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Author

A. Almulla

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Open access Sep 2026

In Vitro Ketamine Attenuates Immune Sensitization in Major Depressive Disorder in a Concentration-Dependent Manner

Background: Major depressive disorder (MDD) is a severe mental illness associated with severe clinical consequences and substantial societal burden. It's characterized by immune-inflammatory dysregulation and immune sensitization. Objective: To determine whether in vitro ketamine attenuates phytohemagglutinin (PHA)/lip...

Y. Zhang, X. Zhuang, M. Niu et al. · 0 citations
Open access Sep 2026

A Systems Biology Model Linking Peripheral NIMETOX Biomarkers to Multilevel Brain Structural and Functional Alterations Across Major Depression and Schizophrenia

Peripheral lipid and antioxidant-related biomarkers may help contextualize brain abnormalities across psychiatric disorders, but their relationships with brain structure, intrinsic activity, and dimensional symptoms remain incompletely characterized. In this cross-sectional study, 93 adults were recruited: 38 with majo...

H. Wu, C. Yang, Y. He et al. · 0 citations
Aug 2026

Psychological stress-associated ceramide and diacylglyceride lipotoxicity as contributors to first-episode depression pathophysiology: A neuroimmune-metabolic-oxidative stress (NIMETOX) perspective.

Early-stage MDD is characterized by lipid dysregulations, which are linked to psychosocial stress exposure, oxidative stress and attenuated reverse cholesterol transport, and may inform the development of future therapeutic strategies.

V. Sirivatanapa, Pannipa Janta, A. Almulla et al. · 0 citations
Review Open access Jul 2026

Unifying the hallmarks of major depression through neuroimmune–metabolic–oxidative (NIMETOX) dysregulation: a mechanistic systems framework

Evidence is presented that peripheral NIMETOX pathways may lead to neuroinflammation, microglial activation, and neuronal damage and that increased lipid load impairs these central pathways, as well as evidence that peripheral NIMETOX pathways may lead to neuroinflammation, microglial activation, and neuronal damage.

Michael Maes, A. Almulla, Drozdstoj Stoyanov et al. · 0 citations

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