ArticleAutophagy2016
Targeting neuronal MAPK14/p38α activity to modulate autophagy in the Alzheimer disease brain.
Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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.
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Who cites it
27 citing papers in PubMed, 59 citations in OpenAlex.
- Preclinical and randomized clinical evaluation of the p38α kinase inhibitor neflamapimod for basal forebrain cholinergic degeneration.Nature communications · 2022Trial
- Integration of network pharmacology, molecular docking, and molecular dynamics simulation to elucidate the mechanism of Psychotria rubra in depression treatment.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026Article
- DNAJB6a deficiency induces tau pathology through IRE1α-Xbp1-induced mitochondria dysfunction.Zoological research · 2026Article
- Single-cell sequencing-based study of ferroptosis mechanisms in heat stroke: identification of key biomarkers and dynamic analysis of the immune microenvironment.BMC medical genomics · 2025Article
- Proteome-wide association studies using summary pQTL data of brain, CSF, and plasma identify 30 risk genes of Alzheimer's disease dementia.Alzheimer's research & therapy · 2025Article
- Correlation of autophagy and Alzheimer's disease with special emphasis on the role of phosphodiesterase-4.3 Biotech · 2025Review
- Article
- Potential association between COVID-19 and neurological disorders: analysis of common genes and therapeutics.Frontiers in neurology · 2024Article
- RNA-binding deficient TDP-43 drives cognitive decline in a mouse model of TDP-43 proteinopathy.eLife · 2023Article
- Article
- Exploring the key ferroptosis-related gene in the peripheral blood of patients with Alzheimer's disease and its clinical significance.Frontiers in aging neuroscience · 2022Article
- Article
- Understanding Abnormal c-JNK/p38MAPK Signaling Overactivation Involved in the Progression of Multiple Sclerosis: Possible Therapeutic Targets and Impact on Neurodegenerative Diseases.Neurotoxicity research · 2021Review
- Activation of CREB-mediated autophagy by thioperamide ameliorates β-amyloid pathology and cognition in Alzheimer's disease.Aging cell · 2021Article
- Identification of Potential Biomarkers of Depression and Network Pharmacology Approach to Investigate the Mechanism of Key Genes and Therapeutic Traditional Chinese Medicine in the Treatment of Depression.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Icariin, an Up-and-Coming Bioactive Compound Against Neurological Diseases: Network Pharmacology-Based Study and Literature Review.Drug design, development and therapy · 2021Review
- P38α MAPK Signaling-A Robust Therapeutic Target for Rab5-Mediated Neurodegenerative Disease.International journal of molecular sciences · 2020Review
- In Vivo Chimeric Alzheimer's Disease Modeling of Apolipoprotein E4 Toxicity in Human Neurons.Cell reports · 2020Article
- Article
- Functions of p38 MAP Kinases in the Central Nervous System.Frontiers in molecular neuroscience · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated autophagic-lysosomal degradation of proteins has been linked to the most common genetic defect in familial Alzheimer disease, and has been correlated with disease progression in both human disease and in animal models. Recently, it was demonstrated that the expression of MAPK14/p38α protein is upregulated in the brain of APP-PS1 transgenic Alzheimer mouse and further that genetic deficiency of Mapk14 in the APP-PS1 mouse stimulates macroautophagy/autophagy, which then leads to reduced amyloid pathology via increasing autophagic-lysosomal degradation of BACE1. The findings resolve at least in the context of the APP-PS1 mouse, prior conflicting in vitro observations that have implicated MAPK14 in autophagic processes, and indicate that inhibition of MAPK14 enzyme activity has potential as a therapeutic approach to mitigate a critical physiological defect within neurons of the Alzheimer disease brain. Moreover, the findings suggest that biomarkers of BACE1 activity could be utilized to evaluate the effects of MAPK14 inhibition and other autophagy-inducing therapeutic approaches in human clinical studies, thereby potentially facilitating the clinical development of such agents.
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What OpenQuestion holds
Registered trials
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.