The Many Faces of Mitochondrial Dysfunction in Depression: From Pathology to Treatment

Caruso, Giuseppe; Benatti, Cristina; Blom, Johanna Maria Catharina; Caraci, Filippo; Tascedda, Fabio

doi:10.3389/fphar.2019.00995

Cited by 42 publications

(55 citation statements)

References 44 publications

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“…Compared to ad libitum-fed controls, mice and rats on an IF diet exhibit less neuronal dysfunction, degeneration and fewer clinical symptoms in models of AD, PD and Huntington’s disease (HD) [ 16 ]. In a different in vivo study carried out by Chaix et al [ 61 ], there were 17 serum metabolites that were higher in TRF than ad libitum feeding group, including anserine and carnosine, which have shown therapeutic potential against the oxidative stress observed in pathologies characterized by cognitive dysfunctions [ 62 , 63 ]. Differently from caloric restriction, IF could prevent cognitive decline in a triple transgenic AD mouse model by acting on mitochondrial dysfunction and oxidative imbalance without reductions in β-amyloid protein and phospho-tau levels [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Association between Time Restricted Feeding and Cognitive Status in Older Italian Adults

et al. 2021

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Background: Due to the increased life expectancy, the prevalence of aging-related health conditions, such as cognitive impairment, dementia and Alzheimer’s disease is increasing. Among the modifiable risk factors, dietary factors have proved to be of primary importance in preserving and improving mental health and cognitive status in older adults, possibly through the modulation of adult neurogenesis, neuronal plasticity and brain signaling. Feeding/fasting timing manipulation has emerged as an innovative strategy to counteract and treat cognitive decline. The aim of this study was to investigate the association between the timing of the feeding period and cognitive status in a cross-sectional cohort of adults living in the Mediterranean area. Methods: Demographic and dietary characteristics of 883 adults living in Southern Italy (Sicily) were analyzed. Food frequency questionnaires were used to calculate the time window between the first and the last meal of an average day. Participants with an eating time window duration of more than 10 h were then identified, as well as those with eating time restricted to less than 10 h (TRF). Results: After adjusting for potential confounding factors, individuals adherent to TRF were less likely to have cognitive impairment, compared to those with no eating time restrictions [odds ratio (OR) = 0.28; 95% confidence intervals (CI): 0.07–0.90]; a similar association was found for individuals having breakfast (OR = 0.37, 95% CI: 0.16–0.89), but not for those having dinner. Conclusions: The results of this study reveal that time restricted eating may be positively associated with cognitive status, and thus exert plausible effects on brain health.

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Section: Discussionmentioning

confidence: 99%

Association between Time Restricted Feeding and Cognitive Status in Older Italian Adults

et al. 2021

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“…Research methods designed to capitalize on mitonuclear interactions and detect incompatibilities as outlined in this review can be applied to other psychiatric disorders, as mitochondrial dysfunction is well documented in schizophrenia ( Goncalves et al, 2015 ; Hjelm et al, 2015 ; Monpays et al, 2016 ; Ben-Shachar, 2017 ; Ni and Chung, 2020 ; Roberts, 2020 ), depression ( Bansal and Kuhad, 2016 ; Allen et al, 2018 ; Caruso et al, 2019 ; Forester et al, 2019 ), autism ( Rossignol and Frye, 2012 ; Goh et al, 2014 ; Varga et al, 2018 ; Bennuri et al, 2019 ; Citrigno et al, 2020 ; Frye, 2020 ; Gevezova et al, 2020 ), and anxiety ( Chakravarty et al, 2013 ; Khalifeh et al, 2016 ; Babenko et al, 2018 ). The studies outlined in this review suggest that mitochondrial dysfunction underlying BD and other psychiatric disorders with genetic overlap may be the consequence of mitonuclear incompatibility, and may be enhanced in admixed populations with mitonuclear genomes originating from different ancestral populations ( Chou and Leu, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

The Role of Mitonuclear Incompatibility in Bipolar Disorder Susceptibility and Resilience Against Environmental Stressors

Gonzalez

2021

Front. Genet.

