RESUMO
Using manual morphometric techniques, we estimated the amount of neuromelanin in hematoxylin and eosin-stained sections of the pars compacta of the substantia nigra of 19 Alzheimer's patients without nigral Lewy bodies and 12 age-matched controls. Our estimates showed that the mean area and areal fraction of neuromelanin were lower in Alzheimer's disease than controls but the number and size of the neuronal cell bodies, nuclei and nucleoli did not differ between the two groups. We speculated that the decreased amount of neuromelanin in nigral neuronal cell bodies could have resulted from neurofibrillary degeneration, retrograde degeneration from damage of nigral dopaminergic terminals in the striatum by the beta amyloid protein of the diffuse plaques and possibly transneuronal degeneration from damage of cell bodies or dendrites of nigral neurons by their plaque- and tangle-ravaged striatal, neocortical and other subcortical nigral connections. We hypothesized that any or all of the above types of degeneration could have lowered the rate of dopamine metabolism and the formation of one of its by-products, neuromelanin. Our study shows that a decrease in the amount of histopathologically-observable nigral neuromelanin commonly occurs in Alzheimer's disease without nigral Lewy bodies.
