Evidence map›Paper›PMID 35246032›Full record

ReviewBMC neuroscience2022

Calmodulin binding proteins and neuroinflammation in multiple neurodegenerative diseases.

Danton H O'Day, Robert J Huber

Open access · goldAbstract readReview
In one paragraph

Review in BMC neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. The soluble state of the HIV-1 Vpu protein forms a complex with CaProtein science : a publication of the Protein Society · 2026
    Article
  7. Targeting TMEM175 in Lysosomal Physiology and Human Diseases.Current stem cell research & therapy · 2026
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. What We Know About TMEM175 in Parkinson's Disease.CNS neuroscience & therapeutics · 2025
    Review
  15. Role of Calmodulin in Neurodegeneration and Neuroprotection.Mini reviews in medicinal chemistry · 2025
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. OsCAMTA3 Negatively Regulates Disease Resistance toInternational journal of molecular sciences · 2024
    Article
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

2 authors at 2 institutions in 1 country.

Danton H O'DayCell and Systems Biology, University of Toronto, Toronto, ON, M5S 3G5, Canada.
Robert J HuberDepartment of Biology, Trent University, 1600 West Bank Drive, Peterborough, ON, K9L 0G2, Canada. roberthuber@trentu.ca.ORCID 0000-0003-2606-6983
Trent University · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium dysregulation ("Calcium Hypothesis") is an early and critical event in Alzheimer's and other neurodegenerative diseases. Calcium binds to and regulates the small regulatory protein calmodulin that in turn binds to and regulates several hundred calmodulin binding proteins. Initial and continued research has shown that many calmodulin binding proteins mediate multiple events during the onset and progression of Alzheimer's disease, thus establishing the "Calmodulin Hypothesis". To gain insight into the general applicability of this hypothesis, the involvement of calmodulin in neuroinflammation in Alzheimer's, amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease, frontotemporal dementia, and other dementias was explored. After a literature search for calmodulin binding, 11 different neuroinflammatory proteins (TREM2, CD33, PILRA, CR1, MS4A, CLU, ABCA7, EPHA1, ABCA1, CH3L1/YKL-40 and NLRP3) were scanned for calmodulin binding domains using the Calmodulin Target Database. This analysis revealed the presence of at least one binding domain within which visual scanning demonstrated the presence of valid binding motifs. Coupled with previous research that identified 13 other neuroinflammation linked proteins (BACE1, BIN1, CaMKII, PP2B, PMCA, NOS, NMDAR, AchR, Ado A2AR, Aβ, APOE, SNCA, TMEM175), this work shows that at least 24 critical proteins involved in neuroinflammation are putative or proven calmodulin binding proteins. Many of these proteins are linked to multiple neurodegenerative diseases indicating that calmodulin binding proteins lie at the heart of neuroinflammatory events associated with multiple neurodegenerative diseases. Since many calmodulin-based pharmaceuticals have been successfully used to treat Huntington's and other neurodegenerative diseases, these findings argue for their immediate therapeutic implementation.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesCalciumCalmodulinCalmodulin-Binding ProteinsHumansNeuroinflammatory DiseasesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesCalciumCalmodulinCalmodulin-Binding ProteinsCalciumCalmodulin binding domainsCalmodulin binding proteinsIQ motifsNeurodegenerationNeuroinflammation

Identifiers

PMID35246032
PMCPMC8896083
OpenAlexW4214876699

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.