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It has been postulated that mitochondrial dysfunction has a significant role in the underlying pathophysiology of bipolar disorder (BD). Mitochondrial functioning plays an important role in regulating synaptic transmission, brain function, and cognition. Neuronal activity is energy dependent and neurons are particularly sensitive to changes in bioenergetic fluctuations, suggesting that mitochondria regulate fundamental aspects of brain function. Vigorous evidence supports the role of mitochondrial dysfunction in the etiology of BD, including dysregulated oxidative phosphorylation, general decrease of energy, altered brain bioenergetics, co-morbidity with mitochondrial disorders, and association with genetic variants in mitochondrial DNA (mtDNA) or nuclear-encoded mitochondrial genes. Despite these advances, the underlying etiology of mitochondrial dysfunction in BD is unclear. A plausible evolutionary explanation is that mitochondrial-nuclear (mitonuclear) incompatibility leads to a desynchronization of machinery required for efficient electron transport and cellular energy production. Approximately 1,200 genes, encoded from both nuclear and mitochondrial genomes, are essential for mitochondrial function. Studies suggest that mitochondrial and nuclear genomes co-evolve, and the coordinated expression of these interacting gene products are essential for optimal organism function. Incompatibilities between mtDNA and nuclear-encoded mitochondrial genes results in inefficiency in electron flow down the respiratory chain, differential oxidative phosphorylation efficiency, increased release of free radicals, altered intracellular Ca2+ signaling, and reduction of catalytic sites and ATP production. This review explores the role of mitonuclear incompatibility in BD susceptibility and resilience against environmental stressors.

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“…Depression has also been associated with mitochondrial dysfunctions and an increase in the formation of reactive oxygen species (ROS) inducing redox to unbalance and reduction in the energy production (adenosine triphosphate-ATP) ( Caruso et al, 2019 ). Oxidative stress activates several transcription factors, such as nuclear factor kappa B (NF-kB) leading to the production of pro-inflammatory cytokines and other inflammatory molecules acting as potent inducers of inducible nitric oxide synthase (iNOS) ( Morris and Berk, 2015 ).…”

Section: Vitamin D and Depressive Symptomsmentioning

confidence: 99%

Vitamin D, Depressive Symptoms, and Covid-19 Pandemic

et al. 2021

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Graphical AbstractRole of vitamin D in the development of depressive symptoms. The synthesis of vitamin D from sunlight is impaired by lockdown and social distance measures imposed by the governments around the world during COVID-10 pandemic. Endogenous vitamin D synthesis initiates in the skin when 7-dehydrocholesterol (7-DHC) is converted in pre-vitamin D3 and then vitamin D3 [25(OH)D3]. It is transported through blood circulation by the vitamin D binding protein (VDBP) to the liver, the kidney, and the brain, where can be converted in its the active form [1,25(OH)2D3]. In the brain, the biological effects of 1,25(OH)2D3 are largely mediated by vitamin D receptor (VDR) through genomic mechanisms, which influence several aspects of serotonin metabolism, such as increasing serotonin synthesis by induction of the tryptophan hydroxylase 2 (TPH2) gene expression; influencing the expression of serotonin reuptake transporter (SERT) and the levels of monoamine oxidase-A (MAO-A), responsible to serotonin catabolism; and indirectly may regulate the synthesis of melatonin that improve the circadian rhythm. This mechanism can be impaired during social isolation and consequent reduction of vitamin D due to low sun exposure during the pandemic, which could contribute to the development of depressive symptoms.

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The Many Faces of Mitochondrial Dysfunction in Depression: From Pathology to Treatment

Cited by 42 publications

References 44 publications

Association between Time Restricted Feeding and Cognitive Status in Older Italian Adults

Association between Time Restricted Feeding and Cognitive Status in Older Italian Adults

The Role of Mitonuclear Incompatibility in Bipolar Disorder Susceptibility and Resilience Against Environmental Stressors

Vitamin D, Depressive Symptoms, and Covid-19 Pandemic

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