The NLRP3 and NLRP1 inflammasomes are activated in Alzheimer’s disease
Open accessAbstract
BACKGROUND: Interleukin-1 beta (IL-1β) and its key regulator, the inflammasome, are suspected to play a role in the neuroinflammation observed in Alzheimer's disease (AD); no conclusive data are nevertheless available in AD patients. RESULTS: mRNA for inflammasome components (NLRP1, NLRP3, PYCARD, caspase 1, 5 and 8) and downstream effectors (IL-1β, IL-18) was up-regulated in severe and MILD AD. Monocytes co-expressing NLRP3 with caspase 1 or caspase 8 were significantly increased in severe AD alone, whereas those co-expressing NLRP1 and NLRP3 with PYCARD were augmented in both severe and MILD AD. Activation of the NLRP1 and NLRP3 inflammasomes in AD was confirmed by confocal microscopy proteins co-localization and by the significantly higher amounts of the pro-inflammatory cytokines IL-1β and IL-18 being produced by monocytes. In MCI, the expression of NLRP3, but not the one of PYCARD or caspase 1 was increased, indicating that functional inflammasomes are not assembled in these individuals: this was confirmed by lack of co-localization and of proinflammatory cytokines production. CONCLUSIONS: The activation of at least two different inflammasome complexes explains AD-associated neuroinflammation. Strategies targeting inflammasome activation could be useful in the therapy of AD.
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In monocytes from mildly cognitively impaired individuals, NLRP3 and caspase-1 were not co-localized and IL-18/IL-1β secretion was not detected.
“In these monocytes, NLRP3 and caspase-1 were also not co-localized and IL-18/IL-1β secretion was not detected”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [75]
The Abstract (Results) reports a lack of inflammasome co-localization and pro-inflammatory cytokine production in mild cognitive impairment (MCI). The Results section on cytokine production says IL-1β and IL-18 were not increased in MCI, but does not say their secretion was undetectable. The claim overstates that finding. (LLM, conf=0.87)
Experimental — accuracy not yet measuredEvidence for activation of functional NLRP3 inflammasomes has been detected in early and intermediate stages of Alzheimer's disease from studies of post-mortem brains.
“Evidence for activation of functional NLRP3 inflammasomes has been detected in early and intermediate stages of AD from studies of post-mortem brains.”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [75]
The Results report functional NLRP3 inflammasome activation in patients with moderate and severe Alzheimer’s disease, but not in those with mild cognitive impairment. The Discussion specifies that the analyses used peripheral blood immune cells, not post-mortem brains; the paper therefore does not support the claimed specimen source or activation at the MCI stage. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn monocytes isolated from mildly cognitively impaired individuals, only an increase in NLRP3 levels, but not in ASC or caspase-1, was observed.
“only an increase in NLRP3 levels, but not in ASC or caspase-1, was observed in monocytes isolated from mildly cognitively impaired (MCI) individuals.”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [75]
The NLRP3 inflammasome might not be active at the mildly cognitively impaired stage of Alzheimer's disease.
“suggesting that the NLRP3 inflammasome might not be active at this stage of disease [75, 76].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [75]
Higher expression of NLRP3, ASC, caspase-1, caspase-5, IL-1β, and IL-18 was found in PBMCs of AD patients.
“The higher expression of NLRP3, ASC, caspase-1, caspase-5, IL-1β, and IL-18 was additionally found in the PBMCs of AD patients (224, 226, 227).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [226]
Increased expression and activity of NLRP3 inflammasome machinery in circulating immune cells have been reported in patients with depression, bipolar disorder, and ASD.
“Increased expression and activity of the NLRP3 inflammasome machinery in circulating immune cells of patients affected by depression (245), bipolar disorder (246), and ASD (226), have been reported.”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [226]
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- Authors
- Saresella, M., La Rosa, F., Piancone, F., Zoppis, M., Marventano, I., Calabrese, E., Rainone, V., Nemni, R., Mancuso, R., & Clerici, M.
- Affiliations
- Don Carlo Gnocchi Foundation (IT)
- University of Milan (IT)
- Corresponding author
- Saresella, Marina
- ORCID
- Venue
- Molecular Neurodegeneration
- Published
- 2016-03-03
- Volume
- 11
- Issue
- 1
- Pages
- 23-23
- ISSN
- 1750-1326 (ISSN-L)
- PMC
- PMC4778358
- OpenAlex
- W2291436232
- Cited by
- 489
- References
- 70
- Citations by year
- 2026: 41 · 2025: 36 · 2024: 54 · 2023: 69 · 2022: 56 · 2021: 70 · 2020: 45 · 2019: 37 · 2018: 43 · 2017: 28 · 2016: 10
- FWCI
- 20.45
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Molecular Neurodegeneration (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Funders
- Ministero della Salute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- Alzheimer's disease, NLRP3 inflammasome, NLRP1 inflammasome, neuroinflammation, IL-1β, IL-18, PYCARD, caspase-1, caspase-8, monocytes, mild cognitive impairment, inflammasome activation, inflammatory cytokines
- MeSH terms
- NLR Proteins, NLR Family, Pyrin Domain-Containing 3 Protein, Adult, Alzheimer Disease, Carrier Proteins, Cells, Cultured, Humans, Signal Transduction, Reactive Oxygen Species, Caspase 1, Adaptor Proteins, Signal Transducing, Apoptosis Regulatory Proteins, Interleukin-1beta, Inflammasomes
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