miR regulatory mechanisms in experimental VCID.

Reviews of cellular or molecular mechanism of demyelination process and therapeutic strategies for remyelination via OPCs and other potential targets in aging and stroke.

In this review, we summarized the pathogenesis of idiopathic 
normal
 pressure hydrocephalus (iNPH) and its pathophysiological features that lead to neurological deficits. We also reviewed the current treatment strategies for iNPH and discussed prospective future therapies.

As monotherapy in patients with generalized myasthenia gravis, rituximab displays higher efficacy to prevent disease relapses compared to other oral immunosupressants.

Schematic shows the mechanism of EPC-EXs^miR-126 on treating ischemic stroke in diabetes. Overexpression of miR-126 enhanced the therapeutic effects of EPC-EXs on diabetic ischemic stroke by reducing cell apoptosis in acute phase and promoting angiogenesis and neurogenesis to promote neurological function recovery in chronic phase.

Activated phagocytic microglia may regulate the formation of abnormal neural circuits in temporal lobe epilepsy (TLE). After an epileptogenic injury, microglia in hippocampus was activated with up-regulated lysosomal molecules including CD68, LAMP1, LYZ, and LAPTM5. The expressions of phagocytosis-related molecules like C1QA, C1QB, C3, and TYROBP were also up-regulated. Activated phagocytic microglia could engulf apoptosis neurons, newborn neurons, and synapse with the help of complement and TYROBP, thus regulating the abnormal neural circuits and epileptogenesis in TLE. In chronic stage, the occurrence of spontaneous seizures further activated microglia and complements and exacerbated abnormal neuronal circuits.

It is the first time to demonstrate that a disrupted dissociation pattern of DMN still exists in recuperative herpes zoster patients compared with healthy controls even the rash disappeared and pain was relieved. This study could provide heuristic cues for future research about herpes zoster transition mechanism.

Schematic illustration of AQP4 polarity loss being induced by Poldip2 in mouse bacterial meningitis model. Poldip2 induced the upregulation and activation of MMPs, which mediates the cleavage of β-DG. Due to β-DG being responsible for AQP4 anchoring to astrocytic endfeet, the degradation of β-DG results in AQP4 polarity loss. In the present mechanism study, Poldip2 siRNA and the UK383367 were used to inhibit Poldip2 expression and MMP activity, respectively.

Promoter methylation of a 7-gene panel can be helpful in brain tumor diagnosis or characterization, and MS-HRM is a suitable method for its analysis.

This study, for the first time, confirmed the association between RORA and migraine.

The changes in outpatient visits and inpatient services from the neurology department in a tertiary hospital in Shanghai, China, where there was no official city lockdown during the pandemic. A. It indicates the clinic visits from January 2019 to July 2020. Clinic visits dropped by 36.6% in February 2020 as compared to that in February in 2019, with a partial rebound as the effects of the pandemic waned; B. It indicates the inpatient services in stroke and all neurological diseases from January 2019 to July 2020. Inpatient services in stroke and all neurological diseases dropped by 27.4% and 23.8%, respectively, in February 2020 as compared to that in February in 2019 and then rose rapidly to a nearly normal status