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store-operated calcium entry in neuroglia

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Neuroscience Bulletin 2014年第1期30卷 125-133页

作者： Alexei Verkhratsky Vladimir Parpura Faculty of Life sciences The University of Manchester Achucarro Center for Neuroscience IKERBASQUE Basque Foundation for Science 48011 Bilbao Spain and Department of Neurosciences University of the Basque Country UPV/EHU Department of Neurobiology Center for Glial Biology in Medicine Atomic Force Microscopy & Nanotechnology aboratories Civitan International Research Center Evelyn F. McKnight Brain Institute University of Alabama Department of Biotechnology University or Rijeka

Neuroglial cells are homeostatic neural cells. Generally, they are electrically non-excitable and their activation is associated with the generation of complex intracellular Ca^2＋ signals that define the ＂Ca^2＋ excitability＂ of glia. In mammalian glial cells the major source of Ca^2＋ for this excitability is the lumen of the endoplasmic reticulum （ER）, which is ultimately （re）filled from the extracellular space. This occurs via store-operated Ca^2＋ entry （sOCE） which is supported by a specific signaling system connecting the ER with plasmalemmal Ca^2＋ entry. Here, emptying of the ER Ca^2＋ store is necessary and sufficient for the activation of sOCE, and without Ca^2＋ influx via sOCE the ER store cannot be refilled. The molecular arrangements underlying sOCE are relatively complex and include plasmalemmal channels, ER Ca^2＋ sensors, such as stromal interaction molecule, and possibly ER Ca^2＋ pumps （of the sERCA type）. There are at least two sets of plasmalemmal channels mediating sOCE, the Ca2＊-release activated channels, Orai, and transient receptor potential （TRP） channels. The molecular identity of neuroglial sOCE has not been yet identified unequivocally. However, it seems that Orai is predominantly expressed in microglia, whereas astrocytes and oligodendrocytes rely more on TRP channels to produce sOCE. In physiological conditions the sOCE pathway is instrumental for the sustained phase of the Ca^2＋ signal observed following stimulation of metabotropic receptors on glial cells.

关键词： calcium signaling astrocyte oligodendrocyte microglia store-operated calcium entry TRP sTIM Orai

Integrated lipidomics and proteomics network analysis highlights lipid and immunity pathways associated with alzheimer's disease

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Translational Neurodegeneration 2020年第3期9卷 458-472页

作者： Jin Xu Giulia Bankov Min Kim Asger Wretlind Jodie Lord Rebecca Green Angela Hodges Abdul Hye Dag Aarsland Latha Velayudhan Richard J.B.Dobson Petroula Proitsi Cristina Legido-Quigley on behalf of the AddNeuroMed Consortium Institute of Pharmaceutical science King's College LondonLondonUK. Institute of Psychiatry Psychology&NeuroscienceKing's College LondonLondonUK. steno Diabetes Center Copenhagen GentofteDenmark Center for Age Related Medicine Stavanger University HospitalStavangerNorway 不详

Background:There is an urgent need to understand the pathways and processes underlying alzheimer's disease(AD)for early diagnosis and development of effective *** study was aimed to investigate alzheimer's dementia using an unsupervised lipid,protein and gene multi-omics integrative ***:A lipidomics dataset comprising 185 AD patients,40 mild cognitive impairment(MCI)individuals and 185 controls,and two proteomics datasets(295 AD,159 MCI and 197 controls)were used for weighted gene CO-expression network analyses(WGCNA).Correlations of modules created within each modality with clinical AD diagnosis,brain atrophy measures and disease progression,as well as their correlations with each other,were *** ontology enrichment analysis was employed to examine the biological processes and molecular and cellular functions of protein modules associated with AD *** species were annotated in the lipid modules associated with AD *** associations between established AD risk loci and the lipid/protein modules that showed high correlation with AD phenotypes were also ***:Five of the 20 identified lipid modules and five of the 17 identified protein modules were correlated with clinical AD diagnosis,brain atrophy measures and disease *** lipid modules comprising phospholipids,triglycerides,sphingolipids and cholesterol esters were correlated with AD risk loci involved in immune response and lipid *** five protein modules involved in positive regulation of cytokine production,neutrophil-mediated immunity,and humoral immune responses were correlated with AD risk loci involved in immune and complement systems and in lipid metabolism(the APOE ε4 genotype).Conclusions:Modules of tightly regulated lipids and proteins,drivers in lipid homeostasis and innate immunity,are strongly associated with AD phenotypes.

