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Article ; Online: Mitochondria in the Central Nervous System in Health and Disease: The Puzzle of the Therapeutic Potential of Mitochondrial Transplantation.

Tripathi, Kuldeep / Ben-Shachar, Dorit

2024 Volume 13, Issue 5

Abstract: Mitochondria, the energy suppliers of the cells, play a central role in a variety of cellular processes essential for survival or leading to cell death. Consequently, mitochondrial dysfunction is implicated in numerous general and CNS disorders. The ... ...

Abstract	Mitochondria, the energy suppliers of the cells, play a central role in a variety of cellular processes essential for survival or leading to cell death. Consequently, mitochondrial dysfunction is implicated in numerous general and CNS disorders. The clinical manifestations of mitochondrial dysfunction include metabolic disorders, dysfunction of the immune system, tumorigenesis, and neuronal and behavioral abnormalities. In this review, we focus on the mitochondrial role in the CNS, which has unique characteristics and is therefore highly dependent on the mitochondria. First, we review the role of mitochondria in neuronal development, synaptogenesis, plasticity, and behavior as well as their adaptation to the intricate connections between the different cell types in the brain. Then, we review the sparse knowledge of the mechanisms of exogenous mitochondrial uptake and describe attempts to determine their half-life and transplantation long-term effects on neuronal sprouting, cellular proteome, and behavior. We further discuss the potential of mitochondrial transplantation to serve as a tool to study the causal link between mitochondria and neuronal activity and behavior. Next, we describe mitochondrial transplantation's therapeutic potential in various CNS disorders. Finally, we discuss the basic and reverse-translation challenges of this approach that currently hinder the clinical use of mitochondrial transplantation.
MeSH term(s)	Humans ; Mitochondria/metabolism ; Central Nervous System/metabolism ; Brain/metabolism ; Central Nervous System Diseases/metabolism ; Mitochondrial Diseases/metabolism
Language	English
Publishing date	2024-02-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells13050410
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Article ; Online: Update of Mitochondrial Network Analysis by Imaging: Proof of Technique in Schizophrenia.

Yatchenko, Yekaterina / Ben-Shachar, Dorit

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2277, Page(s) 187–201

Abstract: Mitochondria, similar to living cells and organelles, have a negative membrane potential, which ranges between (-108) and (150) mV as compared to (-70) and (-90) mV of the plasma membrane. Therefore, permeable lipophilic cations tend to accumulate in the ...

Abstract	Mitochondria, similar to living cells and organelles, have a negative membrane potential, which ranges between (-108) and (150) mV as compared to (-70) and (-90) mV of the plasma membrane. Therefore, permeable lipophilic cations tend to accumulate in the mitochondria. Those cations which exhibit fluorescence activity after accumulation into energized systems are widely used to decipher changes in membrane potential by imaging techniques. Here we describe the use of two different dyes for labeling mitochondrial membrane potential (Δψ
Language	English
Publishing date	2021-06-02
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1270-5_13
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Article ; Online: The bimodal mechanism of interaction between dopamine and mitochondria as reflected in Parkinson's disease and in schizophrenia.

Ben-Shachar, Dorit

Journal of neural transmission (Vienna, Austria : 1996)

2019 Volume 127, Issue 2, Page(s) 159–168

Abstract: Parkinson's disease (PD) and schizophrenia (SZ) are two CNS disorders in which dysfunctions in the dopaminergic system and mitochondria are major pathologies. The symptomology of both, PD a neurodegenerative disorder and SZ a neurodevelopmental disorder, ...

