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Exercised blood plasma promotes hippocampal neurogenesis in the alzheimer's disease rat brain

Journal of sport and Health science 2024年第2期13卷 245-255页

作者： Cecilie skarstad Norevik Aleksi M.Huuha Ragnhild N.RФsbjФrgen Linda Hildegard Bergersen kamilla Jacobsen Rodrigo Miguel-dos-santos Liv Ryan Belma skender Jose Bianco N.Moreira Asgeir kobro-Flatmoen Menno P.Witter Nathan scrimgeour Atefe R.Tari Cardiac Exercise Research group(CERg) Department of Circulation and Medical ImagingNorwegian University of Science and Technology7491TrondheimNorway Department of Neurology and Clinical Neurophysiology St.Olavs University Hospital7030TrondheimNorway Institute of Oral Biology University of Oslo0372OsloNorway Department of Physiology Federal University of SergipeS~ao Cristov~ao49100-000SergipeBrazil centre of Molecular Inflammation Research Department of Clinical and Molecular MedicineNorwegian University of Science and Technology7491TrondheimNorway kavli Institute for systems Neuroscience Centre for Neural Computationand Egil and Pauline Braathen and Fred Kavli Centre for Cortical MicrocircuitsNorwegian University of Science and Technology7030TrondheimNorway k.g.jebsen centre for alzheimer’s disease Norwegian University of Science and Technology7030TrondheimNorway

Background:Exercise training promotes brain plasticity and is associated with protection against cognitive impairment and alzheimer’s disease(AD).These beneficial effects may be partly mediated by blood-borne *** we used an in vitro model of AD to investigate effects of blood plasma from exercise-trained donors on neuronal viability,and an in vivo rat model of AD to test whether such plasma impacts cognitive function,amyloid pathology,and ***:Mouse hippocampal neuronal cells were exposed to AD-like stress using amyloid-βand treated with plasma collected from human male donors 3 h after a single bout of high-intensity *** in vivo studies,blood was collected from exercise-trained young male Wistar rats(high-intensity intervals 5 days/week for 6 weeks).Transgenic AD rats(Mcgill-R-Thyl-APP)were inj ected 5 times/fortnight for 6 weeks at2 months or 5 months of age with either(a)plasma from the exercise-trained rats,(b)plasma from sedentary rats,or(c)*** function,amyloid plaque pathology,and neurogenesis were *** plasma used for the treatment was analyzed for 23 ***:Plasma from exercised donors enhanced cell viability by 44.1%(p=0.032)and reduced atrophy by 50.0%(psed plasma treatment did not alter cognitive function or amyloid plaque pathology but did increase hippocampal neurogenesis by~3 fold,regardless of pathological stage,when compared to saline-treated *** of 7 cytokines were significantly reduced in exercised plasma compared to sedentary ***:Our proof-of-concept study demonstrates that plasma from exercise-trained donors can protect neuronal cells in culture and promote adult hippocampal neurogenesis in the AD rat *** effect may be partly due to reduced pro-inflammatory signaling molecules in exercised plasma.

关键词： Cytokines High-intensity interval training Inflammation Neurons Plasma transfusion

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CHIT1-positive microglia act as culprits for spinal motor neuron aging

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science China(Life sciences) 2024年第4期67卷 847-848页

作者： Zhao Wang Wantong Cai Weihong song Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine Vision and Brain Health)Institute of AgingKey Laboratory of Alzheimer’s Disease of Zhejiang ProvinceThe Second Affiliated HospitalWenzhou Medical UniversityWenzhou 325035China

Aging is one of the primary factors in spinal cord-associated disorders(Roberts,1990).However,the effects of aging on the spinal cord and the age-specific mechanisms underlying this relationship remain *** neurons(MNs... 详细信息

关键词： aging Roberts positive

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Circadian rhythm disruption and retinal dysfunction:a bidirectional link in alzheimer’s disease?

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Neural Regeneration Research 2024年第9期19卷 1967-1972页

作者： Laura Carrero DesireéAntequera Cristina Municio Eva Carro group of Neurodegenerative diseases Hospital Universitario 12 de Octubre Research Institute(imas12)MadridSpainNetwork Center for Biomedical Research in Neurodegenerative Diseases(CIBERNED)ISCIIIMadridSpain PhD Program in Neuroscience Autonoma de Madrid UniversityMadridSpain Neurobiology of alzheimer’s disease Unit Functional Unit for Research into Chronic DiseasesInstituto de Salud Carlos IIIMadridSpainNetwork Centre for Biomedical Research in Neurodegenerative Diseases(CIBERNED)ISCIIIMadridSpain

Dysfunction in circadian rhythms is a common occurrence in patients with alzheimer’s disease.A predominant function of the retina is circadian synchronization,carrying information to the brain through the retinohypothalamic tract,which projects to the suprachiasmatic ***,alzheimer’s disease hallmarks,including amyloid-β,are present in the retinas of alzheimer’s disease patients,followed/associated by structural and functional ***,the mechanistic link between circadian dysfunction and the pathological changes affecting the retina in alzheimer’s disease is not fully understood,although some studies point to the possibility that retinal dysfunction could be considered an early pathological process that directly modulates the circadian rhythm.

