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BackgroundPsychiatric disorders have seriously affected human life, one of the risk genes related to psychosis is the methylenetetrahydrofolatereductase (MTHFR) gene. This gene has a potential role in psychiatric disorders. Therefore, a meta-analysis is conducted to investigate the correlations between two prevalent MTHFR single nucleotide polymorphisms (SNPs), MTHFR C677T, A1298C, severe psychological disorders (schizophrenia, major depression, bipolar disorder).MethodsA total of 81 published studies were screened and selected by a search of electronic databases up to April 2022. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the association between MTHFR polymorphism and psychiatric disorders susceptibility by using random effect models.ResultsWe found that MTHFR C677T polymorphism is significantly related to schizophrenia and major depression in the overall population. MTHFR C677T has been linked to an increased risk of bipolar disorder in the recessive model (TT vs. CT + CC). Ethnic subgroup analysis shows that schizophrenia and major depression significantly correlate with MTHFR C677T and A1298C in Asian populations but not Caucasians. Besides, schizophrenia is correlated substantially with MTHFR C677T in the African population. However, the MTHFR A1298C polymorphism is only marginally linked to major depression.ConclusionFindings of the current study revealed that MTHFR may contribute to the common pathogenesis of psychiatric diseases and that its variants may be essential in controlling the expression of psychosis-related genes. This study could help the researchers and health specialists in the early diagnosis and treatment of psychiatric disorders.

Da-Bu-Yin-Wan (DBYW) and Qian-Zheng-San (QZS), two classic traditional Chinese medicinal formulas, were clinically employed to treat Parkinson's disease (PD). Our previous studies demonstrated neuroprotective effects of them on mitochondrial function in PD mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The purpose of this research was to investigate their possible mechanisms in the light of mitochondrial ATP-sensitive potassium (mitoKATP) channels. The neuroprotective effect of DBYW and QZS on dopamine (DA) neurons in substantia nigra (SN) in the MPTP-induced PD mice was investigated by behavioral test (pole test) and immunohistochemistry. Adenosine triphosphate (ATP) level in the midbrain tissue was detected by firefly luciferase method. MitoKATP channel subunits SUR1 and Kir6.2 mRNA and protein expressions were tested by real-time PCR (RT-PCR) and Western blot. It was observed that DBYW and/or QZS served to ameliorate MPTP-induced behavioral impairment and prevent the loss of substantia nigra dopamine neurons, as well as increase ATP level in the midbrain tissue and downregulate SUR1 expression at mRNA and protein levels with no marked influence on Kir6.2. We concluded that DBYW and QZS exhibit neuroprotective effects probably through the regulation of ATP level and mitoKATP channel subunit expressions.

To investigate the effect of Da-Bu-Yin-Wan and Qian-Zheng-San (DBYW and QZS) on mitochondrial mass in Parkinson’s disease (PD) cell model induced by 1-Methyl-4-phenylpyridinium Ion (MPP + ). The SH-SY5Y cell was selected and treated with MPP + . The PD model was intervened with DBYW and QZS. CCK-8 method was used to detect the survival rate of cells in each group. Mitochondria was labeled by mitoTracker ® Red CMXRos probe and observed by laser scanning confocal microscope, and ImageJ software was used to process images and measure mitochondrial form factors; Tetramethylrhodamine methyl ester was used to detect mitochondrial membrane potential (ΔΨm); Luciferase method was used to detect cellular ATP levels; Western-Blot technique was applied to detect the expression levels of Parkin protein, and the expression levels of Mfn1, Mfn2, OPA1, Drp1, and Fis1. We found that DBYW and QZS treatment significantly increased the cell survival rate, form factor (F-factor), mitochondrial activity and ΔΨm after MPP + treatment, while the increase of ATP levels was not significant. In addition, the results of western blot analysis showed that the MPP + induced increase in the expression of Drp1 and Fis1, as well as decrease in Parkin, Mfn1, Mfn2, and OPA1 were all partially revised by DBYW and QZS. In summary, our data strongly suggested that DBYW and QZS treatment can exert protective effects against PD related neuronal injury through regulation the homeostasis between mitochondrial fission and fusion.

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Acupuncture help alleviate depression-like behaviors, but the neural mechanisms behind such anti-depressive impacts are still unknown. Abnormalities in the perineuronal net (PNN) have been documented in multiple psychiatric disorders. The modulation and neural mechanism of PNNs in the antidepressant process of electroacupuncture (EA) at Baihui (GV20) and Yintang (GV29) points were investigated in this work. A rat depression model was induced by chronic unpredicted mild stress (CUMS). Acupuncture was performed on model rats in the EA group at GV20 and GV29 acupoints every other day for 30 min each time. The fluoxetine (FLX) group of model rats were gavaged with 10 mg/kg fluoxetine each day. Immunohistochemistry and western blot assays were used to evaluate the density and components of PNNs, the protein expression levels of the main synthase of GABA, GAD67, and of the synaptic proteins GLuA1, and PSD95 in the pre-limbic (PrL) and sub-limbic (IL) of mPFC. We found that four weeks of CUMS could decrease the levels of PNN component proteins aggrecan and brevican and GAD67. Electroacupuncture exhibited significant anti-depressive effects on depressive rats by altering the levels of PNNs. Specifically, aggrecan and brevican are involved in the anti-depression mechanism of electroacupuncture. After electroacupuncture treatment, the decreased expression of GAD67, GLuA1 and PSD95 in the mPFC induced by CUMS for four weeks was also reversed. This indicates that the mechanism of acupuncture's antidepressant effect may be based on reversing the stress-induced decline in PNN expression, the functional impairment of GABA neurons, and the regulation of excitatory synaptic expression.