PMID- 8786385 OWN - NLM STAT- MEDLINE DCOM- 19960920 LR - 20190512 IS - 0022-3069 (Print) IS - 1554-6578 (Electronic) IS - 0022-3069 (Linking) VI - 55 IP - 3 DP - 1996 Mar TI - Correlation of astrocytic S100 beta expression with dystrophic neurites in amyloid plaques of Alzheimer's disease. PG - 273-9 AB - The neurite extension factor S100 beta is overexpressed by activated astrocytes associated with amyloid-containing plaques in Alzheimer's disease, and has been implicated in dystrophic neurite formation in these plaques. This predicts (a) that the appearance of S100beta- immunoreactive (S100beta+) astrocytes precedes that of dystrophic neurites in diffuse amyloid deposits and (b) that the number of these astrocytes correlates with the degree of dystrophic neurite proliferation in neuritic plaques. As a test of the first prediction, we determined the number of S100beta+ astrocytes associated with different plaque types: diffuse non-neuritic, diffuse neuritic, dense-core neuritic, and dense-core non-neuritic. Diffuse non-neuritic plaques had small numbers of associated S100beta+ astrocytes (1.3 +/- 0.1 S100beta astrocytes per plaque [mean +/- SEM]; 80% of plaques had one or more). These astrocytes were most abundant in diffuse neuritic plaques (4.2 +/- 0.2; 100%), were somewhat less numerous in dense-core neuritic plaques (1.6 +/- 0.2; 90%), and were only rarely associated with dense-core non-neuritic plaques (0.15 +/- 0.05; 12%). As a test of the second prediction, we correlated the number of S100beta+ astrocytes per plaque with the area of beta-amyloid precursor protein (beta-APP) immunoreactivity per plaque (an index of the size of the plaques' dystrophic neurite shells) and found a significant positive correlation (r = 0.74, p < 0.001). This correlation was also evident at the tissue level: the numbers of S100beta+ astrocytes per plaque-rich field correlated with the total area beta-APP immunoreactivity in these fields (r = 0.66, p < 0.05). These correlations support the idea that astrocytic activation and S100 beta overexpression are involved in the induction and maintenance of dystrophic neurites in amyloid deposits, and support the concept of a glial cytokine-mediated cascade underlying the progression of neuropathological changes in Alzheimer's disease. FAU - Mrak, R E AU - Mrak RE AD - Department of Veterans' Affairs Medical Center, Little Rock, Arkansas, USA. FAU - Sheng, J G AU - Sheng JG FAU - Griffin, W S AU - Griffin WS LA - eng GR - P01 AG012411/AG/NIA NIH HHS/United States GR - AG10208/AG/NIA NIH HHS/United States GR - AG12411/AG/NIA NIH HHS/United States GR - AG27414/AG/NIA NIH HHS/United States PT - Journal Article PT - Research Support, U.S. Gov't, P.H.S. PL - England TA - J Neuropathol Exp Neurol JT - Journal of neuropathology and experimental neurology JID - 2985192R RN - 0 (Amyloid beta-Protein Precursor) SB - IM MH - Aged MH - Alzheimer Disease/*pathology MH - Amyloid beta-Protein Precursor/genetics/*metabolism MH - Astrocytes/*metabolism MH - Humans MH - Immunohistochemistry MH - Middle Aged MH - Neurites/*pathology PMC - PMC3833601 MID - NIHMS524648 EDAT- 1996/03/01 00:00 MHDA- 1996/03/01 00:01 PMCR- 2013/11/19 CRDT- 1996/03/01 00:00 PHST- 1996/03/01 00:00 [pubmed] PHST- 1996/03/01 00:01 [medline] PHST- 1996/03/01 00:00 [entrez] PHST- 2013/11/19 00:00 [pmc-release] AID - 10.1097/00005072-199603000-00002 [doi] PST - ppublish SO - J Neuropathol Exp Neurol. 1996 Mar;55(3):273-9. doi: 10.1097/00005072-199603000-00002.