Parkinson\'s disease is the second most prevalent neurodegenerative disease after Alzheimer\'s disease, mostly happened in the elder population and the prevalence gradually increased with age. Parkinson\'s disease is a movement disorder that severely affects patients\' daily life. The mechanism of Parkinson\'s disease still remains unknown, however, studies already proved that the damage or absence of dopaminergic neurons located in the substantia nigra and the decreased dopamine in the striatum are significantly related to Parkinson\'s disease. To date, the mainstream treatment of Parkinson\'s disease has been achieved by alleviating its associated morbid symptoms, such as the use of levodopa, carbidopa, dopamine receptor agonists, monoamine oxidase type B inhibitors, anticholinergic drugs, etc. However, strong side effects, even toxicity, have been reported after using these drugs, with reduced effectiveness over time. Plant compounds have shown good therapeutic effects in neurodegenerative diseases as a less toxic treatment. In this review, we have compiled several natural plant compounds and classified the currently reported compounds for therapeutic use based on their structural parent nuclei and constituent elements. We wish to inspire new ideas for the treatment of Parkinson\'s disease by summarizing their mechanisms.

Parkinson\'s disease (PD) is a common neurodegenerative disease that affects the motor system and progressively worsens with age. Current treatment options for PD mainly target symptoms, due to our limited understanding of the etiology and pathophysiology of PD. A variety of preclinical models have been developed to study different aspects of the disease. The models have been used to elucidate the pathogenesis and for testing new treatments. These models include cell models, non-mammalian models, rodent models, and non-human primate models. Over the past few decades, Caenorhabditis elegans (C. elegans) has been widely adopted as a model system due to its small size, transparent body, short generation time and life cycle, fully sequenced genome, the tractability of genetic manipulation and suitability for large scale screening for disease modifiers. Here, we review studies using C. elegans as a model for PD and highlight the strengths and limitations of the C. elegans model. Various C. elegans PD models, including neurotoxin-induced models and genetic models, are described in detail. Moreover, met.

Schizophrenia is a chronic disorder characterized by specific positive and negative primary symptoms, social behavior disturbances and cognitive deficits (e.g., impairment in working memory and cognitive flexibility). Mounting evidence suggests that altered excitability and inhibition at the molecular, cellular, circuit and network level might be the basis for the pathophysiology of neurodevelopmental and neuropsychiatric disorders such as schizophrenia. In the past decades, human and animal studies have identified that glutamate and gamma-aminobutyric acid (GABA) neurotransmissions are critically involved in several cognitive progresses, including learning and memory. The purpose of this review is, by analyzing emerging findings relating to the balance of excitatory and inhibitory, ranging from animal models of schizophrenia to clinical studies in patients with early onset, first-episode or chronic schizophrenia, to discuss how the excitatory-inhibitory imbalance may relate to the pathophysiology of disease phenotypes such as cognitive deficits and negative symptoms, and highlight directions for appropriate therapeutic strategies.

Autism spectrum disorder (ASD) is becoming increasingly prevalent of late. Methylenetetrahydrofolate reductase (MTHFR) has a significant role in folate metabolism. Owing to the inconsistencies and inconclusiveness on the association between MTHFR single nucleotide polymorphism (SNP) and ASD susceptibilities, a meta-analysis was conducted to settle the inconsistencies.
For this meta-analysis, a total of 15 manuscripts published up to January 26, 2020, were selected from PubMed, Google Scholar, Medline, WangFang, and CNKI databases using search terms \"MTHFR\" OR \"methylenetetrahydrofolate reductase\" AND \"ASD\" OR \"Autism Spectrum Disorders\" OR \"Autism\" AND \"polymorphism\" OR \"susceptibility\" OR \"C677T\" OR \"A1298C\".
The findings of the meta-analysis indicated that MTHFR C677T polymorphism is remarkably associated with ASD in the five genetic models, viz., allelic, dominant, recessive, heterozygote, and homozygote. However, the MTHFR A1298C polymorphism was not found to be significantly related to ASD in the five genetic models. Subgroup analyses revealed significant associations of ASD with the MTHFR (C677T and A1298C) polymorphism. Sensitivity analysis showed that this meta-analysis was stable and reliable. No publication bias was identified in the associations between MTHFRC677T polymorphisms and ASD in the five genetic models, except for the one with regard to the associations between MTHFRA1298C polymorphisms and ASD in the five genetic models.
This meta-analysis showed that MTHFR C677T polymorphism is a susceptibility factor for ASD, and MTHFR A1298C polymorphism is not associated with ASD susceptibility.

Impulse control disorders (ICDs) are characterized by generalized difficulty controlling emotions and behaviors. ICDs are a broad group of the central nervous system (CNS) disorders including conduct disorder, intermittent explosive, oppositional-defiant disorder, antisocial personality disorder, kleptomania, pyromania and other illnesses. Although they all share a common feature (aberrant impulsivity), their pathobiology is complex and poorly understood. There are also currently no ICD-specific therapies to treat these illnesses. Animal models are a valuable tool for studying ICD pathobiology and potential therapies. The zebrafish (Danio rerio) has become a useful model organism to study CNS disorders due to high genetic and physiological homology to mammals, and sensitivity to various pharmacological and genetic manipulations. Here, we summarize experimental models of impulsivity and ICD in zebrafish and highlight their growing translational significance. We also emphasize the need for further development of zebrafish ICD models to improve our understanding of their pathogenesis and to search for novel therapeutic treatments.

