Technology
Mitochondrial dysfunction is increasingly recognized as a critical factor in schizophrenia (SZ). Impaired activity of Complex I (CoI) of the mitochondrial respiratory chain has been identified, with aberrant expression of CoI subunit NDUFV2 and its pseudogene (NDUFV2P1) playing a key role.
NDUFV2P1 shows increased expression in SZ, inversely correlating with NDUFV2 protein levels and CoI-driven respiration. These findings point to the pseudogene as a novel regulatory mechanism underlying mitochondrial dysfunction in SZ. This technology offers a dual approach:
1. Therapeutic interventions, including gene therapy, to restore mitochondrial function by modulating pseudogene expression.
2. Diagnostic tools to identify SZ subtypes and enable personalized treatment strategies through pseudogene expression profiling.
The approach holds potential for broad applicability to other mitochondrial-related diseases such as such as Parkinson’s disease, Alzheimer’s, type II diabetes and several cancers.
Advantages
- Targets a novel mechanism involving NDUFV2P1, directly addressing mitochondrial dysfunction.
- Offers both therapeutic and diagnostic solutions, enhancing precision medicine.
- Provides a foundation for personalized treatment by linking pseudogene expression to disease mechanisms.
- Potential applicability beyond schizophrenia to other mitochondrial-linked conditions.
Applications
- Therapeutics: Development of gene therapy to mitigate Complex I deficits by targeting NDUFV2P1 expression and restoring mitochondrial function.
- Diagnostics: Use of NDUFV2P1 expression as a biomarker for early detection, prognosis, and treatment stratification in SZ.
Business Development Contacts