SLIT and NTRK-like protein-5 (SliTrk5) is one of the six members of SliTrk protein family, which is widely expressed in the central nervous system (CNS), regulating and participating in many essential steps of central nervous system development, including axon and dendritic growth, neuron differentiation, and synaptogenesis. SliTrk5, as a neuron transmembrane protein, contains two important conservative domains consisting of leucine repeats (LRRs) located at the amino terminal in the extracellular region and tyrosine residues (Tyr) located at the carboxyl terminal in the intracellular domains. These special structures make SliTrk5 play an important role in the pathological process of the CNS. A large number of studies have shown that SliTrk5 may be involved in the pathogenesis of CNS diseases, such as obsessive-compulsive-disorder (OCD), attention deficit/hyperactivity disorder (ADHD), glioma, autism spectrum disorders (ASDs), and Parkinson’s disease (PD). Targeting SliTrk5 is expected to become a new target for the treatment of CNS diseases, promoting the functional recovery of CNS. The purpose of this article is to review the current research progression of the role of SliTrk5 in CNS and its potential mechanisms in CNS diseases.

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Epilepsy, characterized by recurrent seizures and abnormal brain discharges, is the third most common chronic disorder of the Central Nervous System (CNS). Although significant progress has been made in the research on antiepileptic drugs (AEDs), approximately one-third of patients with epilepsy are refractory to these drugs. Thus, research on the pathogenesis of epilepsy is ongoing to find more effective treatments. Many pathological mechanisms are involved in epilepsy, including neuronal apoptosis, mossy fiber sprouting, neuroinflammation, and dysfunction of neuronal ion channels, leading to abnormal neuronal excitatory networks in the brain. CK2 (Casein kinase 2), which plays a critical role in modulating neuronal excitability and synaptic transmission, has been shown to be associated with epilepsy. However, there is limited research on the mechanisms involved. Recent studies have suggested that CK2 is involved in regulating the function of neuronal ion channels by directly phosphorylating them or their binding partners. Therefore, in this review, we will summarize recent research advances regarding the potential role of CK2 regulating ion channels in epilepsy, aiming to provide more evidence for future studies.

BackgroundThe dementia and affective disorders are common non-motor features in patients with essential tremor (ET). However, the relationship of ET with cognitive impairments and affective disorders remains controversial. This meta-analysis aimed to analyze the association of ET with dementia and affective disorders.MethodsOriginal studies published from January 1999 to October 2019 were systematically searched from the database of Medline (OvidSP), EMBASE (OvidSP), and the Cochrane Central Register of Controlled Trials. Pooled standard mean difference (SMD, random effect model), odds ratios (ORs), relative risk (RR), and 95% CI were calculated.ResultsCompared with the Non-ET group, patients with ET had significantly lower Mini-Mental State Examination (MMSE) score (SMD, −1.16; 95% CI, −1.75 to −0.58; p = 0.0001) and had significantly higher depressive and anxiety symptoms scale score (SMD, 0.55; 95% CI, 0.22–0.87; p = 0.0009). The OR for dementia and affective disorders in individuals with ET compared with individuals without ET was 2.49 (95% CI, 2.17–2.85, p < 0.00001). While there was no significant difference in Montreal Cognitive Assessment (MoCA) score between ET and Non-ET groups (SMD, −0.52; 95% CI, −0.16 to 0.13; p = 0.23), there was a significant difference in the risk of mortality between ET and Non-ET groups (RR = 4.69, 95% CI, 2.18–10.07).ConclusionThe non-motor symptoms should not be neglected among patients with ET. However, the causal relationship between ET and dementia, depression, and anxiety is unclear.