The DOI matches its Crossref record; 362 of the 362 references it cites were found in a registry or an index.
Neuroinflammatory processes in Alzheimer’s disease
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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“These cells undergo a classical M1 inflammatory activation in response of amyloid deposition, leading to a proinflammatory milieu in the brain (Wyss-Coray, 2006; Heneka et al., 2010).”
From Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease (2012) · cites this paper as Heneka et al., 2010
In the citing paper
“Consequently, age-related immune changes and those that occur during AD share many similarities and the distinction between the two processes remains unclear (89).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [89]
In the citing paper
“In fact, neuroinflammation is closely related to neurodegenerative diseases, as Huntington’s [133], Alzheimer’s [134] and Parkinson’s disease [135] and neuropsychiatric disorders, such as major depressive disorder, bipolar disorder and anxiety [136].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [134]
Citations
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Role of Pro-Inflammatory Cytokines Released from Microglia in Neurodegenerative Diseases
Smith, J. A., Das, A., Ray, S. K., & Banik, N. L. (2012) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2011.10.004 · Cited by 1,165
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Heterogeneity of CNS myeloid cells and their roles in neurodegeneration
Prinz, M., Priller, J., Sisodia, S. S., & Ransohoff, R. M. (2011) · Nature Neuroscience · doi:10.1038/nn.2923 · Cited by 674
Glycogen synthase kinase-3 signaling in Alzheimer’s disease
Lauretti, E., Dincer, O., & Praticò, D. (2020) · Biochimica et biophysica acta. Molecular cell research · doi:10.1016/j.bbamcr.2020.118664 · Cited by 543
Brain metabolic dysfunction at the core of Alzheimer's disease
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Metadata
- 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.
- Venue
- Journal of Neural Transmission
- Published
- 2010-07-15
- Volume
- 117
- Issue
- 8
- Pages
- 919-947
- ISSN
- 0300-9564 (ISSN-L)
- 1435-1463
- 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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