Inflammation and Alzheimer's disease: relationships between pathogenic mechanisms and clinical expression.
During the past 15 years a variety of inflammatory proteins has been identified in the brains of patients with Alzheimer's disease (AD) postmortem. There is now considerable evidence that in AD the deposition of amyloid-beta (A beta) protein precedes a cascade of events that ultimately leads to a local "brain inflammatory response." Here we reviewed the evidence (i) that inflammatory mechanisms can be a part of the relevant etiological factors for AD in patients with head trauma, ischemia, and Down's syndrome; (ii) that in cerebral A beta disorders the clinical symptoms are determined to a great extent by the site of inflammation; and (iii) that a brain inflammatory response can explain some poorly understood characteristics of the clinical picture, among others the susceptibility of AD patients to delirium. The present data indicate that inflammatory processes in the brain contribute to the etiology, the pathogenesis, and the clinical expression of AD.
Eikelenboom
P
P
Department of Psychiatry, Graduate School Neurosciences Amsterdam, Vrije Universiteit, Valeriuskliniek, The Netherlands.
Rozemuller
J M
JM
van Muiswinkel
F L
FL
D000209:Acute-Phase Proteins / Q000378:metabolism; D000544:Alzheimer Disease / Q000150:complications / Q000276:immunology* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D006259:Craniocerebral Trauma / Q000150:complications; D003693:Delirium / Q000150:complications; D004314:Down Syndrome / Q000150:complications / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism
D000209:Acute-Phase Proteins; D016229:Amyloid beta-Peptides; D018836:Inflammation Mediators