Inflammation, A beta 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 sets: AD patients, nondemented elderly patients with few or no neurofibrillary tangles (NFTs) and amyloid beta peptide (A beta) deposits, i.e. normal controls (NC), and nondemented elderly patients with profuse entorhinal cortex NFTs and neocortical A beta deposits, i.

Inflammation and Alzheimer's disease pathogenesis.

Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The first is that to be pathogenically significant a neurodegenerative mechanism must be primary. The second is that inflammation merely occurs to clear the detritis of already existent pathology.

Complement activation by beta-amyloid in Alzheimer disease.

Alzheimer disease (AD) is characterized by excessive deposition of the beta-amyloid peptide (beta-AP) in the central nervous system. Although several lines of evidence suggest that beta-AP is neurotoxic, a mechanism for beta-AP toxicity in AD brain remains unclear. In this paper we provide both direct in vitro evidence that beta-AP can bind and activate the classical complement cytolytic pathway in the absence of antibody and indirect in situ evidence that such actions occur in the AD brain in association with areas of AD pathology.

Molecular, cellular, and pathologic characterization of HLA-DR immunoreactivity in normal elderly and Alzheimer's disease brain.

Previous studies have suggested that markers of immune function may be present in brain. We have characterized one of the most important of these markers, the human major histocompatibility complex antigen HLA-DR, at molecular, cellular, and pathologic levels. The results show that an antigen with the correct molecular weight for HLA-DR and the appropriate immunoreactivity for HLA-DR monoclonal antibodies is present in nondemented elderly (ND) and Alzheimer's disease (AD) brain tissue.

Epidermal growth factor receptor expression in demented and aged human brain.

Immunoreactivity to epidermal growth factor receptor (EGFR) was present in the brain vasculature of 13/13 demented elderly patients, but absent in 9/11 non-demented elderly patients. Of the two positive non-demented patients, one had significant Alzheimer's pathology and the other spinal carcinoma. Ultrastructurally, EGFR is localized to the lumenal surface of endothelial cells.