关键词： alzheimer’s disease amyloid circadian rhythm neurodegeneration retina

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A commentary of“Unravelling the mechanisms of human genomic‘dark matter’in driving aging”:Top 10 scientific Advances of 2023,China

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Fundamental Research 2024年第3期4卷 693-694页

作者： Zhao Wang Chenglin guo Weihong song Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine Vision and Brain Health)Institute of AgingKey Laboratory of Alzheimer's Disease of Zhejiang Provincethe Second Affiliated HospitalWenzhou Medical UniversityWenzhou 325035China

Aging is related to physiological decline and the development of chronic diseases,yet molecular changes and mechanisms underlying the aging process remain *** certain“dark matter”,such as transposable elements with viral origins in the genome,be activated and participate in the aging process?Excitingly,a study by Liu and colleagues revealed that the reactivation of endogenous retroviruses(ERVs)during aging enhances senescence[1].By using cross-species models and multiple techniques,the team uncovered the unusual role of ERV reactivation as a hallmark and driver of *** authors identified that ERV expression is associated with cellular and tissue aging(Fig.1).They found that the accumulation of human ERV group k(HERVk)retrovirus-like particles(RVLPs)mediates aging-promoting effects in recipient cells.

关键词： aging mechanisms driving

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FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

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Neural Regeneration Research 2025年第7期20卷 2068-2083页

作者： Jing Yao Yuan Li Xi Liu Wenping Liang Yu Li Liyong Wu Zhe Wang Weihong song The National Clinical Research Center for geriatric disease Xuanwu HospitalCapital Medical UniversityBeijingChina Department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina Department of Neurosurgery Xuanwu HospitalCapital Medical UniversityBeijingChina Department of Pediatrics The Second Affiliated Hospital and Yuying Children’s HospitalKey Laboratory of Alzheimer’s Disease of Zhejiang ProvinceInstitute of AgingWenzhou Medical UniversityWenzhouZhejiang ProvinceChina Oujiang Laboratory(Zhejiang Laboratory for Regenerative Medicine Visionand Brain Health)WenzhouZhejiang ProvinceChina

alzheimer's disease is characterized by deposition of amyloid-β,which forms extracellular neuritic plaques,and accumulation of hyperphosphorylated tau,which aggregates to form intraneuronal neurofibrillary tangles,in the *** NLRP3 inflammasome may play a role in the transition from amyloid-βdeposition to tau phosphorylation and *** NLRP3 is primarily found in brain microglia,and tau is predominantly located in neurons,it has been suggested that NLRP3 expressed by microglia indirectly triggers tau phosphorylation by upregulating the expression of pro-inflammatory ***,we found that neurons also express NLRP3 in vitro and in vivo,and that neuronal NLRP3 regulates tau *** biochemical methods,we mapped the minimal NLRP3 promoter and identified FUBP3 as a transcription factor regulating NLRP3 expression in *** primary neurons and the neuroblastoma cell line Neuro2A,FUBP3 is required for endogenous NLRP3 expression and tau phosphorylation only when amyloid-βis *** the brains of aged wild-type mice and a mouse model of alzheimer's disease,FUBP3 expression was markedly increased in cortical *** analysis suggested that FUBP3 plays a role in neuron-mediated immune *** also found that FUBP3 trimmed the 5′end of DNA fragments that it bound,implying that FUBP3 functions in stress-induced *** findings suggest that neuronal NLRP3 may be more directly involved in the amyloid-β-to–phospho-tau transition than microglial NLRP3,and that amyloid-βfundamentally alters the regulatory mechanism of NLRP3 expression in *** that FUBP3 was only expressed at low levels in young wild-type mice and was strongly upregulated in the brains of aged mice and alzheimer's disease mice,FUBP3 could be a safe therapeutic target for preventing alzheimer's disease progression.

