The Pharmaceutical Properties of Sulforaphane and Its Role in Tumor and Neurodegenerative Diseases / 生物化学与生物物理进展

Sulforaphane is a naturally occurring active substance derived from cruciferous vegetables with potent antioxidant and anticancer properties. Researches have shown that sulforaphane has good bioavailability and can be absorbed by the small intestine through passive transport, followed by excretion in the form of urine via the hydrophobic acid pathway. In addition, since sulforaphane is easy to be absorbed and metabolized, wrapping sulforaphane with nanomaterials can improve its bioavailability and stability, prolong its action time in human body, and better utilize its therapeutic effect. In terms of mechanism of action, sulforaphane can activate Nrf2 and HSF1 signaling pathways, induce the expression of phase II detoxification enzymes HO-1, NADPH, GST and HSP, thus regulating the concentration of oxidative stress ROS in vivo; inhibit NF-κB signaling pathway, thus suppressing the expression of inflammatory factors TNF-α, IL-1 and IL-6; regulate epigenetic modifications, thus inhibiting HDAC and DNMT, and increasing the concentration of histone H3 and H4. By regulating the expression levels of the above factors, sulforaphane can affect the occurrence and development of cancer, neurodegenerative diseases and other diseases. In recent years, several phase I/II clinical trials have shown that sulforaphane has good drug-generating properties. For example, researchers have found that patients with skin cancer have not shown any health problems and their corresponding functional problems have improved greatly after long-term use of sulforaphane. This suggests that in the future sulforaphane has a very high medicinal potential for the treatment of cancer and neurodegenerative diseases. In this paper, we review the pharmacokinetics, target of action and safety of sulforaphane and its research progress in tumor and neurodegenerative diseases to provide a reference for the future application of sulforaphane in the treatment of tumor and neurodegenerative diseases.

Functions and roles of connective tissue growth factor in nervous systems / 中国组织工程研究

BACKGROUND:Recent studies have shown that connective tissue growth factor not only participates in the development of neurons,but also participates in the pathogenesis of neurodegenerative diseases,depression,epilepsy,etc.It can also be used as a therapeutic target to develop related drugs,thereby improving the patients'quality of life. OBJECTIVE:To summarize the biological functions of connective tissue growth factor and the mechanisms involved in neurodegenerative diseases and depression,as well as the progress in intervention with connective tissue growth factor and related emerging treatments. METHODS:The first author searched relevant articles published from January 1996 to December 2022 in PubMed and Web of Science.The key words were"connective tissue growth factor,nervous system,depression,Alzheimer disease,epilepsy,Parkinson disease,epilepsy,amyotrophic lateral sclerosis,FG-3019"in English.After reading,screening and sorting,the articles consistent with the content of the review were collected.Finally,51 articles were selected for review. RESULTS AND CONCLUSION:Connective tissue growth factor participates in multiple biological activities such as fibrosis,cell adhesion,and cell development under different conditions through four different structural domains.Connective tissue growth factor is up-regulated in lesion sites of neurodegenerative diseases,depression and epilepsy.After interfering with the expression of connective tissue growth factor,the symptoms improve or disappear,suggesting that connective tissue growth factor plays an important role in the progression of these diseases.The development of novel therapeutic strategies and intervention targets around connective tissue growth factor is very promising therapeutic research.More research is needed to identify the mechanism of action to transfer from basic medical studies to clinical studies and to achieve safer and more effective treatments.

