TY - JOUR
T1 - Amyloid β-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain exists
AU - Butterfield, D. Allan
AU - Griffin, Sue
AU - Munch, Gerald
AU - Pasinetti, Giulio Maria
PY - 2002/6
Y1 - 2002/6
N2 - Alzheimer's disease (AD) brain is characterized by excess deposition of amyloid β-peptide (Aβ), particularly the 42-amino acid peptide [Aβ(1-42)] and by extensive oxidative stress. Several sources of the oxidative stress and inflammatory cascades are likely, including that induced by advanced glycation end products, microglial activation, and by Aβ(1-42) and its sequelae. This review briefly examines each of these sources of oxidative stress and inflammation in AD brain and discusses their potential roles in the clinical progression of AD dementia.
AB - Alzheimer's disease (AD) brain is characterized by excess deposition of amyloid β-peptide (Aβ), particularly the 42-amino acid peptide [Aβ(1-42)] and by extensive oxidative stress. Several sources of the oxidative stress and inflammatory cascades are likely, including that induced by advanced glycation end products, microglial activation, and by Aβ(1-42) and its sequelae. This review briefly examines each of these sources of oxidative stress and inflammation in AD brain and discusses their potential roles in the clinical progression of AD dementia.
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U2 - 10.3233/JAD-2002-4309
DO - 10.3233/JAD-2002-4309
M3 - Review article
C2 - 12226538
AN - SCOPUS:0036592636
SN - 1387-2877
VL - 4
SP - 193
EP - 201
JO - Journal of Alzheimer's Disease
JF - Journal of Alzheimer's Disease
IS - 3
ER -