关键词： 5′end trimming alzheimer's disease amyloid-beta amyloid-β-dependent transcription FUBP3 inflammasome inflammation neuron NLRP3 tau transcription factor

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soluble alpha-synuclein post-translational modifications:unexpected regulators of pathological alpha-synuclein amplification

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Neural Regeneration Research 2024年第5期19卷 959-960页

作者： simran kapila Yuhan sun Chao Peng shujing Zhang Department of Neurology David Geffen School of MedicineUniversity of CaliforniaLos AngelesCAUSA Molecular Biology Institute Brain Research InstituteMary S.Easton Center for Alzheimer’s ResearchUniversity of CaliforniaLos AngelesCAUSA

The build-up of misfoldedα-synuclein(α-syn)in the central nervous system is the pathological hallmark of a number of neurodegenerative diseases that are known asα-*** include Parkinson’s disease(PD),Parkinson’s disease with dementia(PDD),dementia with Lewy body(LB),multiple system atrophy(MsA),and a subset of alzheimer’s *** evidence underscores that the intercellular transmission and amplification of pathologicalα-syn are critical processes underlying the progression ofα-synucleinopathies(Peng et al.,2020),and as such,the study of these processes could lead to the identification of promising therapeutics to mitigate disease *** previous studies have focused solely on pathological seeds in relation to disease progression.

关键词： pathological diseases

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sIL1 improves cognitive impairment in APP23/Ps45 mice by regulating amyloid precursor protein processing and Aβ generation

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Zoological Research 2024年第4期45卷 845-856页

作者： Qunxian Wang Yanshuang Jiang Zijun Meng Xiangjun Dong Dongjie Hu Liangye Ji Weihui Zhou Weihong song Chongqing key Laboratory of Child Neurodevelopment and Cognitive Disorders Ministry of Education Key Laboratory of Child Development and DisordersNational Clinical Research Center for Child Health and DisordersChina International Science and Technology Cooperation Base of Child Development and Critical DisordersChildren's Hospital of Chongqing Medical UniversityChongqing 400000China second Affiliated Hospital and Yuying Children’s Hospital Institute of AgingKey Laboratory of Alzheimer’s Disease of Zhejiang ProvinceWenzhou Medical UniversityWenzhouZhejiang 325000China Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine Vision and Brain Health)WenzhouZhejiang 325001China

sIL1,an endoplasmic reticulum(ER)-resident protein,is reported to play a protective role in alzheimer’s disease(AD).However,the effect of sIL1 on amyloid precursor protein(APP)processing remains *** this study,the role of sIL1 in APP processing was explored both in vitro and in *** the in vitro experiment,sIL1 was either overexpressed or knocked down in cells stably expressing the human swedish mutant *** the in vivo experiment,AAV-sIL1-EgFP or AAV-EgFP was microinjected into APP23/Ps45 mice and their wild-type *** blotting(WB),immunohistochemistry,RNA sequencing(RNA-seq),and behavioral experiments were performed to evaluate the relevant *** indicated that sIL1 expression decreased in APP23/Ps45 *** of sIL1 significantly decreased the protein levels of APP,presenilin-1(Ps1),and C-terminal fragments(CTFs)of APP in vivo and in ***,knockdown of sIL1 increased the protein levels of APP,β-site APP cleavage enzyme 1(BACE1),Ps1,and CTFs,as well as APP mRNA expression in 2EB2 ***,sIL1 overexpression reduced the number of senile plaques in APP23/Ps45 ***,Y-maze and Morris Water maze tests demonstrated that sIL1 overexpression improved cognitive impairment in APP23/Ps45 *** findings indicate that sIL1 improves cognitive impairment in APP23/Ps45 mice by inhibiting APP amyloidogenic processing and suggest that sIL1 is a potential therapeutic target for AD by modulating APP processing.

关键词： alzheimer’s disease sIL1 APP processing Cognitive impairment

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The role of inflammasomes in human diseases and their potential as therapeutic targets

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signal Transduction and Targeted Therapy 2024年第2期9卷 479-508页

作者： Jing Yao keenan sterling Zhe Wang Yun Zhang Weihong song The National Clinical Research Center for geriatric disease Xuanwu HospitalCapital Medical UniversityBeijing 100053China Townsend Family Laboratories Department of PsychiatryBrain Research CenterThe University of British Columbia2255 Wesbrook MallVancouverBC V6T 1Z3Canada key Laboratory of Neurodegenerative diseases Ministry of EducationBeijingP.R.China Zhejiang Clinical Research Center for Mental Disorders Key Laboratory of Alzheimer’s Disease of Zhejiang ProvinceSchool of Mental Health and The Affiliated Kangning HospitalInstitute of AgingWenzhou Medical UniversityWenzhouZhejiang 325000China Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine Vision and Brain Health)WenzhouZhejiang 325000China

