ReviewMolecular neurobiology2015
ATF4: a Novel Potential Therapeutic Target for Alzheimer's Disease.
Review in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- The mRNA Expression Levels of General Transcription Factors Altered in Alzheimer Cases Possibly Due to Amyloid Beta 1-42 Exposure.Noro psikiyatri arsivi · 2026Article
- The dual role of ATF4 in neurons: from stress adaptation to therapeutic intervention.Frontiers in molecular neuroscience · 2026Review
- Epigenetic Mechanisms Shaping Spine Regulation: Unveiling the Role of Cytoskeletal Dynamics and Localized Protein Synthesis.Molecular neurobiology · 2025Review
- NADCell death & disease · 2024Article
- pyPAGE: A framework for Addressing biases in gene-set enrichment analysis-A case study on Alzheimer's disease.PLoS computational biology · 2024Article
- ATF4 inhibits tumor development and mediates p-GCN2/ASNS upregulation in colon cancer.Scientific reports · 2024Article
- Induction of proteasomal activity in mammalian cells by lifespan-extending tRNA synthetase inhibitors.GeroScience · 2024Article
- Overexpression of ATF4 Inhibits Ferroptosis to Alleviate Anxiety Disorders by Activating the TGF-β Signaling Pathway.Neuropsychiatric disease and treatment · 2024Article
- Soluble and insoluble protein aggregates, endoplasmic reticulum stress, and vascular dysfunction in Alzheimer's disease and cardiovascular diseases.GeroScience · 2023Review
- Intestinal activating transcription factor 4 regulates stress-related behavioral alterations via paraventricular thalamus in male mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Leucine deprivation results in antidepressant effects via GCN2 in AgRP neurons.Life metabolism · 2023Article
- The expression pattern of GDF15 in human brain changes during aging and in Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Adipose-derived stem cells (ADSCs) inhibit the expression of anti-apoptosis proteins through up-regulation of ATF4 on breast cancer cells.Annals of translational medicine · 2021Article
- Pathogenesis and promising therapeutics of Alzheimer disease through eIF2α pathway and correspondent kinases.Metabolic brain disease · 2020Review
- Epigallocatechin-3-Gallate (EGCG) Improves Cognitive Deficits Aggravated by an Obesogenic Diet Through Modulation of Unfolded Protein Response in APPswe/PS1dE9 Mice.Molecular neurobiology · 2020Article
- Identification of Temporal Characteristic Networks of Peripheral Blood Changes in Alzheimer's Disease Based on Weighted Gene Co-expression Network Analysis.Frontiers in aging neuroscience · 2019Article
- Integrated Stress Responses to Bacterial Pathogenesis Patterns.Frontiers in immunology · 2018Review
- Endoplasmic reticulum proteostasis impairment in aging.Aging cell · 2017Review
- Neurodegeneration: Keeping ATF4 on a Tight Leash.Frontiers in cellular neuroscience · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activating transcription factor 4 (ATF4) belongs to the activating transcription factor family and its expression is increased upon the stimulation of a diverse array of microenvironmental stresses. ATF4 plays a major role in the development, metabolism, and memory formation. Alzheimer's disease (AD) is a prevalent neurodegenerative disease in aged population. The dominant pathological changes in AD brain, including the neurofibrillary tangles, consist of hyperphosphorylated tau protein, senile plaques composed of β-amyloid proteins, loss of neurons in the whole brain, and dysfunction of synapses. The protein level of ATF4 is upregulated in both AD brain and AD mouse model, indicating its latent roles in the pathogenesis of this disease. In this paper, we reviewed the related literatures about the interaction of ATF4 with the different types of pathological changes in AD brain and pointed out some unsolved problems in this area. We also proposed that a fine regulation of ATF4 in separate neurons or brain regions might be benefit to the therapy of AD.
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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.