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ATP6AP2,a regulator of LRP6/β-catenin protein trafficking,promotes Wnt/β-catenin signaling and bone formation in a cell type dependent manner

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Bone Research 2024年第2期12卷 453-468页

作者： Lei Xiong Hao-Han Guo Jin-Xiu Pan Xiao Ren Daehoon Lee Li Chen Lin Mei Wen-Cheng Xiong department of neurosciences School of MedicineCase Western Reserve UniversityClevelandOH 44106USA Louis Stoke VA Medical Center ClevelandOH 44106USA

Wnt/β-catenin signaling is critical for various cellular processes in multiple cell types,including osteoblast(OB)differentiation and *** how Wnt/β-catenin signaling is regulated in OBs remain ***6AP2,an accessory subunit of V-ATPase,plays important roles in multiple cell types/organs and multiple signaling ***,little is known whether and how ATP6AP2 in OBs regulates Wnt/β-catenin signaling and bone *** we provide evidence for ATP6AP2 in the OB-lineage cells to promote OB-mediated bone formation and bone homeostasis selectively in the trabecular bone *** knocking out(CKO)ATP6AP2 in the OB-lineage cells(Atp6ap2^(Ocn-Cre))reduced trabecular,but not cortical,bone formation and bone *** and cellular biochemical studies revealed that LRP6 and N-cadherin were reduced in ATP6AP2-KO BMSCs and OBs,but not *** in vitro and in vivo studies revealed impairedβ-catenin signaling in ATP6AP2-KO BMSCs and OBs,but not osteocytes,under both basal and Wnt stimulated conditions,although LRP5 was decreased in ATP6AP2-KO osteocytes,but not *** cell biological studies uncovered that osteoblastic ATP6AP2 is not required for Wnt3a suppression ofβ-catenin phosphorylation,but necessary for LRP6/β-catenin and N-cadherin/β-catenin protein complex distribution at the cell membrane,thus preventing their *** of activeβ-catenin diminished the OB differentiation deficit in ATP6AP2-KO *** together,these results support the view for ATP6AP2 as a critical regulator of both LRP6 and N-cadherin protein trafficking and stability,and thus regulatingβ-catenin levels,demonstrating an un-recognized function of osteoblastic ATP6AP2 in promoting Wnt/LRP6/β-catenin signaling and trabecular bone formation.

关键词： LRP6 impaired organs

Autolysosomal acidification impairment as a mediator for TNFR1 induced neuronal necroptosis in Alzheimer’s disease

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Neural Regeneration Research 2024年第9期19卷 1869-1870页

作者： Evridiki Asimakidou Richard Reynolds Anna M.Barron Chih Hung Lo department of Clinical neurosciences University of CambridgeCambridgeUK department of Brain Sciences Faculty of MedicineImperial College LondonLondonUK Lee Kong Chian School of Medicine Nanyang Technological UniversitySingaporeSingapore

Neuronal necroptosis-an emerging form of regulated cell death associated with neuroinflammatory signaling:Alzheimer’s disease(AD)is characterized by the presence of extracellular amyloid-β(Aβ)plaques and intracellular tau neurofibrillary tangles as well as progressive neuronal *** evidence has suggested that prolonged neuroinflammation with increased levels of cytokines,arising from neuronal injury,innate immune responses from glial cells,and peripheral inflammation,leads to neuronal death and AD progression.

关键词： Alzheimer death tau Aβ

Biochemical consequences of glucocerebrosidase 1 mutations in Parkinson’s disease

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Neural Regeneration Research 2024年第4期19卷 725-727页

作者： Jeong Hyun Yoon Chiao-Yin Lee Anthony HV Schapira department of Clinical and Movement neurosciences University College London Institute of Neurology Faculty of Medicine Imperial College London Aligning Science Across Parkinson's(ASAP)Collaborative Research Network

Parkinson’s disease(PD,OMIM#168600)is a common neurodegenerative disorder with a global prevalence of approximately 8.5 *** is characterized by four cardinal motor symptoms:bradykinesia,rigidity,resting tremor,and subsequently by postural *** usually involves non-motor symptoms such as rapid eye movement sleep disorder,dementia,anosmia,and autonomic *** gene glucocerebrosidase 1(GBA1),which encodes the lysosomal enzyme glucocerebrosidase(GCase)(IUBMB:EC 3.***.1.45),shows strong linkage with PD;variants of GBA1 are the commonest genetic association with PD(Sidransky et al.,2009).Several mechanisms may underlie the relationship between GBA1 mutations/variants and the molecular pathology of PD(Figure 1A and B).

