Cited by 433Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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Neuroinflammatory processes in Alzheimer’s disease

Heneka, Michael T., O’Banion, M. Kerry, Terwel, Dick, Kummer, Markus Peter·2010·Journal of Neural Transmission

DOI 10.1007/s00702-010-0438-z

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Abstract

Generation of neurotoxic amyloid beta peptides and their deposition along with neurofibrillary tangle formation represent key pathological hallmarks in Alzheimer's disease (AD). Recent evidence suggests that inflammation may be a third important component which, once initiated in response to neurodegeneration or dysfunction, may actively contribute to disease progression and chronicity. Various neuroinflammatory mediators including complement activators and inhibitors, chemokines, cytokines, radical oxygen species and inflammatory enzyme systems are expressed and released by microglia, astrocytes and neurons in the AD brain. Degeneration of aminergic brain stem nuclei including the locus ceruleus and the nucleus basalis of Meynert may facilitate the occurrence of inflammation in their projection areas given the antiinflammatory and neuroprotective action of their key transmitters norepinephrine and acetylcholine. While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate amyloid precursor protein processing by various means and therefore can establish a vicious cycle. Despite the fact that some aspects of inflammation may even be protective for bystander neurons, antiinflammatory treatment strategies should therefore be considered. Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD. While, the precise molecular mechanism underlying this effect is still unknown, a number of possible mechanisms including cyclooxygenase 2 or gamma-secretase inhibition and activation of the peroxisome proliferator activated receptor gamma may alone or, more likely, in concert account for the epidemiologically observed protection.

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Authors: Heneka, M. T., O’Banion, M. K., Terwel, D., & Kummer, M. P.
Affiliations: University of Bonn (DE)
University of Rochester Medicine (US)
Corresponding author: Heneka, Michael T.
ORCID: Heneka, Michael T.
O’Banion, M. Kerry
Terwel, Dick
Kummer, Markus Peter
Venue: Journal of Neural Transmission
Publisher: Springer Science and Business Media LLC
Published: 2010-07-15
Volume: 117
Issue: 8
Pages: 919-947
ISSN: 0300-9564 (ISSN-L)
1435-1463
DOI: 10.1007/s00702-010-0438-z
OpenAlex: W2085262263
Cited by: 433
References: 362
Citations by year: 2026: 4 · 2025: 10 · 2024: 21 · 2023: 20 · 2022: 17 · 2021: 33 · 2020: 28 · 2019: 22 · 2018: 39 · 2017: 29 · 2016: 31 · 2015: 36 · 2014: 38 · 2013: 41 · 2012: 38
FWCI: 3.38
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Journal of Neural Transmission (publishedVersion)
PubMed (publishedVersion)
Open Repository and Bibliography (University of Luxembourg) (submittedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, nonsteroidal anti-inflammatory drugs, cyclooxygenase-2, gamma-secretase inhibition, PPARγ, neuroprotection
MeSH terms: Alzheimer Disease, Animals, Brain, Humans, Inflammation, Cytokines, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Neurofibrillary Tangles, Inflammation Mediators, Cyclooxygenase 2, Chromogranin A

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