Interaction between autophagy and mesenchymal stem cells in treatment of neurodegenerative diseases / 中国组织工程研究

BACKGROUND:Neuronal autophagy disorder and abnormal protein aggregation are the main pathological changes of neurodegenerative diseases.The relationship and interaction between mesenchymal stem cells and autophagy represent a possible mechanism for the treatment of neurodegenerative diseases. OBJECTIVE:To review the research progress of autophagy and mesenchymal stem cells in the treatment of neurodegenerative diseases and their interaction in order to provide a theoretical basis and new ideas for the treatment of neurodegenerative diseases. METHODS:PubMed and CNKI databases were searched for relevant articles using"autophagy,neurodegenerative diseases,mesenchymal stem cells,Parkinson's disease,Alzheimer's disease"as the search terms in Chinese and English.Totally,59 articles were included for review. RESULTS AND CONCLUSION:(1)Autophagy homeostasis is beneficial for maintaining the stability of the internal and external environment of the central nervous system and for controlling the progression of neurodegenerative disease.(2)As a dynamic circulation mechanism to maintain cell renewal and equilibrium,autophagy can affect the biological functions of mesenchymal stem cells such as migration,survival,differentiation,anti-apoptosis and immune regulation,and optimize their therapeutic efficacy for diseases.(3)Mesenchymal stem cells are an important class of neuroprotective agents that can alleviate pathological features and improve dysfunction in neurodegenerative diseases by regulating the level of cellular autophagy,which may be related to specific cellular conditions and activation levels in catabolic processes.

Does the elbow position change the handgrip strength in Parkinson's disease? / A posição do cotovelo altera a força de preensão manual na doença de Parkinson?

Abstract The flexed elbow is a standardization position on the handgrip strength test, however the literature shows divergence in the values obtained from extended elbow. The aim of this study was to verify if there is such difference in people with Parkinson's disease. Cross-sectional study. Thirty-one elderly individuals with clinical diagnosis of Parkinson's disease, performed 2 handgrip tests, first with extended elbow and second with flexed elbow, with 48 hours of interval. There was not significantly different between positions for handgrip strength (p > 0.05). As well as, the effect size was insignificant (d < 0.19). The main results indicate there was no significant difference between the flexed and the extended protocol, the effect size was negative and very small, it shows there is no clinical effect. Since, there are no difference between elbow positions, The American Society of Hand Therapists standardized position is recommended for testing of handgrip strength.

Resumo O cotovelo flexionado é uma posição padronizada no teste de força de preensão manual, no entanto, a literatura mostra divergências nos valores obtidos com o cotovelo estendido. O objetivo deste estudo foi verificar se existe tal diferença em pessoas com a doença de Parkinson. Estudo transversal. Trinta e um idosos com diagnóstico clínico da doença de Parkinson realizaram 2 testes de preensão manual, o primeiro com o cotovelo estendido e o segundo com o cotovelo flexionado, com intervalo de 48 horas. Não houve diferença significativa entre as posições para a força de preensão manual (p > 0,05). Além disso, o tamanho do efeito foi insignificante (d < 0,19). Os principais resultados indicam que não houve diferença significativa entre o protocolo flexionado e o estendido, o tamanho do efeito foi negativo e muito pequeno, o que mostra que não há efeito clínico. Portanto, não há diferença entre as posições do cotovelo, recomenda-se a posição padronizada da Sociedade Americana de Terapeutas de Mão para o teste de força de preensão manual.

Sleep in the human aging process and circadian sleep rhythm disruptions / Sono no processo de envelhecimento humano e interrupções do ritmo circadiano do sono

The aging process is often related to sleeping difficulties, often due to changes in circadian rhythms. The circadian timing system is centered in the suprachiasmatic nucleus - the master biological clock - which synchronizes the rhythm of oscillators throughout the body, including the sleep-wake cycle. This affects the time, duration and quality of sleep according to the development and aging process, under external and internal influences. This review addresses the human circadian timing system, including endogenous and exogenous influences on circadian rhythms, their age-related particularities, as well as the repercussions of circadian misalignment in neurodegenerative diseases. Circadian rhythms naturally weaken with aging, but there are particularities according to age. Throughout life, sleep and circadian rhythm disorders are strongly bidirectionally related to the pathophysiology of some psychiatric and neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. This knowledge could potentially create valuable opportunities to improve the health of the world's population that is under circadian misalignment and aging.