关键词： alzheimer's disease Dementia Brain atrophy sMRI Rate of cognitive decline Lipidomics Proteomics AD risk loci WGCNA

socio-economic and Psychosocial Determinants of smoking and Passive smoking in Older Adults

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Biomedical and Environmental sciences 2013年第6期26卷 453-467页

作者： ZHANG Dong Mei HU Zhi ORTON sophie WANG Jia Ji ZHENG Jian Zhong QIN Xia CHEN Ruo Ling school of Health Administration Anhui Medical University Centre for Health and social Care Improvement School of Health and WellbeingUniversity of Wolverhampton Division of Primary Care University of Nottingham school of Public Health and General Practice Guangzhou Medical University Department of Health Administration and service Shanxi Medical University Division of Health and social Care research King's College London

Objective To determine the associations of socio-economic and psychosocial factors with active and passive smoking in older adults. Methods Using a standard interview method, we examined random samples of 6071 people aged 〉 60 years in 5 provinces of China during 2007-2009. Results World age-standardised prevalence for current and former smoking in men was 45.6% and 20.5%, and in women 11.1% and 4.5%. Current smoking reduced with older age but increased with men, low socioeconomic status （sEs）, alcohol drinking, being never-married, pessimistic and depressive syndromes. Former smoking was associated with men, secondary school education, a middle-high income, being a businessman, being widowed, less frequencies of visiting children/relatives and friends, and worrying about children. Among 3774 never-smokers, the prevalence of passive smoking was 31.5%, and the risk increased with women, low sEs, alcohol drinking, being married, having a religious believe, and daily visiting children/relatives. There were sex differences in the associations, and an interaction effect of education and income on smoking and passive smoking. Conclusion Older Chinese had a higher level of smoking and passive smoking than those in high income countries, reflecting China＇s failures in controlling smoking. The associations with low sEs and different psychosocial aspects and sex differences suggest preventative strategies for active and passive smoking.

关键词： smoking second-hand smoke socio-economic Psychosocial Older adults

Observation of an α-synuclein liquid droplet state and its maturation into Lewy body-like assemblies

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Journal of Molecular Cell Biology 2021年第4期13卷 282-294页

作者： Maarten C.Hardenberg Tessa sinnige sam Casford samuel T.Dada Chetan Poudel Elizabeth A.Robinson Monika Fuxreiter Clemens F.Kaminksi Gabriele s.Kaminski schierle Ellen A.A.Nollen Christopher M.Dobson Michele Vendruscolo Centre for Misfolding Diseases Department of ChemistryUniversity of CambridgeCambridge CB21EWUK Department of Chemical Engineering and Biotechnology University of CambridgeCambridge CB3 OASUK MTA-DE Laboratory of Protein Dynamics Department of Biochemistry and Molecular BiologyUniversity of DebrecenHungary European research Institute for the Biology of Aging University Medical Center GroningenUniversity of GroningenGroningen 9713 AVThe Netherlands Present address Bijvoet Centre for Biomolecular research Department of ChemistryUtrecht UniversityUtrecht 3584 CHThe Netherlands

Misfoldedα-synudein is a major component of Lewy bodies,which are a hallmark of Parkinson's disease(PD).A large body of evidence shows thatα-synuclein can aggregate into amyloid fibrils,but the relationship between a-synuclein self-assembly and Lewy body formation remains ***,we show,both in vitro and in a Caenorhabditis elegans model of PD,thatα-synuclein undergoes liquid-liquid phase separation by forming a liquid droplet state,which converts into an amyloid-rich hydrogel with Lewy-body-like *** maturation process towards the amyloid state is delayed in the presence of model synaptic vesicles in *** together,these results suggest that the formation of Lewy bodies may be linked to the arrested maturation ofα-synuclein condensates in the presence of lipids and other cellular components.

