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Parkinson's disease (PD) is characterized by the loss of neuromelanin (NM)-containing neurons in the substantia nigra pars compacta (SNc), and it is divided into two motor subtypes: the postural instability gait difficulty (PIGD) and the tremor dominant (TD) subtypes. With NM-sensitive Magnetic Resonance Imaging (NM-MRI), investigators have been able to accurately detect signal attenuation in SNc of PD; however, the difference of NM loss between PIGD and TD subtypes is still unclear. Thus, the aim of this study was to evaluate the differences in NM-MRI between PD motor subtypes. PD patients were classified into PIGD (n=14) and TD groups (n=9); 20 age and sex matched controls were recruited. We compared the signal intensity contrast ratios in medial and lateral regions of the SNc using NM-MRI in PIGD, TD, and controls, respectively. Remarkable signal attenuation was observed in the lateral part of SNc in PD when compared with the controls, and we were able to detect more severe signal attenuation in the medial part of SNc in PIGD patients in comparison with that in the TD group. Also, the medial part of SNc, ipsilateral to the most clinically affected side, showed the highest power to discriminate the PD motor subtypes (AUC, 81%; sensitivity, 71.4%; specificity, 77.8%). Our results indicated a potential diagnostic value of NM-MRI to discriminate the PD motor subtypes, providing new evidence for the neuropathology-based differences between the two subtypes., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Valproic acid (VPA), a widely prescribed drug for seizures and bipolar disorder, induces apoptosis in microglia, but the underlying mechanism by which microglia apoptosis in response to VPA is not yet known. In this study, we found that the mitochondrial pathway played an important role in VPA-induced apoptosis in both BV-2 microglia and mouse primary microglial cells. In addition, VPA increased the level of phospho-p38 mitogen-activated protein kinase (MAPK), but had no effects on phospho-ERK and phospho-JNK MAPKs. Moreover, p38 inhibitor SB203580 strongly inhibited VPA-induced apoptosis and caspase-3 activation. Taken together, our results clearly demonstrated that VPA could induce apoptosis of microglia via p38 MAPK and mitochondrial apoptosis pathway., (Copyright 2010 Elsevier Ireland Ltd. All rights reserved.)

Oxidative damage to mitochondrial DNA (mtDNA) has been implicated as an important mechanism underlying mitochondrial deficiency in epileptic seizures. In focusing on the role of the DNA repair pathway, we determined the response of the mitochondrial base excision repair (mtBER) pathway in pilocarpine-induced status epilepticus (SE) in hippocampi of male Wistar rats. The expression of 8-oxoguanine DNA glycosylase (OGG1) and polymerase gamma (polgamma) was decreased at both the cellular mRNA and mitochondrial protein levels at 3, 9 and 25h after the onset of SE. The mRNA and protein levels of APE1 were maintained, but the mitochondrial protein level decreased at 3 and 9h and recovered at 25h. Therefore, the mtBER pathway failed to respond to SE induced by pilocarpine. The failure of mitochondrial import might be an important factor responsible for the lowered mtBER enzymes in mitochondria. We hypothesize that the down-regulation of mtBER enzymes may aggravate mtDNA damage and mitochondrial deficiency after the onset of SE., (Copyright 2010 Elsevier Ireland Ltd. All rights reserved.)

Ghrelin, a 28-amino-acid peptide, is mainly secreted by the stomach. Evidence has shown ghrelin to have neuroprotective effects. However, whether ghrelin protects hippocampal neurons against cell death in pilocarpine-induced seizures is unknown. We used Nissl staining to show that ghrelin attenuated the neuronal loss caused by pilocarpine-induced seizures in the hippocampus. Ghrelin exerted the protective action through regulating the phosphatidylinositol-3-kinase and Akt pathway. Moreover, ghrelin treatment reversed the decreased ratio of Bcl-2 to Bax induced by seizures while inhibiting the activated caspase-3. Ghrelin can inhibit hippocampal neuronal damage caused by pilocarpine-induced seizures, which might have therapeutic value in seizures.