O processo de envelhecimento está frequentemente relacionado a dificuldades de dormir, muitas vezes decorrentes de alterações nos ritmos circadianos. O sistema de ronometragem circadiana está centrada no núcleo supraquiasmático - o relógio biológico mestre - o qual sincroniza o ritmo dos osciladores em todo o corpo, incluindo o ciclo sono-vigília. Isso afeta o tempo, a duração e a qualidade do sono de acordo com o processo de desenvolvimento e envelhecimento, sob influências externas e internas. Esta revisão aborda o sistema de temporização circadiana humana, incluindo as influências endógenas e exógenas nos ritmos circadianos, suas particularidades relacionadas à idade, bem como as repercussões do desalinhamento circadiano nas doenças neurodegenerativas. Os ritmos circadianos enfraquecem naturalmente com o envelhecimento, mas há particularidades de acordo com a idade. Ao longo da vida, os transtornos do sono e do ritmo circadiano estão fortemente relacionados bidirecionalmente à fisiopatologia de algumas doenças psiquiátricas e neurodegenerativas, como as doenças de Alzheimer e Parkinson. Esse conhecimento pode potencialmente criar oportunidades valiosas para melhorar a saúde da população mundial que está sob desalinhamento circadiano e envelhecimento.

Neuronal intranuclear inclusion disease misdiagnosed as CIDP： a case report / 中风与神经疾病杂志

@#A middle-aged male patient，had the chief complaint of recurrent lower limb weakness，and he was misdiagnosed with chronic inflammatory demyelinating polyradiculoneuropathy. Later the patient attended the hospital again due to lower limb weakness，recurrent headache，and nausea and vomiting. The cerebral magnetic resonance imaging showed diffuse restricted high-signal lesions at the bilateral cerebral corticomedullary junctions； immunohistochemical staining showed that inclusion bodies strongly stained with P62 and ubiquitin antibodies were observed in the nuclei of some sweat gland cells，adipocytes，and fibroblasts； genetic testing showed 142 times of the abnormal amplification of GGC in the NOTCH2NLC gene. Therefore，a confirmed diagnosis of neuronal intranuclear inclusion disease （NIID） was made. This case suggests that we should pay attention to whether the central nervous system is involved when peripheral neuropathy is observed.

Inositol 1，4，5-trisphosphate receptors and neurodegenerative diseases / 中风与神经疾病杂志

@#Inositol 1，4，5-trisphosphate receptor （IP3R），which is a calcium ion （Ca2+） channel in the endoplasmic reticulum，participates in cellular biological functions through regulating the Ca2+ signal，and it is a key molecule in maintaining the normal function of the central nervous system. In recent years，more and more studies have found that the structural and functional abnormalities of IP3Rs are closely related to the pathogenesis of neurodegenerative diseases such as Alzheimer's disease，Parkinson disease，Huntington disease，and spinocerebellar ataxia. However，it remains unclear how these structural and functional abnormalities affect the function of IP3Rs and the related calcium signal as well as the pathogenesis and severity of neurodegenerative diseases. This paper reviews the role of IP3Rs in neurodegenerative diseases.

Neurodegenerative diseases and neuroinflammation： roles of microglia and astrocytes / 中风与神经疾病杂志

@#The incidence of neurodegenerative diseases （ND） is increasing every year， posing a serious threat to human health. Neuroinflammation plays an important role in the development and progression of ND and is a common pathological feature of many types of ND. As a defense mechanism， neuroinflammation initially has beneficial effects by promoting tissue repair and removing cellular debris， but a persistent inflammatory response is detrimental and can inhibit regeneration and exacerbate nerve injury. Microglia and astrocytes are key regulators in neuroinflammation. Modulating neuroinflammation improves neurological symptoms and slows the progression of ND.

