Evidence map›Paper›PMID 26601962›Full record

ReviewCurrent pharmaceutical design2016

Neuroprotective Mechanisms Mediated by CDK5 Inhibition.

Gohar Mushtaq, Nigel H Greig, Firoz Anwar, Fahad A Al-Abbasi, Mazin A Zamzami, Hasan A Al-Talhi, Mohammad A Kamal

Open access · greenAbstract readReview
In one paragraph

Review in Current pharmaceutical design, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 59 citations in OpenAlex.

  1. A patent review of cyclin-dependent kinase 5 (CDK5) inhibitors (1999-2025).Frontiers in bioengineering and biotechnology · 2026
    Review
  2. Article
  3. Controlling donor and newborn neuron migration and maturation in the eye through microenvironment engineering.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Review
  5. Article
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  7. Review
  8. Multitargeting the Action of 5-HTInternational journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Review
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  16. Article
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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

7 authors at 2 institutions in 2 countries.

Gohar MushtaqDepartment of Biochemistry, College of Science, King Abdulaziz University, Jeddah 21589, Saudi Arabia. gmushtaq2001@gmail.com.
Nigel H GreigDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National, Institute on Aging, National Institutes of Health, Biomedical Research Center, 251 Bayview Boulevard, Baltimore, MD 21224, USA. greign@grc.nia.nih.gov.
Firoz Anwar
Fahad A Al-Abbasi
Mazin A Zamzami
Hasan A Al-Talhi
Mohammad A Kamal
King Abdulaziz University · SANational Institutes of Health · US

Funding

Design And Development Of Experimental Therapeutics ((Systemic & Neurodegenerative Disorders and Alzheimer's Disease)ZIAAG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$16.0M
Intramural NIH HHS ZIA AG000311
6 · The paper itself

Abstract

Cyclin-dependent kinase 5 (CDK5) is a proline-directed serine/threonine kinase belonging to the family of cyclin-dependent kinases. In addition to maintaining the neuronal architecture, CDK5 plays an important role in the regulation of synaptic plasticity, neurotransmitter release, neuron migration and neurite outgrowth. Although various reports have shown links between neurodegeneration and deregulation of cyclin-dependent kinases, the specific role of CDK5 inhibition in causing neuroprotection in cases of neuronal insult or in neurodegenerative diseases is not wellunderstood. This article discusses current evidence for the involvement of CDK5 deregulation in neurodegenerative disorders and neurodegeneration associated with stroke through various mechanisms. These include upregulation of cyclin D1 and overactivation of CDK5 mediated neuronal cell death pathways, aberrant hyperphosphorylation of human tau proteins and/or neurofilament proteins, formation of neurofibrillary lesions, excitotoxicity, cytoskeletal disruption, motor neuron death (due to abnormally high levels of CDK5/p25) and colchicine- induced apoptosis in cerebellar granule neurons. A better understanding of the role of CDK5 inhibition in neuroprotective mechanisms will help scientists and researchers to develop selective, safe and efficacious pharmacological inhibitors of CDK5 for therapeutic use against human neurodegenerative disorders, such as Alzheimer's disease, amyotrophic lateral sclerosis and neuronal loss associated with stroke.

Indexed as

Alzheimer DiseaseAnimalsBrain IschemiaCyclin-Dependent Kinase 5HumansNeuroprotective AgentsStrokeCyclin-Dependent Kinase 5Neuroprotective Agents

Identifiers

PMID26601962
PMCPMC5002348
OpenAlexW2176746291

What OpenQuestion holds

Textmetadata
LicenceTDM
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.