Related Experiment Video
Updated: Jun 20, 2026
05:14
Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra
Published on: September 8, 2021
The interplay between mitochondrial complex I, dopamine and Sp1 in schizophrenia
1Laboratory of Psychobiology, Department of Psychiatry, Rambam Medical Center and Faculty of Medicine, Rappaport Family Institute for Research in the Medical Sciences, Technion IIT, Haifa, Israel. shachar@tx.technion.ac.il
Journal of Neural Transmission (Vienna, Austria : 1996)
|September 29, 2009
Summary
Mitochondrial dysfunction is implicated in schizophrenia, affecting brain development and connectivity. Research reviews evidence of impaired mitochondrial function, particularly Complex I, in schizophrenia patients.
Area of Science:
- Neuroscience
- Genetics
- Cell Biology
Background:
- Schizophrenia is a complex disorder influenced by genetic and environmental factors impacting brain development.
- Clinical heterogeneity and difficulty linking functions to brain substrates impede identifying specific abnormalities.
- Mitochondria are crucial for neuronal function, energy production, and synaptic plasticity.
Purpose of the Study:
- To review evidence supporting mitochondrial dysfunction in schizophrenia.
- To explore the role of mitochondrial Complex I abnormalities.
- To discuss the disease specificity of mitochondrial pathologies in schizophrenia.
Main Methods:
- Review of existing literature on mitochondrial function in schizophrenia.
- Analysis of studies on mitochondrial hypoplasia and oxidative phosphorylation system (OXPHOS) impairments.
- Examination of gene expression alterations related to mitochondria and Complex I subunits.
Main Results:
- Evidence suggests mitochondrial dysfunction, including hypoplasia and OXPHOS impairments, in schizophrenia.
- Abnormalities in mitochondrial Complex I activity and subunit expression are observed.
- Alterations in Complex I are linked to specificity protein 1 (Sp1) and may be modulated by dopamine (DA).
Conclusions:
- Mitochondrial dysfunction is a significant factor in schizophrenia pathophysiology.
- Complex I alterations may represent a disease-specific or state-specific abnormality.
- Mitochondrial dysfunction could be a cause or consequence of disrupted brain connectivity in schizophrenia.
Related Concept Videos
01:27Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders
Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within the...
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within the...
01:29Biological Causes of Schizophrenia
Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.
01:46Electron Transport Chain: Complex I and II
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
01:29Drugs Affecting Neurotransmitter Synthesis
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
01:45Mitochondrial Membranes
A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
01:24Parkinson Disease ll: Pathophysiology
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...