontal and parietal lobes (Lezak, 1995). The strongest correlation with a global measure of dementia is the loss of functional synapses in the midfrontal and lower parietal areas which surround the temporal lobes (Lezak, 1995). The effect of this pattern of neuronal cortical loss is twofold. First it disconnects the temporal lobe structures from the rest of the cerebral cortex. This accounts for the prominence of memory impairments (Lezak, 1995). Second this pattern also disconnects the prefrontal structures from the parietal ones. This accounts for the compromised capacity for attentional tasks (Lezak, 1995). It is thought that besides the effects of SP and NFT, neuronal loss is chiefly related to the depletion of the neurotransmitter acetylcholine (see treatment).Overall PictureIn a study conducted by Brun and Gustafson (1978) [as cited by Cummings, 1988], the regional distribution of SP, NFT, and neuronal loss, was examined in AD patients. The results indicated that the most severely affected areas were the medial temporal and the temporo-parieto-occipital junction region (see figure 1). Two positron emission tomography (PET) studies by Benson et al. (1983) and Foster et al. (1984) [as cited by Cummings, 1988] have confirmed this pattern....