Tualang and Kelulut Honey Reduced Lipopolysaccharidesstimulated Inflammatory Responses of Mic

@#Microglial activity is crucial in maintaining the central nervous system (CNS) homeostasis. However, prolonged microglial activation have been implicated in the pathology of neurodegenerative diseases. Activated microglia will increase the production of inflammatory cytokines, reactive oxygen species (ROS) and alter their surface marker expression levels. This study used Malaysian honey, Tualang honey (TH), and Kelulut honey (KH) to determine lipopolysaccharide (LPS)-stimulated inflammatory responses of microglia. TH and KH at 0.1% were used in the current study as our findings showed no significant difference in the cell viability between BV2 cells treated with 0.1 % of TH and KH and control group. TH and KH reduced the ROS level significantly by 41.62±1.06% and 49.16±0.63%, respectively, and slightly reduced the expression of co-stimulatory molecules, CD40 and CD11b in LPS-activated BV2 cells. Our preliminary findings proposed an in-depth future study on the anti-inflammatory effect of TH and KH on microglial activation.

Neuroprotection of Natural Products Based on Keap1/Nrf2/ARE Signaling Pathway： A Review / 中国实验方剂学杂志

The pathological manifestations of neurodegenerative diseases， such as Alzheimer's disease， Parkinson's disease， and multiple sclerosis， are abnormal protein aggregation and accumulation， microglia activation， and mitochondrial dysfunction， which eventually lead to the gradual loss of neuronal structure or function and deteriorate over time. These pathological processes are related to the production of reactive oxygen species （ROS）， which can cause oxidative stress and damage proteins， lipids， and DNA， leading to cell and tissue injuries. The Kelch-like ECH-associated protein 1 （Keap1）/nuclear factor E2-related factor 2 （Nrf2）/antioxidant response element （ARE） signaling pathway is the main mechanism to maintain the redox balance of the body and defend against oxidative stress injury. Nrf2 activates the expression of a series of antioxidant genes related to ARE through the dissociation of Keap1 and nuclear transfer in the cytoplasm to protect the body from oxidative damage. Therefore， the discovery and study of the Keap1/Nrf2/ARE signaling pathway activator is of great significance for the prevention and treatment of neurodegenerative diseases. Because of the remarkable biological activity and slight side effects， natural products are a treasure trove for new drug research and development. Studies have shown that a variety of natural products can activate the Keap1/Nrf2/ARE signaling pathway and play a neuroprotective role. According to the structural characteristics， natural products can be divided into flavonoids， terpenoids， volatile oils， polyphenols， and phenylpropanoids. This study summarized the underlying mechanism of the Keap1/Nrf2/ARE signaling pathway in regulating diseases and reviewed the research progress on natural products based on this signaling pathway in neuroprotection to provide references for the development of clinical drugs for the prevention and treatment of neurodegenerative diseases.

Progress on the neuroprotective effects of ginsenoside Rg1 / 药学学报

Ginsenoside Rg1 is one of the most important saponins in ginseng. It has a wide range of pharmacological activities. It is considered to be a powerful neuroprotective agent. It has neuroprotective effects such as anti-neuroinflammation, anti-oxidative stress, anti-neuronal apoptosis, and enhancing memory. Rg1 shows a good application prospect in the prevention and treatment of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, stroke, and mental diseases such as depression. This paper reviews the research on the neuroprotective mechanism of Rg1 at home and abroad in recent years, in order to provide new research ideas for the clinical treatment of nervous system diseases.

Role and research progress of circular RNA in Alzheimer’s disease / 解剖学报

[Abstract] The circular RNA (circRNA) is a class of endogenous expressed non-coding RNA that are formed by covalently closed cyclization through reverse splicing. In recent years, a variety of highly conserved and cell-type specific circRNA have been identified in eukaryotes. Alzheimer’ s disease (AD) is a common neurodegenerative disease and the most common cause of dementia in the elderly. Recent studies had shown that circRNA was involved in the pathogenesis and development of AD, such as amyloid β-protein (Aβ) metabolic, neuroinflammation, oxidative stress, autophagy and synaptic plasticity. The role and application value of circRNA in AD pathology are reviewed to provide a theoretical basis for the application of circRNA in the treatment and diagnosis of AD.

