ArticleeNeuro
Amyloid Precursor Protein (APP) Controls the Expression of the Transcriptional Activator Neuronal PAS Domain Protein 4 (NPAS4) and Synaptic GABA Release.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Npas4 is involved in synaptic and cognitive function by regulating the transcription of Neuroligin-1 and N-cadherin.Translational psychiatry · 2026Article
- 5-Hydroxymethylcytosine profiles in circulating cell-free DNA serve as potential biomarkers for diagnosis and classification of adenomyosis.EBioMedicine · 2026Article
- 10H-phenothiazine exerts beneficial effects in spinal muscular atrophy in vitro and in vivo models.Scientific reports · 2025Article
- Single-Cell Multi-Modal Differential Analysis of the Human Neo-Cortex in HIV Infection Reveals Similarities with Hallmarks of Alzheimer's Disease.Research square · 2025Article
- Neuronal activity-dependent gene dysregulation inAmerican journal of physiology. Cell physiology · 2025Article
- Developmental deletion of amyloid precursor protein precludes transcriptional and proteomic responses to brain injury.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Review
- The AICD interactome: implications in neurodevelopment and neurodegeneration.Biochemical Society transactions · 2024Review
- Article
- Brain Iron Dyshomeostasis and Ferroptosis in Alzheimer's Disease Pathophysiology: Two Faces of the Same Coin.Aging and disease · 2024Review
- Biochemical characterization on muscle tissue of a novel biallelicJIMD reports · 2024Article
- Downregulated NPAS4 in multiple brain regions is associated with major depressive disorder.Scientific reports · 2023Article
- Amyloid β-Oligomers Inhibit the Nuclear CaAntioxidants (Basel, Switzerland) · 2023Article
- Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology.Acta neuropathologica communications · 2023Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- Structural Determinant of β-Amyloid Formation: From Transmembrane Protein Dimerization to β-Amyloid Aggregates.Biomedicines · 2022Review
- Regulation of gene expression by the APP family in the adult cerebral cortex.Scientific reports · 2022Article
- Knockdown of Amyloid Precursor Protein: Biological Consequences and Clinical Opportunities.Frontiers in neuroscience · 2022Review
- Mechanism of Cellular Formation and In Vivo Seeding Effects of Hexameric β-Amyloid Assemblies.Molecular neurobiology · 2021Article
- Overexpression of wild-type human amyloid precursor protein alters GABAergic transmission.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The amyloid precursor protein (APP) has been extensively studied as the precursor of the β-amyloid (Aβ) peptide, the major component of the senile plaques found in the brain of Alzheimer's disease (AD) patients. However, the function of APP per se in neuronal physiology remains to be fully elucidated. APP is expressed at high levels in the brain. It resembles a cell adhesion molecule or a membrane receptor, suggesting that its function relies on cell-cell interaction and/or activation of intracellular signaling pathways. In this respect, the APP intracellular domain (AICD) was reported to act as a transcriptional regulator. Here, we used a transcriptome-based approach to identify the genes transcriptionally regulated by APP in the rodent embryonic cortex and on maturation of primary cortical neurons. Surprisingly, the overall transcriptional changes were subtle, but a more detailed analysis pointed to genes clustered in neuronal-activity dependent pathways. In particular, we observed a decreased transcription of neuronal PAS domain protein 4 (NPAS4) in APP-/- neurons. NPAS4 is an inducible transcription factor (ITF) regulated by neuronal depolarization. The downregulation of NPAS4 co-occurs with an increased production of the inhibitory neurotransmitter GABA and a reduced expression of the GABA
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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.