A territory-wide investigation of southern Chinese patients with multiple sclerosis (MS) was conducted in Hong Kong. There were 47 patients, 35 of whom were clinically definite (CDMS), 6 laboratory-supported definite (LSDMS) and 6 clinically probable (CPMS). The prevalence rate was 0.88 per 10(5) population, which is of the same order as in other Oriental populations but much lower than in Caucasoid populations. Comparisons with major Oriental and Caucasian series showed essentially the same clinical picture with only minor variations. In one autopsy case, the lesions were found mainly in the optic nerves and spinal cord, with marked softening in addition to the classical demyelination features. In contrast to findings in Caucasians, the detection rate of oligoclonal bands in the cerebrospinal fluid was low (33% in CDMS patients) and there was no association with human leucocyte antigens. The possible implications of these findings on the pathogenesis of MS are discussed.

Background: Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune nervous system disease that has become increasingly recognized. This retrospective study is aimed to analyze the relations between clinical manifestations and blood brain barrier (BBB) integrity in anti-NMDAR encephalitis patients. Methods: Anti-NMDAR encephalitis patients were admitted to the First Affiliated Hospital of Guangxi Medical University from April 2014 to April 2020. Patients were grouped by the normal BBB and damaged BBB groups according to the cerebrospinal fluid (CSF) albumin/serum albumin (QAlb). Neutrophil-to-lymphocyte ratio (NLR) in peripheral blood was used for estimating the inflammatory status. The modified Rankin Scale (mRS) was used to assess prognosis. Results: Seventy-three anti-NMDAR encephalitis patients were diagnosed based on the autoimmune encephalitis diagnosis criteria of 2016. Fifty-three (72.6%) patients were in the normal BBB group and twenty (27.4%) were in the BBB damaged group. There were no significant differences in gender, age, psychiatric disturbances, epilepsy, speech disorder, motor dysfunction, memory dysfunction, and autonomic dysfunction between the two groups (p>0.05). Nevertheless, the proportions of decreased consciousness, ICU admission, NLR, CSF protein and intrathecal IgG synthesis (IgGIF, IgGLoc) in the damaged BBB group were higher than that in the normal BBB group (p<0.05). Patients (79.2%) with normal BBB had good prognosis compared to patients with damaged BBB (50%) after 2 months follow-up. The median mRS before and after immunotherapy in the damaged BBB group were significantly higher than that in the normal BBB group (p<0.01, p<0.05, respectively). Additionally, QAlb increased was positively correlated with the quantitative intrathecal IgG synthesis (IgGLoc: r=0.66; IgGIF: r=0.433, all p<0.001). Conclusion: The dysfunction of BBB can be helpful in evaluating its prognosis since QAlb showed associations with ICU admission, NLR, a higher CSF protein, intrathecal IgG synthesis (IgGLoc, IgGIF) and mRS score after 2 months follow-up.

HIV-1 transactivator protein (Tat) induces tight junction (TJ) dysfunction and amyloid-beta (Aβ) clearance dysfunction, contributing to the development and progression of HIV-1-associated neurocognitive disorder (HAND). The Rho/ROCK signaling pathway has protective effects on neurodegenerative disease. However, the underlying mechanisms of whether Rho/ROCK protects against HIV-1 Tat-caused dysfunction of TJ and neprilysin (NEP)/Aβ transfer receptor expression have not been elucidated. C57BL/6 mice were administered sterile saline (i.p., 100 μL) or Rho-kinase inhibitor hydroxyfasudil (HF) (i.p., 10 mg/kg) or HIV-1 Tat (i.v., 100 μg/kg) or HF 30 min before being exposed to HIV-1 Tat once a day for seven consecutive days. Evans Blue (EB) leakage was detected via spectrophotometer and brain slides in mouse brains. The protein and mRNA levels of zonula occludens-1 (ZO-1), occludin, NEP, receptor for advanced glycation end products (RAGE), and low-density lipoprotein receptor-related protein 1 (LRP1) in mouse brain microvessels were, respectively, analyzed by Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) analyses. Exposure of the mice to HIV-1 Tat increased the amount of EB leakage, EB fluorescence intensity, blood–brain barrier (BBB) permeability, as well as the RAGE protein and mRNA levels, and decreased the protein and mRNA levels of ZO-1, occludin, NEP, and LRP1 in mouse brain microvessels. However, these effects were weakened by Rho-kinase inhibitor HF. Taken together, these results provide information that the Rho/ROCK signaling pathway is involved in HIV-1 Tat-induced dysfunction of TJ and NEP/Aβ transfer receptor expression in the C57BL/6 mouse brain. These findings shed some light on potentiality of inhibiting Rho/Rock signaling pathway in handling HAND.