Technology
Mitochondrial dysfunction is a key driver of schizophrenia. Our research identifies the pseudogene NDUFV2P1 as a major regulator of the mitochondrial Complex I subunit NDUFV2, directly impacting neuronal energy balance and function.
The pseudogene is overexpressed in SZ, suppressing NDUFV2 and impairing mitochondrial respiration. Overexpression in human and animal models disrupts mitochondrial dynamics, synaptic activity, and ultimately behavior, while downregulation restores normal function.
Recently, we uncovered that NDUFV2P1 also interferes with RNA-binding proteins responsible for transporting NDUFV2 mRNA from the nucleus to mitochondria — revealing a new regulatory mechanism and a clear therapeutic opportunity.
This discovery supports both:
- Therapeutic strategies that restore mitochondrial function by modulating NDUFV2P1; and
- Diagnostic tools using pseudogene expression as a biomarker for precision treatment.
Potential applicability extends beyond schizophrenia to other mitochondrial-linked conditions.
Advantages
- Novel, first-in-class mitochondrial target
- Mechanism-based, clinically relevant approach
- Dual therapeutic and diagnostic use
- Preclinical validation in human and animal models
Applications
- Therapeutics: Gene or RNA-based modulation of NDUFV2P1 to restore mitochondrial and neuronal function in SZ.
- Diagnostics: Use of pseudogene expression as a biomarker for early detection, prognosis, and treatment stratification in SZ.
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