关键词： cerebro consequences

Combining neural progenitor cell transplant and rehabilitation for enhanced recovery after cervical spinal cord injury

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Neural Regeneration Research 2024年第7期19卷 1433-1434页

作者： Camila M.Freria Paul Lu department of neurosciences University of CaliforniaSan DiegoLa JollaCAUSA Veterans Administration San Diego Healthcare System San DiegoCAUSA

Efforts to promote recovery of function after human spinal cord injury(SCI) will likely require interventions to rgeting the corticospinal tract(CST) motor system:the most important pathway for voluntary motor control in *** system has historically been the most refractory to regenerative efforts after *** "nonregeneration" of the CST changed when robust regeneration of the CST into spared tissue was demonstrated by the inactivation of phosphatase and tensin homolog and delivery of inosine.

关键词： cervical progenitor injury

Epitranscriptomic Regulation of NMDA Receptors Rears its Ugly Head in Chemotherapy-Induced Neuropathic Pain

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Neuroscience Bulletin 2024年第8期40卷 1209-1211页

作者： Wing Lam Yu Gerald W.Zamponi department of Clinical neurosciences Hotchkiss Brain InstituteAlberta Children's Hospital Research InstituteUniversity of CalgaryCalgaryAB T2N 4N1Canada

number of different cancer chemotherapy agents such as cisplatin,oxaliplatin,and paclitaxel can lead to nerve damage,thereby giving rise to neuropathic pain states that present with mechanical and cold allodynia[1].Although these pain conditions often resolve after completion of the chemotherapy,a significant portion of patients exhibit longlasting pain that can persist longer than 12 months with a negative impact on the quality of life of affected individuals[1].

关键词： chemotherapy pain damage

A systematic review of salivary biomarkers in Parkinson's disease

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Neural Regeneration Research 2024年第12期19卷 2613-2625页

作者： Maria Ilenia De Bartolo Daniele Belvisi Romina Mancinelli Matteo Costanzo Claudia Caturano Giorgio Leodori Alfredo Berardelli Giovanni Fabbrini Giorgio Vivacqua IRCCS Neuromed PozzilliItaly department of Human neurosciences Sapienza University of RomeRomeItaly department of Anatomical HistologicalForensic Medicine and Orthopedics SciencesSapienza University of RomeRomeItaly department of Experimental Morphology and Microscopy-Integrated Research Center(PRAAB)-Campus Biomedico University of Rome RomeItaly

The search fo r reliable and easily accessible biomarkers in Parkinson's disease is receiving a growing emphasis,to detect neurodegeneration from the prodromal phase and to enforce disease-modifying *** the need for non-invasively accessible biomarke rs,the majo rity of the studies have pointed to cerebrospinal fluid or peripheral biopsies biomarkers,which require invasive collection *** represents an easily accessible biofluid and an incredibly wide source of molecular *** the present study,after presenting the morphological and biological bases for looking at saliva in the search of biomarkers for Parkinson's disease,we systematically reviewed the results achieved so far in the saliva of different cohorts of Parkinson's disease patients.A comprehensive literature search on PubMed and SCOPUS led to the discovery of *** screening and exclusion,34 relevant articles were derived fo r systematic ***-synuclein,the histopathological hallmark of Parkinson's disease,has been the most investigated Parkinson's disease biomarker in saliva,with oligomeric alphasynuclein consistently found increased in Parkinson's disease patients in comparison to healthy controls,while conflicting results have been reported regarding the levels of total alpha-synuclein and phosphorylated alpha-synuclein,and few studies described an increased oligomeric alpha-synuclein/total alpha-synuclein ratio in Parkinson's *** alpha-synuclein,other biomarkers to rgeting diffe rent molecular pathways have been explored in the saliva of Parkinson's disease patients:total tau,phosphorylated tau,amyloid-β1-42(pathological protein aggregation biomarkers);DJ-1,heme-oxygenase-l,metabolites(alte red energy homeostasis biomarkers);MAPLC-3beta(aberrant proteostasis biomarker);cortisol,tumor necrosis factor-alpha(inflammation biomarkers);DNA methylation,miRNA(DNA/RNA defects biomarkers);acetylcholinesterase activity(synaptic and neuronal network

关键词： alpha-synuclein amyloid-beta autophagy DJ-1 neurodegeneration neuroinflammation Parkinson's disease salivary biomarkers tau

