Evidence map›Paper›PMID 22675649›Full record

ArticleInternational journal of Alzheimer's disease2012

Microglial KCa3.1 Channels as a Potential Therapeutic Target for Alzheimer's Disease.

Izumi Maezawa, David Paul Jenkins, Benjamin E Jin, Heike Wulff

Open access · hybridAbstract read
In one paragraph

Article in International journal of Alzheimer's disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Repurposing the KTranslational stroke research · 2024
    Article
  6. Peripheral Administration of the Kv1.3-Blocking Peptide HsTX1[R14A] Improves Cognitive Performance in Senescence Accelerated SAMP8 Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  7. Review
  8. Article
  9. Functional Potassium Channels in Macrophages.The Journal of membrane biology · 2023
    Review
  10. Imaging of KChemMedChem · 2023
    Article
  11. Review
  12. Article
  13. Frontiers in cellular neuroscience · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Izumi MaezawaDepartment of Pathology and Laboratory Medicine, University of California Davis, Davis, CA 95616, USA.
David Paul Jenkins
Benjamin E Jin
Heike Wulff
University of California, Davis · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
The microglial potassium channels Kv1.3 and KCa3.1 as therapeutic targets for neuR01GM076063 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI WULFF, HEIKE · 2006 to 2014
$2.5M
NIA NIH HHS P30 AG010129NIGMS NIH HHS R01 GM076063
6 · The paper itself

Abstract

There exists an urgent need for new target discovery to treat Alzheimer's disease (AD); however, recent clinical trials based on anti-Aβ and anti-inflammatory strategies have yielded disappointing results. To expedite new drug discovery, we propose reposition targets which have been previously pursued by both industry and academia for indications other than AD. One such target is the calcium-activated potassium channel KCa3.1 (KCNN4), which in the brain is primarily expressed in microglia and is significantly upregulated when microglia are activated. We here review the existing evidence supporting that KCa3.1 inhibition could block microglial neurotoxicity without affecting their neuroprotective phagocytosis activity and without being broadly immunosuppressive. The anti-inflammatory and neuroprotective effects of KCa3.1 blockade would be suitable for treating AD as well as cerebrovascular and traumatic brain injuries, two well-known risk factors contributing to the dementia in AD patients presenting with mixed pathologies. Importantly, the pharmacokinetics and pharmacodynamics of several KCa3.1 blockers are well known, and a KCa3.1 blocker has been proven safe in clinical trials. It is therefore promising to reposition old or new KCa3.1 blockers for AD preclinical and clinical trials.

Identifiers

PMID22675649
PMCPMC3364551
OpenAlexW2133747504

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.