S100β protein expression in Alzheimer disease: Potential role in the pathogenesis of neuritic plaques

✍ Scribed by J. G. Sheng; R. E. Mrak; Prof. W. S. T. Griffin

• Publisher: John Wiley and Sons
• Year: 1994
• Tongue: English
• Weight: 748 KB
• Volume: 39
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.490390406

✦ Synopsis

Increased synthesis and release of Sloop protein from activated astrocytes has been implicated in the overgrowth of dystrophic neurites in neuritic plaques in Alzheimer disease (AD). To evaluate the quantitative relationships between tissues levels of Sloop and the numbers of neuritic plaques in AD patients, we counted neuritic plaques, by Tau-2 immunoreactive (Tau-2 + ) labeling, in tissue sections of hippocampus and adjacent temporal cortex and measured the levels of Sloop protein, by Western immunoblot labeling, in samples of analogous regions from contralateral hemisphere of the same patients. In AD, tissue levels of Sloop (two-to fivefold that of controls) were significantly correlated with the number of Tau-2+ plaques (R = 0.82, P < .01). Dual-label immunohistochemical analysis showed that most Sloop + cells were activated GFAP+ astrocytes. These results were substantiated by a significant correlation between Sloop and GFAP tissue levels (R = 0.81, P < .05).

Many of the Sloop' astrocytes were clustered around and within Tau-2+ plaques. Indeed, no Tau-2 + plaques were found without associated activated Sloop ' astrocytes. Our findings provide further evidence of a role for Sloop protein in dysregulation of neurons that leads to apparently nonsensical growth of imperfect neurites in AD, a potential key element in early stages of neuritic plaque pathogenesis.