Similar topography, morphology and pattern of fiber staining of nicotinamide adenine dinucleotide-diaphorase (NADPH-d), parvalbumin, neuropeptide Y, somatostatin and SMI-32 containing structures were demonstratedin the amygdala of the monkey, gorilla, chimpanzee and normal aged human brains. These similarities support the usefulness of experimental paradigms comparing these neurochemical systems in non- human and human primates. While the primate basolateral amygdaloid division developed phylogenetically in tandem with the expansion of neocortical association areas, the greatest increase was observed in humans. Because the lateral amygdaloid nucleus maintains direct synaptic contact with cerebral cortical association areas, and harbors a distinct population of parvalbumin and SMI-32-containing neurons, it was used to test the selective vulnerability hypothesis in Alzheimer's disease (AD). The lateral nucleus showed up to a 50% decrease in cytoarchitectural area features in the pathogenesis of AD. A molecular biology approach was also used to test selective vulnerability. Neuropathologic analysis of AD patients identified clinically with leukoencephalopathy did not support a direct vascular role in the etiology of the disease. Amyloid staining revealed severe cerebral amyloid angiopathy without involvement of white matter vessels. Thus, the increased amyloid burden in the cerebral vasculature does not appear to account for clinically observed leukoencephalopathy in AD patients.
