Muscle spindles provide the greatest contribution to kinesthetic perception. Primary motor cortex (M1) excitability changes in parallel with the intensity of kinesthetic perception inputs from muscle spindles; M1 is therefore involved in kinesthetic perception. However, the causal relationship between changes in kinesthetic sensitivity and M1 excitability is unclear. The purpose of this study was to test whether artificially and sustainably modulated M1 excitability causes changes in kinesthetic sensitivity in healthy individuals. We evaluated motor evoked potentials (MEP) in Experiment 1 and joint motion detection thresholds (JMDT) in Experiment 2 before and after quadripulse transcranial magnetic stimulation (QPS). Nine healthy right-handed male volunteers were recruited. In each experiment, participants received QPS or sham stimulation (Sham) on separate days. MEP amplitude and JMDT were recorded before and at 0, 15, 30, 45, and 60 min after QPS and Sham. Our results showed that M1 excitability and kinesthetic sensitivity increased after QPS, whereas neither changed after Sham. In the five subjects who participated in both experiments, there was a significant moderate correlation between M1 excitability and kinesthetic sensitivity. Thus, the long-lasting change in kinesthetic sensitivity may be due to changes in M1 excitability. In addition, M1 may play a gain adjustment role in the neural pathways of muscle spindle input.It has been reported that many long noncoding RNAs (lncRNA) are abnormally expressed in Parkinson's disease (PD). However, the knowledge about the role of dysregulated lncRNA in the pathological process of PD and the potential molecular regulation mechanism is still limited. Our immunofluorescence data show that miR-126 enhances the aggregation and toxicity of synuclein, while lncRNA OIP5-AS1 reduces the aggregation and toxicity of MPP + induced α-synuclein by targeting miR-126. Luciferase experiments have found that miR-126 regulates α-synuclein by targeting PLK2. Western blot and IP experimental analysis showed that this process is achieved by regulating PLK2/α-synuclein autophagy. In conclusion, our data indicate that OIP5-AS1 promotes the autophagy of PLK2-α-synuclein by targeting the miR-126 axis with pathogenic factors, thus reducing the aggregation toxicity of α-synuclein, which It will help better to understand the mechanism of dopaminergic neuron loss in PD and provide novel treatment options.
  This research aimed to observe the effect of probucol combined with mecobalamin tablets on oxidative stress in patients with diabetic peripheral neuropathy (DPN).
 
  In this prospective study, 104 patients with DPN who were treated in our hospital were included, from August 2018 to January 2020. They were divided into groups of combination (n = 52) and control (n = 52) by using a random number table. All patients took mecobalamin tablets after meals for 3 months (1 tablet/time, 3 times/d). On this basis, patients in the combination group took probucol for 3 months (4 tablets/time, 2 times/d).  https://www.selleckchem.com/products/filgotinib.html  The observation indicators were the Toronto Clinical Scoring System (TCSS)(symptom, sensory, and reflex scores), nerve conduction velocity[sensory nerve conduction velocity (SNCV) and motor nerve conduction velocity(MNCV) of the common peroneal nerve and median nerve], oxidative stress indicators[superoxide dismutase(SOD), malondialdehyde(MDA), glutathione peroxidase(GSH-Px) and catalase(CAT)], clinical efficacy and adv stress response of patients and was worthy of clinical promotion.
  Orexin, a neuropeptide primarily secreted by neurons in the lateral hypothalamus, has been implicated in Parkinson's disease (PD). Studies on the relationship between plasma orexin-A levels and PD are rare.
 
  This study aimed to assess levels of plasma orexin-A in the progression of PD and to evaluate the correlation between orexin-A levels and non-motor symptoms.
 
  Enzyme-linked immunosorbent assay was used to determine plasma orexin-A levels in 117 healthy controls and 121 PD patients, including those with early (n = 68), medium (n = 40) and advanced (n = 13) stages of the disease. Evaluation of motor symptoms and non-motor symptoms in PD patients, such as sleep disorders, cognitive dysfunction, neuropsychiatric symptoms, autonomic nervous dysfunction, hyposmia and PD-related pain, were assessed by the associated scales.
 
  Plasma orexin-A levels were significantly higher in PD patients compared to healthy controls. Orexin-A levels were elevated in early-stage and medium-stage PD compared to healthy contro, cognitive dysfunction, and renal dysfunction.Parkinson's disease (PD) patients with postural instability and gait disorder phenotype (PIGD) are at high risk of cognitive deficits compared to those with tremor dominant phenotype (TD). Alterations of white matter (WM) integrity can occur in patients with normal cognitive functions (PD-N). However, the alterations of WM integrity related to cognitive functions in PD-N, especially in these two motor phenotypes, remain unclear. Diffusion tensor imaging (DTI) is a non-invasive neuroimaging method to evaluate WM properties and by applying DTI tractography, one can identify WM tracts connecting functional regions. Here, we 1) compared the executive function (EF) in PIGD phenotype with normal cognitive functions (PIGD-N) and TD phenotype with normal cognitive functions (TD-N) phenotypes; 2) used DTI tractography to evaluated differences in WM alterations between these two phenotypes within a task-based functional network; and 3) examined the WM integrity alterations related to EF in a whole brain network for PD-05). Compared to the TD-N, PIGD-N group exhibited significantly higher MD and RD in the tracts connecting the left superior temporal gyrus and left insula, and those connecting the right pars opercularis and right insula. Moreover, compared to TD-N, PIGD-N group had significantly higher RD in the tracts connecting right pars opercularis and right pars triangularis, and the tracts connecting right inferior temporal gyrus and right middle temporal gyrus. For the entire PD-N cohort, FAS verbal fluency scores positively correlated with MD in the superior longitudinal fasciculus (SLF). This study confirmed that PIGD-N phenotype has more deficits in verbal fluency task than TD-N phenotype. Additionally, our findings suggest (1) PIGD-N shows more microstructural changes related to FAS verbal fluency task when compared to TD-N phenotype; (2) SLF plays an important role in FAS verbal fluency task in PD-N patients regardless of motor phenotypes.