Evidence map›Paper›PMID 35066762›Full record

ReviewMolecular neurobiology2022

Inflammasome Signaling in the Aging Brain and Age-Related Neurodegenerative Diseases.

Subhashini Brahadeeswaran, Narmadhaa Sivagurunathan, Latchoumycandane Calivarathan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Potential Role of Inflammasomes in Aging.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Inflammaging and Brain Aging.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Molecular hallmarks of ageing in amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Subhashini Brahadeeswaran *Molecular Pharmacology and Toxicology Laboratory, Department of Life Sciences, School of Life Sciences, Central University of Tamil Nadu, Neelakudi Campus, Thiruvarur, Tamil Nadu, 610005, India.
Narmadhaa Sivagurunathan *Molecular Pharmacology and Toxicology Laboratory, Department of Life Sciences, School of Life Sciences, Central University of Tamil Nadu, Neelakudi Campus, Thiruvarur, Tamil Nadu, 610005, India.
Latchoumycandane CalivarathanMolecular Pharmacology and Toxicology Laboratory, Department of Life Sciences, School of Life Sciences, Central University of Tamil Nadu, Neelakudi Campus, Thiruvarur, Tamil Nadu, 610005, India. latchoumycandane@cutn.ac.in.ORCID http://orcid.org/0000-0002-6637-369X
Central University of Tamil Nadu · IN

Funding

Science and Engineering Research Board JRF
6 · The paper itself

Abstract

Inflammasomes are intracellular protein complexes, members of the innate immune system, and their activation and regulation play an essential role in maintaining homeostatic conditions against exogenous and endogenous stimuli. Inflammasomes occur as cytosolic proteins and assemble into a complex during the recognition of pathogen-associated or danger-associated molecular patterns by pattern-recognition receptors in host cells. The formation of the inflammasome complex elicits signaling molecules of proinflammatory cytokines such as interleukin-1β and interleukin 18 via activation of caspase-1 in the canonical inflammasome pathway whereas caspase-11 in the case of a mouse and caspase-4 and caspase-5 in the case of humans in the non-canonical inflammasome pathway, resulting in pyroptotic or inflammatory cell death which ultimately leads to neuroinflammation and neurodegenerative diseases. Inflammasome activation, particularly in microglial cells and macrophages, has been linked to aging as well as age-related neurodegenerative diseases. The accumulation of abnormal/ misfolded proteins acts as a ligand for inflammasome activation in neurodegenerative diseases. Although recent studies have revealed the inflammasomes' functionality in both in vitro and in vivo models, many inflammasome signaling cascade activations during biological aging, neuroinflammation, and neurodegeneration are still ambiguous. In this review, we comprehensively unveil the cellular and molecular mechanisms of inflammasome activation during neuronal aging and age-related neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, prion disease, and amyotrophic lateral sclerosis.

Indexed as

InflammasomesNeurodegenerative DiseasesAgingAnimalsBrainCaspasesMacrophagesMiceNLR Family, Pyrin Domain-Containing 3 ProteinCaspasesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAgingCaspase-1InflammagingInflammasomeNeurodegenerationNeuroinflammation

Identifiers

PMID35066762
OpenAlexW4206948692

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.