关键词： α-synuclein,liquid-liquid phase separation,Parkinson's disease

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Neural Regeneration research 2018年第3期13卷 419-420页

作者： Linyu Wei sharifah Alawieyah syed Mortadza Lin-Hua Jiang sino-uk Joint Laboratory of Brain Function and Injury of Henan Province and Department of Physiology and Neurobiology Xinxiang Medical University school of Biomedical sciences Faculty of Biological Sciences University of Leeds

alzheimer’s disease （AD） is an age-related eurodegenerative disease that represents the most common cause of dementia among the elderly people. With the increasingly aging population, AD has presented an overwhelming healthcare challenge to modern society; the World alzheimer Report 2015 has estimated that 46.8 million people worldwide lived with dementia in 2015 and this number will rise to 74.7 million in 2030 and that the total cost of dementia was 818 billion in Us$ in 2015 and will reach two trillion in 2030. Post-mortem studies have identified two histopathological hallmarks in the brains of AD patients; extracellular senile plaque with elevated deposition of amyloid β （Aβ） peptides, and intracellular neurofibrillary tangle composed of hyper-phosphorylated microtubule-associated protein ***, progressive neuronal loss within the cerebral cortex and hippocampus regions of the brain leads to irreversible decline in, and eventually complete loss of, memory and other cognitive functions that afflict AD patients. The widely-accepted amyloid cascade hypothesis for AD pathogenesis holds that accumulation and aggregation of neurotoxic Aβ peptides, due to imbalance of their generation and clearance as a result of changes in genetic makeup, aging and/or exposure to environmental risk factors, is a major and early trigger of AD. This hypothesis has continuously gained support by preclinical and clinical studies （selkoe and Hardy, 2016）. However, the intensive and costly drug discovery efforts over the past decades based on such a hypothesis have proved extremely frustrating in developing effective therapeutics to treat or slow down the progress of AD, highlighting the need for more research to improve our understanding towards the cellular and molecular mechanisms by which Aβ peptides bring about neurotoxicity and cognitive dysfunction.

关键词： induced neuroinflammation Melastatin-related transient receptor potential 2 channel in A implications to alzheimer’s disease mechanism and development of therapeutics

Toward a biomarker panel measured in CNs-originating extracellular vesicles for improved differential diagnosis of Parkinson’s disease and multiple system atrophy

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Translational Neurodegeneration 2023年第1期12卷 677-680页

作者： Hash Brown Taha simon Hornung suman Dutta Leony Fenwick Otmane Lahgui Kathryn Howe Nour Elabed Irish del Rosario Darice Y.Wong Aline Duarte Folle Daniela Markovic Jose-Alberto Palma Un Jung Kang Roy N.Alcalay Miriam sklerov Horacio Kaufmann Brent L.Fogel Jeff M.Bronstein Beate Ritz Gal Bitan Department of Neurology David Geffen School of MedicineUniversity of California Los AngelesLos AngelesCA 90095USA Department of Integrative Biology and Physiology University of California Los AngelesLos AngelesCA 90095USA Department of Epidemiology Fielding School of Public HealthUniversity of California Los AngelesLos AngelesCA 90095USA Department of Medicine statistics Core Division of General Internal Medicine and Health Services ResearchUniversity of California Los AngelesLos AngelesCA 90095USA Department of Neurology Dysautonomia CenterNew York University School of MedicineNew YorkNY 10016USA Department of Neurology Taub Institute for Research on Alzheimer’s Disease and the Aging BrainColumbia UniversityNew YorkNY 10032USA Department of Neurology Tel Aviv Sourasky Medical CenterTel AvivIsrael Department of Neurology University of North Carolina School of MedicineChapel HillNC 27599USA Department of Neurology The Marlene and Paolo Fresco Institute for Parkinson’s and Movement DisordersNew York University School of MedicineNew YorkNY 10016USA Department of Human Genetics David Geffen School of MedicineUniversity of California Los AngelesLos AngelesCA 90095USA UCLA Clinical Neurogenomics research Center David Geffen School of MedicineUniversity of CaliforniaLos AngelesCA 90095USA Brain research Institute University of CaliforniaLos AngelesCA 90095USA Molecular Biology Institute University of California Los AngelesLos AngelesCA 90095USA Present Address:Division of Peptide Biochemistry TUM School of Life SciencesTechnical University of Munich85354 FreisingGermany

synucleinopathies are neurodegenerative diseases char-acterized by accumulation of misfoldedα-synuclein(α-syn)inclusions in neuronal and/or glial *** differences in the underlying pathophysiology,synucle-inopathies ... 详细信息

关键词： diagnosis atrophy diseases

Clinical management of cerebral small vessel disease:a call for a holistic approach

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Chinese Medical Journal 2021年第2期134卷 127-142页

作者： Una Clancy Jason P.Appleton Carmen Arteaga Fergus N.Doubal Philip M.Bath Joanna M.Wardlaw Centre for Clinical Brain sciences and UK Dementia Research InstituteUniversity of EdinburghChancellor's Building49 Little France CrescentEdinburghEH164SPUK stroke Trials Unit Division of Clinical NeuroscienceUniversity of NottinghamNottingham NG51PBUK stroke University Hospitals Birmingham NHS Foundation TrustMindelsohn WayEdgbastonBirmingham B152GWUK stroke Nottingham University Hospitals NHS TrustNottingham NG51PBUK.

