Alterations in GABAergic Interneurons, Neuroinflammation, and Epigenetics: Potential Targets for Therapeutic Strategies in Schizophrenia - PubMed
6 hours ago
- #epigenetics
- #neuroinflammation
- #schizophrenia
- Schizophrenia (SZ) is a chronic psychiatric disorder affecting cognition, emotions, and behavior.
- Epigenetic changes during early development disrupt GABAergic-glutamatergic neurotransmission, increasing SZ risk.
- Neuroinflammation, driven by microglial reactivity, contributes to SZ pathology and cognitive impairment.
- GABAergic interneuron markers (somatostatin, parvalbumin) are altered by systemic inflammation.
- TLR4 and NF-κB1 are key molecular targets linked to inflammation and gene regulation in SZ.
- Polyphenols (quercetin, EGCG, resveratrol) and valproic acid show anti-inflammatory and epigenetic therapeutic potential.
- Epigenetic modifications in parvalbumin-positive interneurons and glutamate dysfunction play a role in SZ pathogenesis.