Immunochemical and morphometric features of astrocyte reactivity vs. plaque location in Alzheimer's disease.

The quantitative relationship between glial fibrillary acidic protein (GFAP) hyper-reactivity and β-amy- loid protein (βAP) deposition was investigated by double immunoperoxidase labeling of hippocam- pal and entorhinal cortex sections from five Alzheimers disease (AD) cases and five age-matched controls. βAP plaques, which were absent in controls, were found in all AD samples, without significant differences in number or perimeter according to their location among the regions studied. In contrast, the mean number of GFAP (+) cells was significantly greater in the hippocampus than in the entorhinal cortex from AD cases (49 vs.39). Although at lower values (30 vs. 20), predominance of astrocyte hyperplasia in hippocampus as com- pared with entorhinal cortex was also found in control samples. Concomitant astrocyte hypertrophy, as defined by surface density (Sv) values of GFAP-immunoreactive material exceeding those of control means, affected a similar proportion of cells in the hippocampus (73%) and the entorhinal cortex (74%) from AD cases. Since an increased number of GFAP (+) cells in the hippocampus was not accompanied by an increased number and/or perimeter of neighbouring plaques, such differential hyper-reactivity in samples from AD patients, as well as in those with normal aging, seems to depend partially on the regional location of the involved astrocyte.