Amyloid β-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain exists

D. Allan Butterfield, Sue Griffin, Gerald Munch, Giulio Maria Pasinetti

Research output: Contribution to journalReview articlepeer-review

135 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)193-201
Number of pages9
JournalJournal of Alzheimer's Disease
Volume4
Issue number3
DOIs
StatePublished - Jun 2002

ASJC Scopus subject areas

  • Neuroscience (all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

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