Inflammation, Aβ Deposition, and Neurofibrillary Tangle Formation as Correlates of Alzheimer's Disease Neurodegeneration

We evaluated entorhinal cortex and superior frontal gyrus for hallmarks of Alzheimer's disease (AD) pathology, including inflammation, in three patient setsAD patients, nondemented elderly patients with few or no neurofibrillary tangles (NFTs) and amyloid β peptide (Aβ) deposits, i.e. normal co...

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Bibliographic Details
Published in:Journal of neuropathology and experimental neurology 1996-10, Vol.55 (10), p.1083-1088
Main Authors: Lue, Lih-Fen, Brachova, Libuse, Civin, Harold W, Rogers, Joseph
Format: Article
Language:English
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Summary:We evaluated entorhinal cortex and superior frontal gyrus for hallmarks of Alzheimer's disease (AD) pathology, including inflammation, in three patient setsAD patients, nondemented elderly patients with few or no neurofibrillary tangles (NFTs) and amyloid β peptide (Aβ) deposits, i.e. normal controls (NC), and nondemented elderly patients with profuse entorhinal cortex NFTs and neocortical Aβ deposits, i.e. high pathology controls (HPC). Membrane attack complex (C5b-9) immunoreactivity and immune activation of microglia (MHCII expression) were used as general markers for inflammation. Compared to NC patients, AD patients exhibited significant cortical synapse loss, Aβ deposition, NFT formation, and inflammation. HPC patients also had significantly elevated Aβ deposition and NFT formation, but there was no evidence of synapse loss and little or no evidence of inflammation. Across patients and brain regions the measures of inflammation each accounted for significant percentages of the variance in synaptophysin immunoreactivity and each was more highly correlated with synapse estimates than NFT formation or Aβ deposition.
ISSN:0022-3069
1554-6578