Abstract	Parkinson's disease (PD) and schizophrenia (SZ) are two CNS disorders in which dysfunctions in the dopaminergic system and mitochondria are major pathologies. The symptomology of both, PD a neurodegenerative disorder and SZ a neurodevelopmental disorder, is completely different. However, the pharmacological treatment of each of the diseases can cause a shift of symptoms into those characteristic of the other disease. In this review, I describe a pathological interaction between dopamine and mitochondria in both disorders, which due to differences in the extent of oxidative stress leads either to cell death and tissue degeneration as in PD substantia nigra pars compacta or to distorted neuronal activity, imbalanced neuronal circuitry and abnormal behavior and cognition in SZ. This review is in the honor of Moussa Youdim who introduced me to the secrets of research work. His enthusiasm, curiosity and novelty-seeking inspired me throughout my career. Thank you Moussa.
MeSH term(s)	Animals ; Dopamine/metabolism ; Humans ; Mitochondria/metabolism ; Neurons/metabolism ; Neurons/pathology ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Schizophrenia/metabolism ; Schizophrenia/physiopathology
Chemical Substances	Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2019-12-17
Publishing country	Austria
Document type	Journal Article ; Review
ZDB-ID	184163-4
ISSN	1435-1463 ; 0300-9564
ISSN (online)	1435-1463
ISSN	0300-9564
DOI	10.1007/s00702-019-02120-x
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Ui II Zs.150: Show issues

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Article ; Online: Mitochondria play an essential role in the trajectory of adolescent neurodevelopment and behavior in adulthood: evidence from a schizophrenia rat model.

Ene, Hila M / Karry, Rachel / Farfara, Dorit / Ben-Shachar, Dorit

Molecular psychiatry

2022 Volume 28, Issue 3, Page(s) 1170–1181

Abstract: Ample evidence implicate mitochondria in early brain development. However, to the best of our knowledge, there is only circumstantial data for mitochondria involvement in late brain development occurring through adolescence, a critical period in the ... ...

Abstract	Ample evidence implicate mitochondria in early brain development. However, to the best of our knowledge, there is only circumstantial data for mitochondria involvement in late brain development occurring through adolescence, a critical period in the pathogenesis of various psychiatric disorders, specifically schizophrenia. In schizophrenia, neurodevelopmental abnormalities and mitochondrial dysfunction has been repeatedly reported. Here we show a causal link between mitochondrial transplantation in adolescence and brain functioning in adulthood. We show that transplantation of allogenic healthy mitochondria into the medial prefrontal cortex of adolescent rats was beneficial in a rat model of schizophrenia, while detrimental in healthy control rats. Specifically, disparate initial changes in mitochondrial function and inflammatory response were associated with opposite long-lasting changes in proteome, neurotransmitter turnover, neuronal sprouting and behavior in adulthood. A similar inverse shift in mitochondrial function was also observed in human lymphoblastoid cells deived from schizophrenia patients and healthy subjects due to the interference of the transplanted mitochondria with their intrinsic mitochondrial state. This study provides fundamental insights into the essential role of adolescent mitochondrial homeostasis in the development of normal functioning adult brain. In addition, it supports a therapeutic potential for mitochondria manipulation in adolescence in disorders with neurodevelopmental and bioenergetic deficits, such as schizophrenia, yet emphasizes the need to monitor individuals' state including their mitochondrial function and immune response, prior to intervention.
MeSH term(s)	Adult ; Rats ; Humans ; Animals ; Adolescent ; Schizophrenia ; Mitochondria ; Brain ; Neurons ; Disease Models, Animal
Language	English
Publishing date	2022-11-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-022-01865-4
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Zs.A 4812: Show issues

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Article ; Online: Mitochondrial multifaceted dysfunction in schizophrenia; complex I as a possible pathological target.

Ben-Shachar, Dorit

Schizophrenia research

2017 Volume 187, Page(s) 3–10

Abstract: Mitochondria are key players in various essential cellular processes beyond being the main energy supplier of the cell. Accordingly, they are involved in neuronal synaptic transmission, neuronal growth and sprouting and consequently neuronal plasticity ... ...

