Cited by 43Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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

Xu, Ling-zhi, Li, Bing-qiu, Jia, Jian-ping·2019·Molecular Neurobiology

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.

Integrity signals

Registry

Crossref · 10.1007/s12035-018-1242-2

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • DAPK1 is a calcium-dependent serine/threonine kinase highly expressed in the cortex in Alzheimer's disease, after ischemic damage, and in physiological ageing where it may play a role in the decay of learning and memory.

    “DAPK1 (FC = 1.08, p = 0.05) is a calcium-dependent serine/threonine kinase that is highly expressed in the cortex in AD [167], after ischemic damage [154], and in physiological ageing where it has been suggested to play a role in the decay of learning and memory with age [51].”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Xu, L.-Z., Li, B.-Q., & Jia, J.-P.
Venue
Molecular Neurobiology
Published
2018-07-31
Volume
56
Issue
4
Pages
2838-2844
ISSN
  • 0893-7648 (ISSN-L)
  • 1559-1182
OpenAlex
W2886355973
Cited by
42
References
54
Citations by year
2026: 6 · 2025: 6 · 2024: 5 · 2023: 6 · 2022: 7 · 2021: 4 · 2020: 5 · 2019: 2 · 2018: 1
FWCI
0.39
Type
journal article
Language
en
Open access
closed
Locations
  • Molecular Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Beijing Municipal Natural Science Foundation (7184215)
  • Beijing Talents Foundation (2017000020124G251)
  • Key Project of the National Natural Science Foundation of China (81530036)
  • National Key Scientific Instrument and Equipment Development Project (31627803)
  • Mission Program of Beijing Municipal Administration of Hospitals (SML20150801)
  • Beijing Scholars Program; Beijing Brain Initiative from Beijing Municipal Science & Technology Commission (Z161100000216137)
  • CHINA-CANADA Joint Initiative on Alzheimer’s Disease and Related Disorders (81261120571)
  • Beijing Municipal Commission of Health and Family Planning (PXM2017_026283_000002)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
DAPK1, Alzheimer's disease, genetic risk, neurodegeneration, neuropathology, therapeutic target, neuronal injury
MeSH terms
Alzheimer Disease, Animals, Humans, Risk Factors, Biomarkers, Genetic Predisposition to Disease, Molecular Targeted Therapy, Death-Associated Protein Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review