Evidence map›Paper›PMID 38195518›Full record

ReviewTranslational neurodegeneration2024

Death-associated protein kinase 1 as a therapeutic target for Alzheimer's disease.

Tao Zhang, Byeong Mo Kim, Tae Ho Lee

Open access · goldAbstract readReview
In one paragraph

Review in Translational neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  14. Epigenetic Regulation of DAPK1 and Netrin-1 Drives Diabetic Encephalopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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 2 countries.

Tao ZhangFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, Institute of Basic Medicine, School of Basic Medical Sciences, Fujian Medical University, 1 Xuefu North Road, Fuzhou, 350122, Fujian, China.
Byeong Mo KimResearch Center for New Drug Development, AgingTarget Inc., 10F Ace Cheonggye Tower, 53, Seonggogae-Ro, Uiwang-Si, 16006, Gyeonggi-Do, Korea. bmkim@agingtarget.com.
Tae Ho LeeFujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, Institute of Basic Medicine, School of Basic Medical Sciences, Fujian Medical University, 1 Xuefu North Road, Fuzhou, 350122, Fujian, China. tlee0813@fjmu.edu.cn.ORCID 0000-0001-5968-1478
Fujian Medical University · CNInstitute of Aging · CA

Funding

National Natural Science Foundation of China 81970993National Natural Science Foundation of China 82001128National Natural Science Foundation of China 82271449Natural Science Foundation of Fujian Province 2021J01672
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent form of dementia in the elderly and represents a major clinical challenge in the ageing society. Neuropathological hallmarks of AD include neurofibrillary tangles composed of hyperphosphorylated tau, senile plaques derived from the deposition of amyloid-β (Aβ) peptides, brain atrophy induced by neuronal loss, and synaptic dysfunctions. Death-associated protein kinase 1 (DAPK1) is ubiquitously expressed in the central nervous system. Dysregulation of DAPK1 has been shown to contribute to various neurological diseases including AD, ischemic stroke and Parkinson's disease (PD). We have established an upstream effect of DAPK1 on Aβ and tau pathologies and neuronal apoptosis through kinase-mediated protein phosphorylation, supporting a causal role of DAPK1 in the pathophysiology of AD. In this review, we summarize current knowledge about how DAPK1 is involved in various AD pathological changes including tau hyperphosphorylation, Aβ deposition, neuronal cell death and synaptic degeneration. The underlying molecular mechanisms of DAPK1 dysregulation in AD are discussed. We also review the recent progress regarding the development of novel DAPK1 modulators and their potential applications in AD intervention. These findings substantiate DAPK1 as a novel therapeutic target for the development of multifunctional disease-modifying treatments for AD and other neurological disorders.

Indexed as

Alzheimer DiseaseAgedAmyloid beta-PeptidesCentral Nervous SystemDeath-Associated Protein KinasesHumansNeurofibrillary TanglesAmyloid beta-PeptidesDeath-Associated Protein KinasesAlzheimer’s diseaseAmyloid-βDeath-associated protein kinase 1Neuronal cell deathTauTherapeutic target

Identifiers

PMID38195518
PMCPMC10775678
OpenAlexW4390725672

What OpenQuestion holds

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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.