Magnetic Resonance Imaging Studies of Neurodegenerative Disease: From Methods to Translational Research / 神经科学通报·英文版

Neurodegenerative diseases (NDs) have become a significant threat to an aging human society. Numerous studies have been conducted in the past decades to clarify their pathologic mechanisms and search for reliable biomarkers. Magnetic resonance imaging (MRI) is a powerful tool for investigating structural and functional brain alterations in NDs. With the advantages of being non-invasive and non-radioactive, it has been frequently used in both animal research and large-scale clinical investigations. MRI may serve as a bridge connecting micro- and macro-level analysis and promoting bench-to-bed translational research. Nevertheless, due to the abundance and complexity of MRI techniques, exploiting their potential is not always straightforward. This review aims to briefly introduce research progress in clinical imaging studies and discuss possible strategies for applying MRI in translational ND research.

Prevention and alleviation of neurodegenerative diseases： time restricted feeding / 上海预防医学

With the rapid development of aging around the world， the incidence and prevalence of age-related dementia have increased significantly， leading to a huge burden on patients， families and society. So far， there are no drugs that can completely reverse degeneration of the nervous system. The core pathological mechanisms of dementia are not clear， and the occurrence and progression of degenerative diseases in the nervous system appears to be only rely on the prevention through lifestyle interventions. Among lifestyle interventions， a large amount of laboratory evidence and a small amount of epidemiological evidence suggest that time restricted feeding have excellent effects on preventing the occurrence and progression of degenerative diseases in the nervous system. However， due to the lack of evidence in human population， the application of time restricted feeding lacks scientific basis. By synthesizing the existing evidence， this review discussed the pathway network of time restricted feeding that antagonizes the nervous system degradation， suggesting that future studies should focus on population evidence and the combined effects of multiple effect pathways.

Corynoxine B targets at HMGB1/2 to enhance autophagy for α-synuclein clearance in fly and rodent models of Parkinson's disease

Parkinson's disease (PD) is the most common neurodegenerative movement disease. It is featured by abnormal alpha-synuclein (α-syn) aggregation in dopaminergic neurons in the substantia nigra. Macroautophagy (autophagy) is an evolutionarily conserved cellular process for degradation of cellular contents, including protein aggregates, to maintain cellular homeostasis. Corynoxine B (Cory B), a natural alkaloid isolated from Uncaria rhynchophylla (Miq.) Jacks., has been reported to promote the clearance of α-syn in cell models by inducing autophagy. However, the molecular mechanism by which Cory B induces autophagy is not known, and the α-syn-lowering activity of Cory B has not been verified in animal models. Here, we report that Cory B enhanced the activity of Beclin 1/VPS34 complex and increased autophagy by promoting the interaction between Beclin 1 and HMGB1/2. Depletion of HMGB1/2 impaired Cory B-induced autophagy. We showed for the first time that, similar to HMGB1, HMGB2 is also required for autophagy and depletion of HMGB2 decreased autophagy levels and phosphatidylinositol 3-kinase III activity both under basal and stimulated conditions. By applying cellular thermal shift assay, surface plasmon resonance, and molecular docking, we confirmed that Cory B directly binds to HMGB1/2 near the C106 site. Furthermore, in vivo studies with a wild-type α-syn transgenic drosophila model of PD and an A53T α-syn transgenic mouse model of PD, Cory B enhanced autophagy, promoted α-syn clearance and improved behavioral abnormalities. Taken together, the results of this study reveal that Cory B enhances phosphatidylinositol 3-kinase III activity/autophagy by binding to HMGB1/2 and that this enhancement is neuroprotective against PD.

