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Parvalbumin-lmmunoreactive Neurons in the Neocortex are Resistant to Degeneration in Alzheimer's Disease

Patrick R. Hof M.D., Kevin Cox B.A., Warren G. Young Ph.D., Marco R. Celio M.D., Joseph Rogers Ph.D., John H. Morrison Ph.D.
DOI: http://dx.doi.org/10.1097/00005072-199107000-00006 451-462 First published online: 1 July 1991


Recent studies have stressed the fact that specific neuronal subtypes may display a differential sensitivity to degeneration in Alzheimer's disease. For example, large pyramidal neurons have been shown to be vulnerable, whereas smaller neurons are resistant to pathology. Using a monoclonal antibody against the calcium-binding protein parvalbumin, we investigated the possible changes in a subpopulation of intemeurons in two cortical areas known to be strongly damaged in Alzheimer's disease. In the prefrontal cortex as well as in the inferior temporal cortex, we observed no differences in parvalbumin-immunoreactive cell counts or cell size in Alzheimer's disease brains as compared to control cases. Moreover, the general cellular morphology of these neurons was preserved in the Alzheimer's disease cases, in that their perikarya and dendritic arborizations were intact. These results suggest that parvalbumin-immunoreactive cells represent a neuronal subset resistant to degeneration, and further support the hypothesis that the pathological process in Alzheimer's disease involves specific neuronal subtypes with particular morphological and molecular characteristics.

Key Words
  • Alzheimer's disease
  • Calcium-binding proteins
  • γ-aminobutyric acid
  • Interneurons
  • Neocortex, human
  • Quantitative neuroanatomy