2018
DOI: 10.1038/s41386-018-0228-0
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Sex differences in schizophrenia: estrogen and mitochondria

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Cited by 14 publications
(9 citation statements)
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References 5 publications
(17 reference statements)
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“…Female patients show later onset of the disorder, less negative and cognitive symptoms, and increased fecundity compared to male patients. This could be explained by the buffering effects of estrogen interacting with the expression of the mitochondrial genome, that is, with the epistasis emerging from the interaction between nuclear and mitochondrial genes . Furthermore, mitochondrial dysfunction has been repeatedly observed in patients with schizophrenia .…”
Section: Evidence Rebutting Hypotheses That Schizophrenia Risk Varianmentioning
confidence: 99%
“…Female patients show later onset of the disorder, less negative and cognitive symptoms, and increased fecundity compared to male patients. This could be explained by the buffering effects of estrogen interacting with the expression of the mitochondrial genome, that is, with the epistasis emerging from the interaction between nuclear and mitochondrial genes . Furthermore, mitochondrial dysfunction has been repeatedly observed in patients with schizophrenia .…”
Section: Evidence Rebutting Hypotheses That Schizophrenia Risk Varianmentioning
confidence: 99%
“…after menopause) [ 6 , 11 , 12 ]. On the other hand, estrogens have direct neuroprotective actions, for example by decreasing neuro-inflammation, promoting synaptic plasticity, and by influencing major neurotransmitter systems relevant for schizophrenia, such as dopamine signaling [ 12 , 14 16 ]. Through their influence on dopaminergic signaling, estrogens reduce impulsivity and risk for substance abuse in women [ 9 12 , 16 ].…”
Section: Introductionmentioning
confidence: 99%
“…As a multifaceted condition, schizophrenia has a wide spectrum of hypotheses, among which alterations and abnormalities within neurotransmission (dopamine hypothesis) seem to be of primary relevance [ 6 , 7 , 8 , 9 , 10 , 11 ]. Other hypotheses refer to genetic predisposition, altered γ-aminobutyric acid (GABA) levels, nicotinic receptors, the endocannabinoid system, inflammation with oxidative stress, sex and developmental differences in brain anatomy, the protective role of estrogens, gut microbiota, or vitamin D deficiency [ 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 ].…”
Section: Introductionmentioning
confidence: 99%