Cerebral small vessel disease(sVD)is a common global brain disease that causes cognitive impairment,ischemic or hemorrhagic stroke,problems with mobility,and neuropsychiatric *** brain damage,seen as focal white and deep grey matter lesions on brain magnetic resonance imaging(MRI)or computed tomography(CT),typically accumulates"covertly"and may reach an advanced state before being detected incidentally on brain scanning or causing *** have typically presented to different clinical services or been recruited into research focused on one clinical manifestation,perhaps explaining a lack of awareness,until recently,of the full range and complexity of *** this review,we discuss the varied clinical presentations,established and emerging risk factors,relationship to sVD features on MRI or CT,and the current state of knowledge on the effectiveness of a wide range of pharmacological and lifestyle *** core message is that effective assessment and clinical management of patients with sVD,as well as future advances in diagnosis,care,and treatment,will require a more"joined-up"’*** approach should integrate clinical expertise in stroke neurology,cognitive,and physical *** requires more clinical trials in order to improve pharmacological interventions,lifestyle and dietary modifications.A deeper understanding of the pathophysiology of sVD is required to steer the identification of novel *** essential prerequisite to accelerating clinical trials is to improve the consistency,and standardization of clinical,cognitive and neuroimaging endpoints.

关键词： Dementia Magnetic resonance imaging Mild cognitive impairment Risk factors small vessel disease stroke symptoms Treatment

structures of α-synuclein filaments from human brains with Lewy pathology

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四川生理科学杂志 2022年第9期44卷 1669-1669页

作者： Yang Yang Medical research Council Laboratory of Molecular Biology Cambridge UK Thermo Fisher scientific Eindhoven The Netherlands Department of Pathology and Laboratory Medicine Indiana University School of Medicine Indianapolis IN USA Department of Clinical and Movement Neurosciences Queen Square Institute of Neurology University College London London UK Queen square Brain Bank for Neurological Disorders Institute of Neurology University College London London UK Department of Neurodegenerative Disease Queen Square Institute of Neurology University College London London UK Department of Neuropathology Metropolitan Institute of Gerontology Tokyo Japan Department of Medical and Molecular Genetics Indiana University School of Medicine Indianapolis IN USA Division of Neurology Sagamihara National Hospital Sagamihara Japan Molecular research Centre for Children’s Mental Development United School of Child Development University of Osaka Osaka Japan Department of Brain and Neurosciences Metropolitan Institute of Medical Science Tokyo Japan

Parkinson's disease(PD)is the most common movement disorder,with resting tremor,rigidity,bradykinesia and postural instability being major symptoms(1).Neuropathologically,it is characterised by the presence of abundant filamentous inclusions ofα-synuclein in the form of Lewy bodies and Lewy neurites in some brain cells,including dopaminergic nerve cells of the substantia nigra(2).PD is increasingly recognised as a multisystem disorder,with cognitive decline being one of its most common non-motor *** patients with PD develop dementia more than 10 years after diagnosis(3).PD dementia(PDD)is clinically and neuropathologically similar to dementia with Lewy bodies(DLB),which is diagnosed when cognitive impairment precedes parkinsonian motor signs or begins within one year from their onset(4).In PDD,cognitive impairment develops in the setting of well-established *** PD and DLB,multiple system atrophy(MsA)is the third major synucleinopathy(5).It is characterised by the presence of abundant filamentousα-synuclein inclusions in brain cells,especially oligodendrocytes(Papp�Lantos bodies).We previously reported the electron cryo-microscopy(cryo-EM)structures of two types ofα-synuclein filaments extracted from the brains of individuals with MsA(6).Each filament type is made of two different *** we report that the cryo-EM structures ofα-synuclein filaments from the brains of individuals with PD,PDD and DLB are made of a single protofilament(Lewy fold)that is markedly different from the protofilaments of *** findings establish the existence of distinct molecular conformers of assembledα-synuclein in neurodegenerative disease.

关键词： markedly diagnosis rigidity