Abstract	Mitochondria are key players in various essential cellular processes beyond being the main energy supplier of the cell. Accordingly, they are involved in neuronal synaptic transmission, neuronal growth and sprouting and consequently neuronal plasticity and connectivity. In addition, mitochondria participate in the modulation of gene transcription and inflammation as well in physiological responses in health and disease. Schizophrenia is currently regarded as a neurodevelopmental disorder associated with impaired immune system, aberrant neuronal differentiation and abnormalities in various neurotransmitter systems mainly the dopaminergic, glutaminergic and GABAergic. Ample evidence has been accumulated over the last decade indicating a multifaceted dysfunction of mitochondria in schizophrenia. Indeed, mitochondrial deficit can be of relevance for the majority of the pathologies observed in this disease. In the present article, we overview specific deficits of the mitochondria in schizophrenia, with a focus on the first complex (complex I) of the mitochondrial electron transport chain (ETC). We argue that complex I, being a major factor in the regulation of mitochondrial ETC, is a possible key modulator of various functions of the mitochondria. We review biochemical, molecular, cellular and functional evidence for mitochondrial impairments and their possible convergence to impact in-vitro neuronal differentiation efficiency in schizophrenia. Mitochondrial function in schizophrenia may advance our knowledge of the disease pathophysiology and open the road for new treatment targets for the benefit of the patients.
Language	English
Publishing date	2017-09
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	639422-x
ISSN	1573-2509 ; 0920-9964
ISSN (online)	1573-2509
ISSN	0920-9964
DOI	10.1016/j.schres.2016.10.022
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Zs.A 2351: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 543: Show issues

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Article ; Online: Gene expression dynamics following mithramycin treatment: A possible model for post-chemotherapy cognitive impairment.

Asor, Eyal / Ben-Shachar, Dorit

Clinical and experimental pharmacology & physiology

2018 Volume 45, Issue 10, Page(s) 1028–1037

Abstract: Chemotherapy-induced cognitive changes is a major burden on a substantial number of cancer survivors. The mechanism of this sequel is unknown. In this study, we followed long-term effects of early in life mithramycin (MTR) treatment on behaviour and on ... ...

Abstract	Chemotherapy-induced cognitive changes is a major burden on a substantial number of cancer survivors. The mechanism of this sequel is unknown. In this study, we followed long-term effects of early in life mithramycin (MTR) treatment on behaviour and on the normal course of alterations of gene expression in brain. Between post-natal days (PND) 7 and 10, male rats were divided into 2 groups, 1 receiving MTR (0.1 mg/kg s.c. per day) and the other receiving saline. At PND11, frontal cortex tissue samples were dissected from 4 rats from each group. At PND 65 the remaining rats underwent behavioural tests after which all the rats were decapitated and their prefrontal cortex incised. Rats treated transiently with MTR early in life, showed impairments in spatial working memory and anxious-like behaviour in adulthood. The immediate molecular effect of MTR was expressed in a limited number of altered genes of different unconnected trajectories, which were simultaneously distorted by the drug. In contrast, 3 months later we observed a change in the expression of more than 1000 genes that converged into specific cellular processes. Time-dependent gene expression dynamics of several genes was significantly different between treated and untreated rats. The differences in the total number of altered genes and in gene expression trends, immediately and long after MTR treatment cessation, suggest the evolution of a new cellular homeostatic set point, which can lead to behavioural abnormalities following chemotherapy treatment.
MeSH term(s)	Animals ; Anxiety/complications ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/complications ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/physiopathology ; Gene Expression Regulation/drug effects ; Male ; Memory, Short-Term/drug effects ; Phenotype ; Plicamycin/adverse effects ; Rats ; Spatial Memory/drug effects
Chemical Substances	Plicamycin (NIJ123W41V)
Language	English
Publishing date	2018-07-11
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	189277-0
ISSN	1440-1681 ; 0305-1870 ; 0143-9294
ISSN (online)	1440-1681
ISSN	0305-1870 ; 0143-9294
DOI	10.1111/1440-1681.12975
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Zs.A 990: Show issues

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Article ; Online: VDAC genes down-regulation in brain samples of individuals with schizophrenia is revealed by a systematic meta-analysis.

Segev, Shaked / Yitzhaky, Assif / Ben Shachar, Dorit / Hertzberg, Libi

Neuroscience research

2023 Volume 192, Page(s) 83–92

Abstract: Mitochondrial dysfunction was shown to be involved in schizophrenia pathophysiology. Abnormal energy states can lead to alterations in neural function and thereby to the cognitive and behavioral aberrations characteristics of schizophrenia. Voltage- ... ...

