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Distribution of interleukin‐1‐immunoreactive microglia in cerebral cortical layers: implications for neuritic plaque formation in Alzheimer’s disease
Author(s) -
Jin Sheng,
W. Sue T. Griffin,
M.C. Royston,
Robert E. Mrak
Publication year - 1998
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.1365-2990.1998.00122.x
Subject(s) - microglia , senile plaques , alzheimer's disease , pathology , neuroscience , medicine , biology , disease , inflammation
Activated microglia overexpressing interleukin‐1 (IL‐1) are prominent neuropathological features of Alzheimer’s disease. We used computerized image analysis to determine the number of IL‐1α‐immunoreactive (IL‐1α + ) microglia in cytoarchitectonic layers of parahippocampal gyrus (Brodmann’s area 28) of Alzheimer and control patients. For cortical layers I and II, the numbers of IL‐1α + microglia were similar in Alzheimer and control patients. For layers III–VI, the numbers of IL‐1α + microglia were higher than that seen in layers I–II for both Alzheimer and control patients. Moreover, for layers III–VI, the number of IL‐1α + microglia in Alzheimer patients was significantly greater than that in control patients (relative Alzheimer values of threefold for layer III–V and twofold for layer VI; P <0.05 in each case). The cortical laminar distribution of IL‐1α + microglia in Alzheimer patients correlated with the cortical laminar distribution of β‐amyloid precursor protein‐immunoreactive (β‐APP + ) neuritic plaques found in Alzheimer patients ( r =0.99, P <0.005). Moreover, the cortical laminar distribution of IL‐1α + microglia in control patients also correlated with the cortical laminar distribution of β‐APP + neuritic plaques found in Alzheimer patients ( r =0.91, P <0.05). These correlations suggest that pre‐existing laminar distribution patterns of IL‐1α + microglia (i.e. that seen in control patients) are important in determining the observed laminar distribution of β‐APP + neuritic plaques in Alzheimer patients. These findings provide further support for our hypothesis that IL‐1 is a key driving force in neuritic plaque formation in Alzheimer’s disease.