Analysis of SOD1 and C9orf72 mutations in patients with amyotrophic lateral sclerosis in Antioquia, Colombia / Análisis de mutaciones en los genes SOD1 y C9orf72 en pacientes con esclerosis lateral amiotrófica, Antioquia, Colombia

Introduction: Amyotrophic lateral sclerosis is a neurodegenerative disease with a possible multifactorial origin characterized by the progressive degeneration of motor neurons. There is a relatively high prevalence of this disease in Antioquia; however, there is no published genetic study to date in Colombia. Despite its unknown etiopathogenesis, more genetic risk factors possibly involved in the development of this disease are constantly found. Objetives: To evaluate G93A and D90A mutations in SOD1 gene and a short tandem repeat in C9orf72 within a cohort of amyotrophic lateral sclerosis patients from Antioquia, Colombia. Materials y methods: Thirty-four patients previously diagnosed with amyotrophic lateral sclerosis were included in the study. Peripheral blood samples were used for DNA extraction and genotyping. Results: No mutations were found in SOD1 (G93A and D90A) in any of the patients, while C9orf72 exhibited an allele with a statistically significant high prevalence in the study sample (8 hexanucleotide repeats of CAGCAG). Conclusions: These results suggest an association between this short tandem repeat (STR) in C9orf72 and the presence of amyotrophic lateral sclerosis in the studied population. However, this association should be established in a larger sample size and with controls from the same population. In addition, there also seems to be a genetic anticipation effect for the disease regarding this locus, since patients with this genotype present an earlier onset.

Introducción. La esclerosis lateral amiotrófica es una enfermedad neurodegenerativa con un posible origen multifactorial, caracterizado por una degeneración progresiva de las neuronas motoras. Hay una gran prevalencia relativa de esta enfermedad en Antioquia; sin embargo, no hay publicaciones de estudios genéticos en Colombia. A pesar de su etiopatogénesis desconocida, hay varios factores de riesgo genético que se encuentran constantemente en el desarrollo de esta enfermedad. Objetivo. Evaluar las mutaciones G93A y D90A del gen SOD1 y una repetición corta en tándem (Short Tandem Repeat, STR) en el locus C9orf72, en una cohorte de pacientes con esclerosis lateral amiotrófica en Antioquia, Colombia. Materiales y métodos. Se incluyeron 34 pacientes previamente diagnosticados en el estudio. Una muestra de sangre periférica se usó para extraer el ADN y, posteriormente, genotipificarlo. Resultados. No se encontraron mutaciones en el gen SOD1 (G93A y D90A), mientras que el C9orf72 exhibe un alelo con una significativa prevalencia en los pacientes del estudio (8 repeticiones del hexanucleótido G4C2). Conclusiones. Se sugiere una asociación entre la repetición en tándem en C9orf72 y la presencia de la esclerosis lateral amiotrófica en la población estudiada. Sin embargo, se sugiere hacer estudios adicionales e incluir un grupo control de la misma población. Además, se detecta un fenómeno de anticipación genética de la enfermedad, dado que los pacientes con el alelo de 8 repeticiones en C9orf72 presentan una edad temprana de aparición de los síntomas.

Bioinformatics study on role of IL-17 signaling in manganese poisoning and manganese-related neurodegenerative diseases / 环境与职业医学