Bioinspired nanotransducers for neuromodulation

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Nano Research 2024年第2期17卷 618-632页

作者： Fan Yang Xiang Wu Sa Cai Guosong Hong department of Materials Science and Engineering Stanford UniversityStanfordCA 94305USA Wu Tsai neurosciences Institute Stanford UniversityStanfordCA 94305USA School of Science Shenzhen Campus of Sun Yat-sen UniversityShenzhen 518107China

The field of neuromodulation has experienced significant advancements in the past decade,owing to breakthroughs in disciplines such as materials science,genetics,bioengineering,photonics,and *** convergence of these fields has resulted in the development of nanotransducers,devices that harness the synergies of these diverse *** nanotransducers,essential for neuromodulation,often draw inspiration from energy conversion processes found in nature for their unique *** this review,we will delve into the latest advancements in wireless neuromodulation facilitated by optical,magnetic,and mechanical *** will examine their working principles,properties,advantages,and limitations in comparison to current methods for deep brain neuromodulation,highlighting the impact of natural systems on their design and ***,we will underscore potential future directions,emphasizing how continued progress in materials science,neuroscience,and bioengineering might expand the horizons of what is achievable with nanotransducer-enabled neuromodulation.

关键词： bioinspired synthesis neuromodulation mechanoluminescence focused ultrasound nanotransducers sono-optogenetics

Ion Channel Dysregulation Following Intracerebral Hemorrhage

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Neuroscience Bulletin 2024年第3期40卷 401-414页

作者： Xiangyu Zhang Yan Zhang Qiuyang Su Yang Liu Zhe Li V.Wee Yong Mengzhou Xue department of Cerebrovascular Diseases The Second Afliated Hospital of Zhengzhou UniversityZhengzhou 450000China Academy of Medical Science Zhengzhou UniversityZhengzhou 450000China Hotchkiss Brain Institute and department of Clinical neurosciences University of CalgaryCalgaryAB T2N 1N4Canada

Injury to the brain after intracerebral hemorrhage(ICH)results from numerous complex cellular *** present,effective therapy for ICH is limited and a better understanding of the mechanisms of brain injury is necessary to improve *** is increasing evidence that ion channel dysregulation occurs at multiple stages in primary and secondary brain injury following *** channels such as TWIK-related K+channel 1,sulfonylurea 1 transient receptor potential melastatin 4 and glutamate-gated channels affect ion homeostasis in *** in turn participate in the formation of brain edema,disruption of the blood-brain barrier,and the generation of *** this review,we summarize the interaction between ions and ion channels,the effects of ion channel dysregulation,and we discuss some therapeutics based on ion-channel modulation following ICH.

关键词： Intracerebral hemorrhage Ion dyshomeostasis Sulfonylurea 1 transient receptor potential melastatin 4 TWIK-related K+channel 1 N-methyl-Daspartate receptor Transient receptor potential vanilloid 4

Metabolic reprogramming of the inflammatory response in the nervous system:the crossover between inflammation and metabolism

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Neural Regeneration Research 2024年第10期19卷 2189-2201页

作者： Jesus Amo-Aparicio Charles A.Dinarello Ruben Lopez-Vales department of Medicine University of ColoradoAuroraCOUSA Institute of neurosciences and Department Cell BiologyPhysiology and ImmunologyUniversitat Autònoma de BarcelonaBellaterraSpain Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas(CIBERNED) Instituto de Salud Carlos ⅢSpain

Metabolism is a fundamental process by which biochemicals are broken down to produce energy(catabolism) or used to build macromolecules(anabolism). Metabolism has received renewed attention as a mechanism that generates molecules that modulate multiple cellular responses. This was first identified in cancer cells as the Warburg effect, but it is also present in immunocompetent cells. Studies have revealed a bidirectional influence of cellular metabolism and immune cell function, highlighting the significance of metabolic reprogramming in immune cell activation and effector functions. Metabolic processes such as glycolysis, oxidative phosphorylation, and fatty acid oxidation have been shown to undergo dynamic changes during immune cell response, facilitating the energetic and biosynthetic demands. This review aims to provide a better understanding of the metabolic reprogramming that occurs in different immune cells upon activation, with a special focus on central nervous system disorders. Understanding the metabolic changes of the immune response not only provides insights into the fundamental mechanisms that regulate immune cell function but also opens new approaches for therapeutic strategies aimed at manipulating the immune system.

关键词： central nervous system fatty acid oxidation glycolysis inflammation macrophage metabolism microglia neurodegeneration oxidative phosphorylation