ArticleMolecular psychiatry2026
Histone demethylase PHF2 regulates inflammatory genes in Alzheimer's disease.
Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed.
- Cognitive and synaptic impairment induced by deficiency of autism risk gene Smarcc2 and its rescue by histone deacetylase inhibition.Molecular psychiatry · 2026Article
- Microglial Deubiquitinase OTUD7B Stabilizes STAT3 to Promote Neuroinflammation and Cognitive Decline in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Glial cells in chronic inflammation: diversity, dysfunction and therapeutic targeting.Nature reviews. Immunology · 2026Review
- Diminished activity-dependent neuroprotective protein (ADNP) contributes to complement gene elevation in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
A plethora of factors contribute to cognitive impairment in Alzheimer's disease (AD), including neuroinflammation, synaptic dysfunction and gene alteration. In search of transcription factors controlling dysregulated genes in AD, we identified that the histone demethylase PHF2 (KDM7C) was a top-ranking candidate. Significant upregulation of PHF2 was found in AD human postmortem tissues, iPSC-derived neurons from AD patients, and a familial AD mouse model (5xFAD). ChIP-seq analysis and quantitative PCR profiling with bidirectional manipulation of Phf2 revealed that Phf2 regulated many genes critically involved in inflammatory pathways and neurodegeneration, including Stat3, Nfkbia, Nfkb2, Tnfrsf1a, Fgfr1, IL6st, Notch2, and Csf1. Knockdown of Phf2 in 5xFAD mice reduced the expression of inflammatory genes, leading to the substantial reduction of microglia/astrocyte activation and the restoration of glutamatergic synaptic function. Behavioral studies showed that Phf2 knockdown in 5xFAD mice significantly improved performance in the Barnes maze test, indicating a mitigation of spatial memory deficits. Our findings have revealed the epigenetic enzyme PHF2 as a regulator of neuroinflammatory processes in AD, linking its activity to both gene expression and cognitive outcomes. It suggests that targeting PHF2 could be a novel therapeutic approach for AD and other brain disorders involving neuroinflammation.
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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 Socratic graph.