Evidence map›Paper›PMID 30062675›Full record

ReviewMolecular neurobiology2019

DAPK1: a Novel Pathology and Treatment Target for Alzheimer's Disease.

Ling-Zhi Xu, Bing-Qiu Li, Jian-Ping Jia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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  8. Current neuropharmacology · 2024
    Article
  9. Review
  10. Pin1 and Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023
    Review
  11. Article
  12. Review
  13. Review
  14. Article
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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

3 authors at 2 institutions in 1 country.

Ling-Zhi XuInnovation Center for Neurological Disorders, Department of Neurology, Xuan Wu Hospital, Capital Medical University, Beijing, People's Republic of China.
Bing-Qiu LiInnovation Center for Neurological Disorders, Department of Neurology, Xuan Wu Hospital, Capital Medical University, Beijing, People's Republic of China.
Jian-Ping JiaInnovation Center for Neurological Disorders, Department of Neurology, Xuan Wu Hospital, Capital Medical University, Beijing, People's Republic of China. jiajp@vip.126.com.ORCID http://orcid.org/0000-0002-1829-7776
Ministry of Education of the People's Republic of China · CNCapital Medical University · CN

Funding

Beijing Municipal Commission of Health and Family Planning PXM2017_026283_000002Beijing Municipal Natural Science Foundation 7184215Beijing Scholars Program; Beijing Brain Initiative from Beijing Municipal Science & Technology Commission Z161100000216137Beijing Talents Foundation 2017000020124G251CHINA-CANADA Joint Initiative on Alzheimer's Disease and Related Disorders 81261120571Key Project of the National Natural Science Foundation of China 81530036Mission Program of Beijing Municipal Administration of Hospitals SML20150801National Key Scientific Instrument and Equipment Development Project 31627803
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease and seriously damages the health of elderly population. Clinical drug research targeting at classic pathology hallmarks, such as amyloid-β (Aβ) and tau protein, failed to achieve effective cognitive improvement, suggesting that the pathogenesis of AD is much complicated, and there are still other unknown and undetermined important factors. Death-associated protein kinase 1 (DAPK1) is a calcium/calmodulin-dependent serine/threonine kinase that plays an important role in various neuronal injury models. Mounting evidence has demonstrated that DAPK1 variants are associated with AD risk. The activation of DAPK1 is also involved in AD-related neurodegeneration in the brain. Exploring the roles of DAPK1 in AD might help us understand the pathogenic mechanisms and find a novel promising therapeutic target in AD. Therefore, in this review, we comprehensively summary the main progress of DAPK1 in the AD studies from genetic risk, neuropathological process, and clinical potential implications.

Indexed as

Molecular Targeted TherapyAlzheimer DiseaseAnimalsBiomarkersDeath-Associated Protein KinasesGenetic Predisposition to DiseaseHumansRisk FactorsBiomarkersDeath-Associated Protein KinasesAlzheimer’s diseaseDeath-associated protein kinase 1NeuropathologyTherapeuticsVariants

Identifiers

PMID30062675
OpenAlexW2886355973

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.