Recent studies have revealed that select neuronal populations may display a differential sensitivity to degeneration in
Alzheimer's disease. For example, large pyramidal neurons have been shown to be vulnerable, whereas small, local circuit neurons appear to be resistant to the pathologic process. More significantly, interneurons that contain the
calcium-binding proteins parvalbumin and
calbindin are particularly resistant to degeneration in
Alzheimer's disease. Using a polyclonal antibody to the
calcium-binding protein calretinin, we analyzed the possible changes in the subset of interneurons containing this
protein in two neocortical areas that are generally devastated in
Alzheimer's disease. In the prefrontal cortex as well as in the inferior temporal cortex, we observed no difference in the density of
calretinin-immunoreactive neurons in
Alzheimer's disease brains as compared to control cases. Moreover, the cellular morphology of these neurons was well preserved in the
Alzheimer's disease cases. These data suggest that
calretinin-immunoreactive neurons, like other
calcium-binding protein-containing interneurons, are resistant to degeneration in
Alzheimer's disease. The results support the notion that the pathological process in
Alzheimer's disease involves specific cellular populations sharing particular morphological and neurochemical characteristics. In addition, it is possible that the presence of
calcium-binding proteins confers a certain degree of resistance to degeneration in specific neuronal subsets.