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PubMedDate not supplied

Neuroimmunology of Alzheimer's disease: a conference report.

A multidisciplinary group met under the auspices of the National Institute on Aging and the Dell Foundation at the Princess Resort in San Diego, CA on April 5-6, 1991. The meeting was organized by Dr. Caleb E. Finch, University of Southern California, Dr. Zaven Khachaturian, National Institute on Aging, Dr. William Markesbery, University of Kentucky, Dr. Patrick McGeer, University of British Columbia, and Dr. Joseph Rogers, Institute for Biogerontology Research, and covered recent data suggesting neuroimmune correlates of Alzheimer's disease (AD). These findings span many of the major immune system phenomena, from major histocompatibility complex (MHC) antigens through cytokines and the complement cascade and suggest that some facets of AD pathogenesis may be immune related.

Alzheimer Disease↗
PubMed2005

[Cardiovascular manifestations in rheumatoid arthritis].

Rheumatoid arthritis (RA) is a chronic inflammatory disease, characterized by a polyarticular joint inflammation which eventually leads to joint destruction and general disability. Besides these polyarticular manifestations, several systemic immune phenomena have been described. An increased mortality in RA patients is evident and is mainly caused by an increased cardiovascular risk. The correlation between disease activity and mortality highlighted the important role of the systemic inflammatory reaction in induction and progression of vascular damaging processes. Endothelial dysfunction and vascular inflammation are important, mechanisms in atherosclerosis and induced by conventional risk factors and systemic inflammation. It has been shown that the deleterious influence of conventional risk factors is aggravated by inflammatory mediators, mainly by pro-inflammatory cytokines. In addition, certain inflammatory mediators exert damaging effects to blood vessels. Especially CRP, merely considered as a risk indicating parameter in the past, has attracted remarkable attention. Also certain RA specific immune phenomena are of considerable proatherosclerotic potential. At least in part, they could be responsible for the excess mortality in RA patients. The newer TNFalpha blocking agents interfere with different mechanisms responsible for induction and perpetuation of atherosclerotic processes. Time will show whether they make a remarkable impact on the cardiovascular mortality in RA patients.

Arthritis, Rheumatoid↗