Background Manganese (Mn) is one of the environmental factors of Parkinson's disease (PD), and long-term exposure to Mn can cause nerve damage. It is important to explore the common mechanism of neurotoxic effects of Mn and neurodegenerative diseases (NDD), especially PD, for early diagnosis of the disease. Objective To comprehensively analyze the core messenger RNA (mRNA)-microRNAs (miRNAs) co-expressed in frontal cortex of NDD patients and neuronal cells exposed to Mn via bioinformatics, and to reveal the potential common mechanism between Mn-induced neurotoxicity and NDD, especially PD. Methods Difference of the mRNAs from frontal cortex of NDD patients (GSE150696) and human neuroblastoma (SH-SY5Y) cells exposed to Mn were analyzed by R software; Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed on the overlapping differentially expressed genes (DEGs). The miRNAs were predicted using the miRNet database, mRNA-miRNA interactions were identified by the starBase and miRTarBase databases, and mRNA-miRNA regulatory networks were constructed with Cytoscape software. The core miRNAs associated with PD (GSE77667) were incorporated into Weighted Gene Co-Expression Network Analysis (WGCNA) and the mRNA-miRNA regulatory network was comparatively analyzed. Results A total of 34 overlapping DEGs were identified in the frontal cortical of NDD patients and the neuronal cells exposed to Mn, mainly enriched in interleukin-17 (IL-17) signaling pathway, cyclic adenosine monophosphate (cAMP) signaling pathway, and primary immunodeficiency. Based on the results of database prediction, 52 miRNAs with 71 pairs of interaction relationships were finally included to construct the miRNA-mRNA regulatory network. Six core miRNAs were screened by WGCNA: hsa-let-7i-5p, hsa-mir-155-5p, hsa-mir-219-2-3p, hsa-mir-221-3p, hsa-mir-485-3p, and hsa-mir-509-3-5p, among which hsa-let-7i-5p interacted with the target gene FBXW2 and hsa-mir-155-5p interacted with the target gene CCL2. The results of the KEGG analysis indicated that CCL2 was closely related to the IL-17 signaling pathway. Conclusion There are similar molecular regulatory mechanisms involved in the neurotoxicity of Mn and NDD, and the IL-17 signaling pathway may play a role in Mn-related NDD through CCL2 and hsa-mir-155-5p.

Recent advance in calcium-regulated autophagy in neurodegenerative diseases / 中华神经医学杂志

Imbalance of calcium homeostasis and abnormal autophagy are important pathogenesis mechanisms for neurodegenerative diseases, as PD, AD, and amyotrophic lateral sclerosis (ALS); and correlation is noted between imbalance of calcium homeostasis and abnormal autophagy. A number of studies have reported that different calcium storage compartments of cells can affect autophagy via calcium channels or Ca 2+-related signal proteins, such as cytoplasm calcium release-activated calcium modulator 1 (Orai1) and transient receptor potential canonical channel (TRPC), endoplasmic reticulum calcium channel inositol 1,4,5-triphosphate receptor (IP3R), mitochondrial calcium uniporter (MCU) related to Ca 2+ uptake, lysosomal calcium channel transient receptor potential channel mucolipin 1(TRPML1) and two-pore channels, cytoplasmic Ca 2+/calmodulin-dependent kinase kinase β (CaMKKβ)/AMP-activated protein kinase(AMPK) pathway. This review summarizes the research progress on autophagy regulated by Ca 2+ in intracellular calcium storage compartments and cytoplasm in neurodegenerative diseases, with a view to further understand the pathogenesis of these diseases.

Recent advance in role of galectin-3 in central neurodegenerative diseases / 中华神经医学杂志

Galectin-3 (Gal3) is a multipotent protein involved in cell activation, proliferation and migration, which plays an important role in a variety of physiological and pathological processes. Recent studies have shown that Gal3 plays an important role in the pathogenesis of central nervous system degenerative diseases, but its specific mechanism is not clear. This article reviews the research progress on the mechanism and expression of Gal3 in central nervous system degenerative diseases, and discusses the application value of Gal3 as a new therapeutic target in central nervous system degenerative diseases, so as to provide new scientific basis for early prevention and treatment of central nervous system degenerative diseases.

Recent advance in protein homeostasis mediated by liquid-liquid phase separation in neurodegenerative diseases / 中华神经医学杂志

Numerous studies have suggested that liquid-liquid phase separation (LLPS) may be involved in occurrence and progression of neurodegenerative diseases through mediating immune inflammation, transcriptional regulation, protein homeostasis, genomic stability, and oxidative stress, and regulation of LLPS-mediated protein homeostasis has attracted particular attention. Therefore, this paper reviews the research progress of mechanism of protein homeostasis regulation in neurodegenerative diseases in recent years, and discusses the prospect of LLPS related research.