Neurodevelopmental disorders (NDDs) caused by aberrant brain growth and development are life-long, debilitating illnesses that markedly impair the quality of life. Animal models are a valuable tool for studying NDD pathobiology and therapies. Mounting evidence suggests the zebrafish (Danio rerio) as a useful model organism to study NDDs, possessing both high physiological homology to humans and sensitivity to pharmacological and genetic manipulations. Here, we summarize experimental models of NDDs in zebrafish and highlight the growing translational significance of zebrafish NDD-related phenotypes. We also emphasize the need in further development of zebrafish models of NDDs to improve our understanding of their pathogenesis and therapeutic treatments.

Esophageal cancer (EC) is a frequent malignant tumor in our world, and has a highly morbidity and mortality. It was reported that genetic factors play vital roles in its pathogenesis. Here, we performed a case - control study to evaluate the COL6A3 genetic variants and EC risk in a Chinese Han cohort. All subjects were genotyped with the Agena MassARRAY platform. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression after adjusting age and gender. We found that rs6720283 (G > A) allele had significantly enhanced EC risk (OR = 1.32, 95% CI = 1.11 alculate p = 0.002). Stratified analysis was performed by gender, age, alcohol drinking, BMI, TNM stage and lymph node metastasis, the results showed that rs7436, rs115510139 and rs6720283 were significantly associated with the risk of EC in different groups (all p < 0.05). Besides, no statistical significant was found between the COL6A3 gene polymorphisms and clinicopathological parameters such as TNM stage and lymph node metastasis among EC patients (p > 0.05). In conclusions, our study found that COL6A3 variants were associated with risk of EC in the Chinese population.

Family-based design is one of the most popular designs in genetic studies. Transmission disequilibrium test (TDT) for family trio design is optimal only under the additive trait model and may lose power under the other trait models. The TDT-type tests are powerful only when the underlying trait model is correctly specified. Usually, the true trait model is unknown, and the selection of the TDT-type test is problematic. Several methods, which are robust against the mis-specification of the trait model, have been proposed. In this paper, we propose a new efficiency robust procedure for family trio design, namely, the weighted TDT (WTDT) test.
We combine information of the largest two TDT-type tests by using weights related to the three TDT-type tests and take the weighted sum as the test statistic.
Simulation results demonstrate that WTDT has power close to, but much more robust than, the optimal TDT-type test based on a single trait model. WTDT also outperforms other efficiency robust methods in terms of power. Applications to real and simulated data from Genetic Analysis Workshop (GAW15) illustrate the practical application of the WTDT method.
WTDT is not only efficiency robust to model mis-specifications but also efficiency robust against mis-specifications of risk allele.

Despite the high prevalence of medicinal use and abuse of opioids, their neurobiology and mechanisms of action are not fully understood. Experimental (animal) models are critical for improving our understanding of opioid effects in vivo. As zebrafish (Danio rerio) are increasingly utilized as a powerful model organism in neuroscience research, mounting evidence suggests these fish as a useful tool to study opioid neurobiology. Here, we discuss the zebrafish opioid system with specific focus on opioid gene expression, existing genetic models, as well as its pharmacological and developmental regulation. As many human brain diseases involve pain and aberrant reward, we also summarize zebrafish models relevant to opioid regulation of pain and addiction, including evidence of functional interplay between the opioid system and central dopaminergic and other neurotransmitter mechanisms. Additionally, we critically evaluate the limitations of zebrafish models for translational opioid research and emphasize their developing utility for improving our understanding of evolutionarily conserved mechanisms of pain-related, addictive, affective and other behaviors, as well as for fostering opioid-related drug discovery.

BACKGROUND: Hypertension is the most common chronic disease, and most important risk factor for cardiovascular disease. This meta-analysis aimed to explore the association between hepatic lipase gene (LIPC) gene -250G/A (rs2070895) and -514C/T (rs1800588) polymorphisms and the susceptibility to hypertension.
METHODS: Published studies were searched using the PubMed, Embase and Cochrane Library databases. Newcastle-Ottawa Scale (NOS) was used to assess the quality of the included studies. Sensitivity analysis was performed using \"leave one out\" method. Egger\'s test was used to evaluate the publication bias. The random effect model was used to calculate the pooled effect size if P < 0.05 or I2 ≥ 50%; otherwise, the fixed effect model was selected.
RESULTS: Four eligible studies, including 2599 participants, were enrolled in the included studies from 2007 to 2014. Quality evaluation revealed that each study had high NOS scores ranged from 5 to 7. The LIPC rs1800588 polymorphism was not found to be associated with the susceptibility to hypertension under all genetic models (T vs C, P = 0.38; CT vs CC, P = 0.46; TT vs CC, P = 0.38; TT vs CC + CT, P = 0.54; TT + CT vs CC, P = 0.34). Notably, the frequencies of the AA+GA genotypes of LIPC rs2070895 polymorphism were related to an increased risk of hypertension (AA+GA vs. GG, OR = 1.1954, 95% CI: 1.0001-1.4288, P = 0.05).
CONCLUSIONS: The LIPC rs2070895 polymorphism was found to be related to an increased risk of hypertension. However, LIPC rs1800588 polymorphism was not associated with the susceptibility to hypertension.