Voluntary wheel running ameliorates depression-like behaviors and brain blood oxygen level-dependent signals in chronic unpredictable mild stress mice.

BACKGROUND: Physical exercise has been long recognized for its therapeutic effects on depressive disorders, but the underlying mechanisms remain largely unknown. In the study, we investigated whether the physical exercise by voluntary wheel running (VWR) alters depression-like behaviors and its impact on brain blood oxygen level-dependent (BOLD) signals in mice. METHODS: Adult male C57BL/6 mice were assigned to one of the following groups; (1) no exercise control (noEx), housed in a standard cage; (2) exercise (Ex), 2h/day in a running wheel apparatus; (3) chronic unpredictable mild stress (CUMS), which was imitating adult stress; and (4) CUMS+Ex. The differences in functional brain changes were determined by BOLD functional magnetic resonance imaging (fMRI). RESULTS: The results showed that VWR exercise significantly reversed the CUMS-induced behavioral abnormalities. Base on the fMRI amplitude of low-frequency fluctuation (ALFF) analysis, we found that VWR exercise could restore the CUMS-induced excessive BOLD activation in parts of limbic system, such as cortex, hippocampus and corpus callosum. Furthermore, CUMS-induced BOLD suppressive regions were also partially attenuated by VWR exercise, such as amygdala, cerebellum anterior lobe, thalamus, midbrain, and pontine. Most of these regions are involved in mood-regulating circuit, suggesting dysfunction of the circuit in CUMS model of depression, and VWR exercise could adjust the mood-regulating circuit. CONCLUSIONS: These results suggested that VWR exercise ameliorated depression-like behaviors and brain BOLD signals in CUMS induced depression mice.

A novel mutation R190H in the AT-hook 1 domain of MeCP2 identified in an atypical Rett syndrome.

BACKGROUND: Mutations in Methyl-CpG binding protein 2 (MECP2) have been identified as the disease-causing mutations in Rett Syndrome (RTT). However, no mutation in the AT-hook 1 domain of MECP2 has been reported in RTT yet. The function of AT-hook 1 domain of MECP2 has not been described either. METHODS: The clinical and radiological features of a girl with progressive hyperactivity and loss of acquired linguistic and motor functions were presented. Next generation sequencing was used to screen the causative gene. Effect of the mutant protein on histone 3 methylation was assessed in vitro experiment. RESULTS: The patient was diagnosed with an atypical RTT at the age of nine. Magnetic resonance imaging revealed a loss of whole-brain volume and abnormal myelination. Genetic analysis identified a de novo novel missense mutation of MECP2 (NM_004992, c.570G->A, p.Arg190His). This mutation is located in the AT-hook 1 domain of MeCP2 protein. Overexpression of the mutant MeCP2 in cultured neuroblastoma cells SH-SY5Y revealed increased level of dimethylated histone 3 lysine 9, a transcriptional repressor marker. CONCLUSION: A novel missense mutation in AT-hook 1 domain of MeCP2 was identified in a patient with atypical RTT. Clinical data and in vitro experiment result imply that R190H mutation in AT-hook1 may cause dysfunction of MeCP2 and be a pathogenic variant.

Solitary fibrous tumor of the central nervous system: report of 2 cases and review of literature.

Solitary fibrous tumors (SFTs) rarely occur in the central nervous system (CNS). Involvement of the brainstem and pineal gland is rarely recorded. Herein, we represent 2 cases of SFTs and firstly report SFT of the pineal gland. Cranial MR imaging showed isointense to hypointense signal intensity, and marked enhancement. Microscopically, the tumors showed characteristic "patternless-pattern" architecture. Elongated tumour cells formed fascicles alternating with hypocellular densely collagenous stroma. Immunohistochemistry for CD34, BCL2, and CD99 favors the definitive diagnosis of SFT. It is difficult to predict prognosis in patients with intraventricular SFT. In general, complete surgical resection may offer the best chance of a favorable clinical outcome.