ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
STAT1 negatively regulates spatial memory formation and mediates the memory-impairing effect of Aβ.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- TNF-α induces type I IFN signalling to suppress neurogenesis and recruit T cells.Nature communications · 2026Article
- The presynaptic protein bassoon is a biofluid biomarker of synaptic pathology in multiple sclerosis.EBioMedicine · 2026Article
- ROS-Driven STAT1 S-Glutathionylation Sustains IFNγ Signaling and Pro-Inflammatory Microglial Polarization.Antioxidants (Basel, Switzerland) · 2025Article
- Decoding the role of glucocorticoid-regulated kinase 1 in Alzheimer's disease: a promising path toward novel therapeutic strategies.Inflammopharmacology · 2025Review
- Mapping dynamic molecular changes in hippocampal subregions after traumatic brain injury through spatial proteomics.Clinical proteomics · 2024Article
- STAT3 ameliorates truncated tau-induced cognitive deficits.Neural regeneration research · 2024Article
- Mesenchymal Stem Cells from Familial Alzheimer's Patients Express MicroRNA Differently.International journal of molecular sciences · 2024Article
- Protein retention in the endoplasmic reticulum rescues Aβ toxicity in Drosophila.Neurobiology of aging · 2023Article
- Transcriptomic and glycomic analyses highlight pathway-specific glycosylation alterations unique to Alzheimer's disease.Scientific reports · 2023Article
- Mechanism of action deconvolution of the small-molecule pathological tau aggregation inhibitor Anle138b.Alzheimer's research & therapy · 2023Article
- Differential expression of interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) in Alzheimer's disease and HIV-1 associated neurocognitive disorders.Scientific reports · 2023Article
- Unique aspects of IFN-γ/STAT1 signaling in neurons.Immunological reviews · 2022Review
- Lead-exposure associated miRNAs in humans and Alzheimer's disease as potential biomarkers of the disease and disease processes.Scientific reports · 2022Article
- Concerted type I interferon signaling in microglia and neural cells promotes memory impairment associated with amyloid β plaques.Immunity · 2022Article
- Super-resolution study of PIAS SUMO E3-ligases in hippocampal and cortical neurons.European journal of histochemistry : EJH · 2021Article
- Illuminating Neural Circuits in Alzheimer's Disease.Neuroscience bulletin · 2021Review
- Article
- STAT3 ameliorates cognitive deficits via regulation of NMDAR expression in an Alzheimer's disease animal model.Theranostics · 2021Article
- Microglia Impede Oligodendrocyte Generation in Aged Brain.Journal of inflammation research · 2021Article
- STAT3 ameliorates cognitive deficits by positively regulating the expression of NMDARs in a mouse model of FTDP-17.Signal transduction and targeted therapy · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducer and activator of transcription-1 (STAT1) has an important role in inflammation and the innate immune response, but its role in the central nervous system is less well understood. Here, we examined the role of STAT1 in spatial learning and memory, and assessed the involvement of STAT1 in mediating the memory-impairing effect of amyloid-beta (Aβ). We found that water maze training downregulated STAT1 expression in the rat hippocampal CA1 area, and spatial learning and memory function was enhanced in Stat1-knockout mice. Conversely, overexpression of STAT1 impaired water maze performance. STAT1 strongly upregulated the expression of the extracellular matrix protein laminin β1 (LB1), which also impaired water maze performance in rats. Furthermore, Aβ impaired spatial learning and memory in association with a dose-dependent increase in STAT1 and LB1 expression, but knockdown of STAT1 and LB1 both reversed this effect of Aβ. This Aβ-induced increase in STAT1 and LB1 expression was also associated with a decrease in the expression of the N-methyl-D-aspartate receptor (NMDAR) subunits, NR1, and NR2B. Overexpression of NR1 or NR2B or exogenous application of NMDA reversed Aβ-induced learning and memory deficits as well as Aβ-induced STAT1 and LB1 expression. Our results demonstrate that STAT1 negatively regulates spatial learning and memory through transcriptional regulation of LB1 expression. We also identified a novel mechanism for Aβ pathogenesis through STAT1 induction. Notably, impairment of spatial learning and memory by this STAT1-mediated mechanism is independent of cAMP responsive element-binding protein signaling.
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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.