TY - JOUR
T1 - Inflammation and Alzheimer's disease
T2 - Relationships between pathogenic mechanisms and clinical expression
AU - Eikelenboom, P.
AU - Rozemuller, J. M.
AU - Van Muiswinkel, F. L.
PY - 1998/1/1
Y1 - 1998/1/1
N2 - 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-β (Aβ) 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 Aβ 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.
AB - 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-β (Aβ) 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 Aβ 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.
KW - Activated microglia
KW - Acute phase response
KW - Alzheimer's disease
KW - Delirium
KW - Down's syndrome
UR - http://www.scopus.com/inward/record.url?scp=0032213445&partnerID=8YFLogxK
U2 - https://doi.org/10.1006/exnr.1998.6920
DO - https://doi.org/10.1006/exnr.1998.6920
M3 - Article
C2 - 9875271
SN - 0014-4886
VL - 154
SP - 89
EP - 98
JO - Experimental neurology
JF - Experimental neurology
IS - 1
ER -