Cited by 782Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Inflammatory processes in Alzheimer's disease

Heneka, Michael T., O'Banion, M. Kerry·2007·Journal of Neuroimmunology

Abstract

Generation and deposition of amyloid beta peptides and neurofibrillary tangle formation are key mechanisms involved in AD pathogenesis. Recent evidence suggests that inflammatory mechanisms represent a third component which, once initiated by degeneration, may significantly contribute to disease progression and chronicity. Various neuroinflammatory mediators including complement activators and inhibitors, chemokines, cytokines, radical oxygen species and inflammatory enzymes are generated and released by microglia, astrocytes and neurons. Degeneration of aminergic brain stem nuclei such as the locus ceruleus and the nucleus baslis of Meynert may facilitate the occurrence of inflammation in their respective projection areas given the antiinflammatory and neuroprotective action of their key products norepinephrine and acetylcholine. While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate APP processing by upregulation of beta secretase 1 and therefore are able to establish a vicious cycle. Despite the fact that some aspects of inflammation may even exert protective effects to bystander neurons, antiinflammatory treatment strategies should therefore be considered. Non-steroidal antiinflammatory drugs have been shown to reduce the risk and delay the onset to develop AD. However, the precise molecular mechanism underlying this effect is still being debated. Several mechanisms including inhibi…

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Crossref · 10.1016/j.jneuroim.2006.11.017

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  • Innate immune function and brain cholesterol metabolism have a role in Alzheimer's disease.

    “Ample evidence suggests a role for innate immune function and brain cholesterol metabolism in Alzheimer's disease (AD) (Mulder and Terwel, 1998;Heneka and O'Banion, 2007).”
  • Inflammatory mechanisms represent an important component which first contribute to defence mechanisms but secondly, stimulated by degeneration, may significantly contribute to disease progression and chronicity.

    “Finally, inflammatory mechanisms represent an important component which, first contribute to defence mechanisms but secondly, stimulated by degeneration, may significantly contribute to disease progression and chronicity [15, 150, 151].”

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Authors
Heneka, M. T., & O'Banion, M. K.
Affiliations
University of Münster (DE)
Venue
Journal of Neuroimmunology
Publisher
Elsevier BV
Published
2007-03
Volume
184
Issue
1-2
Pages
69-91
ISSN
0165-5728 (ISSN-L)
OpenAlex
W1993993136
Cited by
782
References
34
Citations by year
2026: 7 · 2025: 13 · 2024: 20 · 2023: 26 · 2022: 27 · 2021: 36 · 2020: 26 · 2019: 32 · 2018: 45 · 2017: 41 · 2016: 48 · 2015: 51 · 2014: 57 · 2013: 47 · 2012: 59
FWCI
6.53
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neuroimmunology (publishedVersion)
  • PubMed (publishedVersion)
  • Open Repository and Bibliography (University of Luxembourg) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, neuroinflammation, amyloid-beta, neurofibrillary tangles, microglia, astrocytes, complement system, chemokines, cytokines, reactive oxygen species, locus coeruleus, nucleus basalis of Meynert, norepinephrine, acetylcholine, APP processing, beta-secretase 1, nonsteroidal anti-inflammatory drugs, cyclooxygenase-2, gamma-secretase, PPARγ
MeSH terms
Alzheimer Disease, Animals, Anti-Inflammatory Agents, Humans, Inflammation, Neuroglia, Neurons, Apoptosis, Inflammation Mediators

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