Early intraneuronal amyloid triggers neuron-derived inflammatory signaling in APP transgenic rats and human brain
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Significance: This work provides evidence that soluble and oligomeric amyloid protein stokes neuronal inflammation during the earliest stages of Alzheimer’s disease. Identifying neuron-derived factors that engage the brain’s immune system will provide insight into how vulnerable neurons might interact with other immune cells to propagate cytotoxic signaling cascades and cellular dysfunction during disease development.
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Soluble and oligomeric amyloid protein-burdened neurons exhibit a unique inflammatory profile; this neuron-specific inflammatory response may precede insoluble Aβ plaque and tau tangle formation, implicating intraneuronal Aβ accumulation as a very early event in AD development and suggesting a significant immunological component to AD pathogenesis.
“Recently, Welikovitch et al. found that soluble and oligomeric amyloid protein-burdened neurons exhibited a unique inflammatory profile. This neuron-specific inflammatory response may even precede insoluble Aβ plaque and tau tangle formation, implicating the intraneuronal accumulation of Aβ as a very early event during AD development and suggesting that there is a significant immunological comp”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [47]
Observations of neuron-derived immune signaling at early stages of neurodegenerative disease indicate that this may play a role in disease progression.
“Indeed, observations of neuron‐derived immune signaling at early stages of neurodegenerative disease indicate that this may play a role in disease progression (Dutta et al, 2020; Welikovitch et al, 2020).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Welikovitch et al, 2020
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Proinflammatory effects of M-CSF and Aβ in hippocampal organotypic cultures
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Role of neuroinflammation in neurodegeneration development
Zhang, W., Xiao, D., Mao, Q., & Xia, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01486-5 · Cited by 1,668 · see citing works
“This neuron-specific inflammatory response may even precede insoluble Aβ plaque and tau tangle formation, implicating the intraneuronal accumulation of Aβ as a very early event during AD development and suggesting that there is a significant immunological component to AD pathogenesis.(47) In addition to aggregates, ti…”
BackgroundMechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease
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Microglial large extracellular vesicles propagate early synaptic dysfunction in Alzheimer’s disease
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<scp>mTOR</scp> signaling and Alzheimer's disease: What we know and where we are?
Davoody, S., Asgari Taei, A., Khodabakhsh, P., & Dargahi, L. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14463 · Cited by 96 · see citing works
- Authors
- Welikovitch, L. A., Do Carmo, S., Maglóczky, Z., Malcolm, J. C., Lőke, J., Klein, W. L., Freund, T., & Cuello, A. C.
- Affiliations
- McGill University (CA)
- Department of Pharmacology and Therapeutics, McGill University, Montreal, QC H3G 1Y6, Canada;
- HUN-REN Institute of Experimental Medicine (HU)
- Szent Borbála Kórház (HU)
- Northwestern University (US)
- University of Oxford (GB)
- Corresponding author
- Cuello, A. Claudio
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2020-03-06
- Volume
- 117
- Issue
- 12
- Pages
- 6844-6854
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC7104377
- OpenAlex
- W3009672833
- Cited by
- 116
- References
- 93
- Citations by year
- 2026: 15 · 2025: 15 · 2024: 19 · 2023: 15 · 2022: 20 · 2021: 21 · 2020: 10 · 2019: 1
- FWCI
- 9.92
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Repository of the Academy's Library (Library of the Hungarian Academy of Sciences) (acceptedVersion)
- Funders
- Gouvernement du Canada | Canadian Institutes of Health Research (PJT-364544)
- National Research, Development and Innovation Office (2017-1.2.1-NKP-2017-00002)
- 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, intraneuronal amyloid-beta, neuroinflammation, microglial activation, amyloid-beta oligomers, tau tangles, laser microdissection, human brain
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Brain, Disease Models, Animal, Female, Humans, Inflammation, Male, Neurons, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Rats, Rats, Transgenic, Plaque, Amyloid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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