Inflammasomes are large protein complexes that play a major role in sensing inflammatory signals and triggering the innate immune *** inflammasome complex has three major components:an upstream sensor molecule that is connected to a downstream effector protein such as caspase-1 through the adapter protein *** formation typically occurs in response to infectious agents or cellular *** active inflammasome then triggers caspase-1 activation,followed by the secretion of pro-inflammatory cytokines and pyroptotic cell *** inflammasome activation and activity contribute to the development of diabetes,cancer,and several cardiovascular and neurodegenerative *** a result,recent research has increasingly focused on investigating the mechanisms that regulate inflammasome assembly and activation,as well as the potential of targeting inflammasomes to treat various *** clinical trials are currently underway to evaluate the therapeutic potential of several distinct inflammasome-targeting ***,understanding how different inflammasomes contribute to disease pathology may have significant implications for developing novel therapeutic *** this article,we provide a summary of the biological and pathological roles of inflammasomes in health and *** also highlight key evidence that suggests targeting inflammasomes could be a novel strategy for developing new disease-modifying therapies that may be effective in several conditions.

关键词： inflam therapeutic potential

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XBP1 splicing contributes to endoplasmic reticulum stress-induced human islet amyloid polypeptide up-regulation

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genes & diseases 2024年第5期11卷 350-359页

作者： Yun Zhang susan Lin Jing Yao Wantong Cai Huaqiu Chen Ailikemu Aierken Zhe Wang Weihong song National Clinical Research Center for geriatric Disorders Xuanwu HospitalCapital Medical UniversityBeijing 100053China Townsend Family Laboratories Department of PsychiatryThe University of British Columbia2255 Wesbrook MallVancouverBC V6T 1Z3Canada Institute of Aging Key Laboratory of Alzheimer’s Disease of Zhejiang ProvinceSchool of Mental Health and the Affiliated Kangning HospitalWenzhou Medical UniversityWenzhouZhejiang 325000China Oujiang Laboratory(Zhejiang Lab for Regenerative Medicine Vision and Brain Health)WenzhouZhejiang 325001China

As a pathological hallmark of type 2 diabetes mellitus(T2DM),islet amyloid is formed by the aggregation of islet amyloid polypeptide(IAPP).Endoplasmic reticulum(ER)stress interacts with IAPP aggregates and has been implicated in the pathogenesis of *** examine the role of ER stress in T2DM,we cloned the hIAPP promoter and analyzed its promoter activity in human *** found that ER stress significantly enhanced hIAPP promoter activity and expression in human b-cells via triggering X-box binding protein 1(XBP1)*** identified a binding site of XBP1 in the hIAPP *** of this binding site by substitution or deletion mutagenesis significantly diminished the effects of ER stress on hIAPP promoter *** of XBP splicing by MkC3946 treatment inhibited ER stress-induced hIAPP up-regulation and improved human b-cell survival and *** study uncovers a link between ER stress and IAPP at the transcriptional level and may provide novel insights into the role of ER stress in IAPP cytotoxicity and the pathogenesis of T2DM.

关键词： b-cell function Endoplasmic reticulum stress Islet amyloid polypeptide Type 2 diabetes mellitus XBP1

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Treadmill training in Parkinson's disease:possible role of prefrontal modifications in the improved cortical-subcortical network function

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Neural Regeneration Research 2024年第2期19卷 407-408页

作者： Hao Ding Amgad Droby Abdul Rauf Anwar Jeffrey M.Hausdorff Bahman Nasseroleslami Anat Mirelman Inbal Maidan Muthuraman Muthuraman Department of Neurology University Hospital WürzburgWürzburgGermany Academic Unit of Neurology Trinity College Dublinthe University of DublinDublinIreland Department of Neurology Sackler Faculty of MedicineTel Aviv UniversityTel AvivIsrael sagol school of Neuroscience Tel Aviv UniversityTel AvivIsrael Biomedical Engineering centre UET Lahore(KSK Campus)LahorePakistan Laboratory for Early Markers of Neurodegeneration(LEMON) Center for the Study of MovementCognitionand Mobility(CMCM)Neurological InstituteTel Aviv Sourasky Medical CenterTel AvivIsrael Department of Physical Therapy Sackler Faculty of MedicineTel Aviv UniversityTel AvivIsrael Rush alzheimer’s disease Center and Department of Orthopaedic surgery Rush University Medical CenterChicagoILUSA

Parkinson’s disease(PD)is a complex neurodegenerative disorder characterized by a range of motor symptoms such as bradykinesia,resting tremor,rigidity,and postural instability,as well as non-motor symptoms,such as de... 详细信息

关键词： rigidity fatigue

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