Abstract	Mitochondrial dysfunction was shown to be involved in schizophrenia pathophysiology. Abnormal energy states can lead to alterations in neural function and thereby to the cognitive and behavioral aberrations characteristics of schizophrenia. Voltage-dependent anion-selective channels (VDAC) are located in the outer mitochondrial membrane and are involved in mitochondrial energy production. Only few studies explored VDAC genes' expression in schizophrenia, and their results were not consistent. We conducted a systematic meta-analysis of ten brain samples gene expression datasets (overall 368 samples, 179 schizophrenia, 189 controls). In addition, we conducted a meta-analysis of three blood samples datasets (overall 300 samples, 167 schizophrenia, 133 controls). Pairwise correlation analysis was conducted between the VDAC and proteasome subunit genes' expression patterns. VDAC1, VDAC2 and VDAC3 showed significant down-regulation in brain samples of patients with schizophrenia. They also showed significant positive correlations with the proteasome subunit genes' expression levels. Our findings suggest that VDAC genes might play a role in mitochondrial dysfunction in schizophrenia. VDAC1 was down-regulated also in blood samples, which suggests its potential role as a biomarker for schizophrenia. The correlation with proteasome subunits, which were previously shown to be down-regulated in a subgroup of the patients, suggests that our findings might characterize a subgroup of the patients. This direction has the potential to lead to patients' stratification and more precisely-targeted therapy and necessitates further study.
MeSH term(s)	Humans ; Down-Regulation ; Proteasome Endopeptidase Complex/genetics ; Schizophrenia/genetics ; Protein Isoforms/genetics ; Gene Expression ; Brain
Chemical Substances	Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Protein Isoforms
Language	English
Publishing date	2023-01-27
Publishing country	Ireland
Document type	Meta-Analysis ; Journal Article
ZDB-ID	605842-5
ISSN	1872-8111 ; 0168-0102 ; 0921-8696
ISSN (online)	1872-8111
ISSN	0168-0102 ; 0921-8696
DOI	10.1016/j.neures.2023.01.012
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Zs.A 1993: Show issues

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Article ; Online: Impaired heme metabolism in schizophrenia-derived cell lines and in a rat model of the disorder: Possible involvement of mitochondrial complex I.

Ifhar, Lee S / Ene, Hila M / Ben-Shachar, Dorit

European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology

2019 Volume 29, Issue 5, Page(s) 577–589

Abstract: Accumulating data point to heme involvement in neuropsychiatric disorders. Heme plays a role in major cellular processes such as signal transduction, protein complex assembly and regulation of transcription and translation. Its synthesis involves the ... ...

Abstract	Accumulating data point to heme involvement in neuropsychiatric disorders. Heme plays a role in major cellular processes such as signal transduction, protein complex assembly and regulation of transcription and translation. Its synthesis involves the mitochondria, which dysfunction, specifically that of the complex I (Co-I) of the electron transport chain is involved in the pathophysiology of schizophrenia (SZ). Here we aimed to demonstrate that deficits in Co-I affect heme metabolism. We show a significant decrease in heme levels in Co-I deficient SZ-derived EBV transformed lymphocytes (lymphoblastoid cell lines - LCLs) as compared to healthy subjects-derived cells (n = 9/cohort). Moreover, protein levels assessed by immunoblotting and mRNA levels assessed by qRT-PCR of heme catabolic enzyme, heme Oxygenase 1 (HO-1), and protein levels of heme downstream target phosphorylated eukaryotic initiation factor 2-alpha (Peif2a/eif2a) were significantly elevated in SZ-derived cells. In contrast, protein and mRNA levels of heme synthesis rate limiting enzyme aminolevulinic acid synthase-1 (ALAS1) were unchanged in SZ derived LCLs. In addition, inhibition of Co-I by rotenone in healthy subjects-derived LCLs (n = 4/cohort) exhibited an initial increase followed by a later decrease in heme levels. These findings were associated with opposite changes in heme's downstream target and HO-1 level, similar to our findings in SZ-derived cells. We also show a brain region specific pattern of impairment in Co-I subunits and in HO-1 and PeIF2α/eIF2α in the Poly-IC rat model of SZ (n = 6/cohort). Our results provide evidence for a link between CoI and heme metabolism both in-vitro and in-vivo suggesting its contribution to SZ pathophysiology.
MeSH term(s)	Adult ; Animals ; Cell Line ; Electron Transport Complex I/metabolism ; Female ; Hemeproteins/metabolism ; Humans ; Interferon Inducers/toxicity ; Male ; Middle Aged ; Mitochondria/metabolism ; Poly I-C/toxicity ; Rats ; Schizophrenia/chemically induced ; Schizophrenia/metabolism ; Young Adult
Chemical Substances	Hemeproteins ; Interferon Inducers ; Electron Transport Complex I (EC 7.1.1.2) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2019-04-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1082947-7
ISSN	1873-7862 ; 0924-977X
ISSN (online)	1873-7862
ISSN	0924-977X
DOI	10.1016/j.euroneuro.2019.03.011
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Zs.A 3288: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 630: Show issues

