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Human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND) remains prevalent in the anti-retroviral (ART) era. While there is a complex interplay of many factors in the neuropathogenesis of HAND, decreased neurotrophic synthesis has been shown to contribute to synaptic degeneration which is a hallmark of HAND neuropathology. Dynasore Brain derived neurotrophic factor (BDNF) is the most abundant and synaptic-promoting neurotrophic factor in the brain and plays a critical role in both learning and memory. Reduced BDNF levels can worsen neurocognitive impairment in HIV-positive individuals across several domains. In this paper, we review the evidence from pre-clinical and clinical studies showing the neuroprotective roles of BDNF against viral proteins, effect on co-morbid mental health disorders, altered human microbiome and ART in HAND management. Potential applications of BDNF modulation in pharmacotherapeutic, cognitive and behavioral interventions in HAND are also discussed. Finally, research gaps and future research direction are identified with the aim of helping researchers to direct efforts to make these BDNF driven interventions improve the quality of life of patients living with HAND. © 2020 Michael et al.Objective Tourette syndrome (TS) is a childhood-onset neuro-developmental disorder and the genetic factors play an important role in its etiology. As pericentrin (PCNT) binds to disruption-in-schizophrenia 1 (DISC1) and is a risk factor for many mental illnesses, we aimed to investigate the effect of PCNT on TS in the Chinese Han population. Methods Five tag single nucleotide polymorphisms (SNPs) (rs17371795, rs2839227, rs2839228, rs6518291 and rs9983522) in PCNT were screened in 407 TS nuclear family trios and 506 healthy persons by the TaqMan assays real-time. A common case-control study was designed to recognize differences in the genetic distributions. Additionally, we conducted a family based association study including transmission disequilibrium test, haplotype relative risk, and haplotype-based haplotype relative risk for these SNPs. Results The allele frequencies revealed a significant difference of rs17371795, rs2839227 and rs2839228 between TS patients and controls (for rs17371795 P=0.002, OR=0.691, 95% CI=0.547-0.874; for rs2839227 P=0.001, OR=0.682, 95% CI=0.540-0.860; for rs2839228 P=0.028, OR=0.775, 95% CI=0.618-0.973) and genotypic distributions showed a positive association only in rs17371795 and rs2839227 (for rs17371795 P=0.010; for rs2839227 P=0.008). Moreover, only rs2839227 remained significant after Bonferroni correction (P less then 0.01). Conclusion Our study suggested genetic variability at the PCNT locus may be associated with TS risk in the Chinese Han population. © 2020 Liu et al.Purpose Most patients exhibiting psychiatric manifestations often remain undetected, misdiagnosed, and inappropriately managed. This cross-sectional study aims to ascertain the level of knowledge of mental illnesses among nonpsychiatric healthcare workers and their attitudes toward patients with mental illness in Makkah, Saudi Arabia. Patients and Methods A cross-sectional study was conducted in four public hospitals in Makkah from November 2017 to February 2018. A total of 407 participants were involved. A self-reported structured questionnaire was used, and data were collected electronically. Results Of 407 respondents, 183 (45%) were females and 244 (55%) were males. The majority of respondents were physicians with medical specialties 116 (28.5%), followed by physicians with surgical specialties 99 (24.3%). More than half 229 (56.3%) of the respondents had work experience of >10 years. Although 128 (31.4%) of the participants lacked adequate knowledge of mental illnesses, only 104 (25.6%) had relevant knowledge.154 (37.8%) respondents displayed favorable (good) attitude, whereas 82 (44.7%) displayed an unfavorable (poor) attitude toward mentally ill patients. Conclusion The study revealed that nearly one-fourth of the participants appear to have adequate knowledge of mental disorders. However, 44.7% have an unfavorable attitude toward patients with mental illnesses. Hence, respondent professionals markedly correlated with both knowledge and attitude toward patients with mental illnesses, and the positive attitude strongly correlated with having adequate knowledge. © 2020 AlSalem et al.Purpose To explore the neuroprotective effects and mechanisms of Apelin (APLN), and to study the regulation of APLN expression by microRNA (miRNA) in epilepsy. Materials and Methods In vitro and in vivo epileptic models were established with hippocampal neurons and Wistar rats. Apoptosis of neurons was identified by flow cytometry. Western blotting was used to detect the expression of proteins, and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to analyze the expression of miRNA and messenger RNA (mRNA). Bioinformatics software was used to predict target genes of miRNA, which were confirmed by dual-luciferase reporter gene system and functional experiments. Results Our study demonstrated protective effects of APLN against neuronal death in epilepsy both in vitro and in vivo. The underlying mechanisms involved are inhibiting the expression of metabotropic glutamate receptor 1 (mGluR1), Bax, and caspase-3; promoting the expression of Bcl-2; and increasing phosphorylated-AKT (p-AKT) levels in neurons. For the first time, we found that miR-182 could negatively regulate both transcriptional and translational levels of APLN, and that the up-regulation of miR-182 inhibited the expression of APLN and Bcl-2, and promoted the expression of Bax and caspase-3. Conclusion APLN could protect the neurons from injury in epilepsy by regulating the expression of apoptosis-associated proteins and mGluR1 and increasing p-AKT levels, which were attenuated by miR-182. Hence, miR-182/APLN may be potential targets for epilepsy control and treatment. © 2020 Dong et al.Objective This research was aimed to investigate the effects of baicalin on 6-hydroxydopamine (6-OHDA)-induced rat model of Parkinson's disease (PD) and the main mechanism of baicalin based on metabolomics. Methods The rat model of PD was induced by 6-OHDA. The protective effects of baicalin on rat model of PD were evaluated by open field test and rotarod test. The anti-PD efficacy of baicalin was evaluated by examining the morphologic changes of neurons and the level of monoamine neurotransmitters in the striatum, the number and morphology of tyrosine hydroxylase (TH)-positive neurons, and oxidative stress. Combined with metabolomics methods, the pharmacodynamic mechanism of baicalin on PD pathogenesis was also explored. Results Baicalin treatment improved the rod time and voluntary movement in rat model of PD (P less then 0.05) by the open field test and rotarod test. In addition, baicalin also protected from oxidative stress injury (P less then 0.05), and regulated the content of monoamine neurotransmitters dopamine, 3,4-dihydroxyphenylacetic acid, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid (P less then 0.