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Article: Gene environment interaction in periphery and brain converge to modulate behavioral outcomes: Insights from the SP1 transient early in life interference rat model.

Asor, Eyal / Ben-Shachar, Dorit

World journal of psychiatry

2016 Volume 6, Issue 3, Page(s) 294–302

Abstract: It is generally assumed that behavior results from an interaction between susceptible genes and environmental stimuli during critical life stages. The present article reviews the main theoretical and practical concepts in the research of gene environment ...

Abstract	It is generally assumed that behavior results from an interaction between susceptible genes and environmental stimuli during critical life stages. The present article reviews the main theoretical and practical concepts in the research of gene environment interaction, emphasizing the need for models simulating real life complexity. We review a novel approach to study gene environment interaction in which a brief post-natal interference with the expression of multiple genes, by hindering the activity of the ubiquitous transcription factor specificity protein 1 (Sp1) is followed by later-in-life exposure of rats to stress. Finally, this review discusses the role of peripheral processes in behavioral responses, with the Sp1 model as one example demonstrating how specific behavioral patterns are linked to modulations in both peripheral and central physiological processes. We suggest that models, which take into account the tripartite reciprocal interaction between the central nervous system, peripheral systems and environmental stimuli will advance our understanding of the complexity of behavior.
Language	English
Publishing date	2016-09-22
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2220-3206
ISSN	2220-3206
DOI	10.5498/wjp.v6.i3.294
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Article ; Online: Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia: Possible Interactions with Cellular Processes.

Bergman, Oded / Ben-Shachar, Dorit

Canadian journal of psychiatry. Revue canadienne de psychiatrie

2016 Volume 61, Issue 8, Page(s) 457–469

Abstract: Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate molecules by the oxidative phosphorylation system (OXPHOS). Linked to numerous signaling pathways and cellular ... ...

Abstract	Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate molecules by the oxidative phosphorylation system (OXPHOS). Linked to numerous signaling pathways and cellular functions, mitochondria, and OXPHOS in particular, are involved in neuronal development, connectivity, plasticity, and differentiation. Impairments in a variety of mitochondrial functions have been described in different general and psychiatric disorders, including schizophrenia (SCZ), a severe, chronic, debilitating illness that heavily affects the lives of patients and their families. This article reviews findings emphasizing the role of OXPHOS in the pathophysiology of SCZ. Evidence accumulated during the past few decades from imaging, transcriptomic, proteomic, and metabolomic studies points at OXPHOS deficit involvement in SCZ. Abnormalities have been reported in high-energy phosphates generated by the OXPHOS, in the activity of its complexes and gene expression, primarily of complex I (CoI). In addition, cellular signaling such as cAMP/protein kinase A (PKA) and Ca(+2), neuronal development, connectivity, and plasticity have been linked to OXPHOS function and are reported to be impaired in SCZ. Finally, CoI has been shown as a site of interaction for both dopamine (DA) and antipsychotic drugs, further substantiating its role in the pathology of SCZ. Understanding the role of mitochondria and the OXPHOS in particular may encourage new insights into the pathophysiology and etiology of this debilitating disorder.
MeSH term(s)	Humans ; Mitochondria/metabolism ; Mitochondrial Diseases/metabolism ; Oxidative Phosphorylation ; Schizophrenia/metabolism ; Signal Transduction/physiology
Language	English
Publishing date	2016-08-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	304227-3
ISSN	1497-0015 ; 0008-4824 ; 0706-7437
ISSN (online)	1497-0015
ISSN	0008-4824 ; 0706-7437
DOI	10.1177/0706743716648290
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