Decades of research in glial biology have investigated mechanisms of neuro-glial interplay,demonstrating that neurons and glia intimately cooperate for energy metabolism in the central nervous system(CNS)(Magistretti ...Decades of research in glial biology have investigated mechanisms of neuro-glial interplay,demonstrating that neurons and glia intimately cooperate for energy metabolism in the central nervous system(CNS)(Magistretti and Allaman,2018).展开更多
The main pathological feature of the neurodegenerative diseases is represented by neuronal death that represents the final step of a cascade of adverse/hostile events.Early in the neurodegenerative process,glial cells...The main pathological feature of the neurodegenerative diseases is represented by neuronal death that represents the final step of a cascade of adverse/hostile events.Early in the neurodegenerative process,glial cells (including astrocytes,microglial cells,and oligodendrocytes) activate and trigger an insidious neuroinflammatory reaction,metabolic decay,blood brain barrier dysfunction and energy impairment,boosting neuronal death.How these mechanisms might induce selective neuronal death in specific brain areas are far from being elucidated.The last two decades of neurobiological studies have provided evidence of the main role of glial cells in most of the processes of the central nervous system,from development to synaptogenesis,neuronal homeostasis and integration into,highly specific neuro-glial networks.In this mini-review,we moved from in vitro and in vivo models of neurodegeneration to analyze the putative role of glial cells in the early mechanisms of neurodegeneration.We report changes of transcriptional,genetic,morphological,and metabolic activity in astrocytes and microglial cells in specific brain areas before neuronal degeneration,providing evidence in experimental models of neurodegenerative disorders,including Parkinson’s and Alzheimer’s diseases.Understanding these mechanisms might increase the insight of these processes and pave the way for new specific glia-targeted therapeutic strategies for neurodegenerative disorders.展开更多
The recognition that neurogenesis does not stop with adolescence has spun off research towards the reduction of brain disorders by enhancing brain regeneration. Adult neurogenesis is one of the tougher problems of dev...The recognition that neurogenesis does not stop with adolescence has spun off research towards the reduction of brain disorders by enhancing brain regeneration. Adult neurogenesis is one of the tougher problems of developmental biology as it requires the generation of complex intracellular and pericellular anatomies, amidst the danger of neuroinflammation. We here review how a multitude of regulatory pathways optimized for early neurogenesis has to be revamped into a new choreography of time dependencies. Distinct pathways need to be regulated, ranging from neural growth factor induced differentiation to mitochondrial bioenergetics, reactive oxygen metabolism, and apoptosis. Requiring much Gibbs energy consumption, brain depends on aerobic energy metabolism, hence on mitochondrial activity. Mitochondrial fission and fusion, movement and perhaps even mitoptosis, thereby come into play. All these network processes are interlinked and involve a plethora of molecules. We recommend a deep thinking approach to adult neurobiology.展开更多
Who drew the borders between central and peripheral nervous sys tem? A complex question but a simple answer. Human anatomy and clinical neurology need to differentiate peripheral nerves from central nervous system ...Who drew the borders between central and peripheral nervous sys tem? A complex question but a simple answer. Human anatomy and clinical neurology need to differentiate peripheral nerves from central nervous system (CNS), peripheral or central disorders, respectively. However, there are no anatomical and functional clefts between peripheral axons and central synaps- es. There is a direct continuity from the periphery to the center, from the receptor to the sensory neuron, from the spinal motor neuron to the muscle, just the neuromuscular junction.展开更多
基金supported by grants from Regione Campania (L.R. N.5 Bando 2003 to MP)the Italian Minister of Research and University (PRIN 2007 to MP,PRIN 2017-2017XJ38A4_003 to GC and MP)UNIMIB (Progetto ID 2019-ATESP-0001 and Progetto ID 2018-CONV-0056 to AV)。
文摘Decades of research in glial biology have investigated mechanisms of neuro-glial interplay,demonstrating that neurons and glia intimately cooperate for energy metabolism in the central nervous system(CNS)(Magistretti and Allaman,2018).
基金supported by grants from Regione Campania(L.R.N.5 Bando 2003,to MP)the Italian Minister of Research and University(PRIN 2007,to MP+1 种基金 PRIN 2017,to GC and MP)UNIMIB(Progetto ID 2019-ATESP-0001 and Progetto ID 2018-CONV-0056,to AV)
文摘The main pathological feature of the neurodegenerative diseases is represented by neuronal death that represents the final step of a cascade of adverse/hostile events.Early in the neurodegenerative process,glial cells (including astrocytes,microglial cells,and oligodendrocytes) activate and trigger an insidious neuroinflammatory reaction,metabolic decay,blood brain barrier dysfunction and energy impairment,boosting neuronal death.How these mechanisms might induce selective neuronal death in specific brain areas are far from being elucidated.The last two decades of neurobiological studies have provided evidence of the main role of glial cells in most of the processes of the central nervous system,from development to synaptogenesis,neuronal homeostasis and integration into,highly specific neuro-glial networks.In this mini-review,we moved from in vitro and in vivo models of neurodegeneration to analyze the putative role of glial cells in the early mechanisms of neurodegeneration.We report changes of transcriptional,genetic,morphological,and metabolic activity in astrocytes and microglial cells in specific brain areas before neuronal degeneration,providing evidence in experimental models of neurodegenerative disorders,including Parkinson’s and Alzheimer’s diseases.Understanding these mechanisms might increase the insight of these processes and pave the way for new specific glia-targeted therapeutic strategies for neurodegenerative disorders.
基金supported by grants from the Italian Ministry of University and Research(MIUR)(SYSBIONET-Italian ROADMAP ESFRI Infrastructures to LA,AMC and MP IVASCOMAR-National Cluster to AMC)+5 种基金Netherlands Organization for Scientific Research(NWO)in the integrated program of WOTRO [W01.65.324.00/project 4] Science for Global DevelopmentSynpol:EU-FP7 [KBBE.2012.3.4-02#311815]Corbel:EU-H2020 [NFRADEV-4-2014-2015#654248]Epipredict:EU-H2020 MSCA-ITN-2014-ETN:Marie Sk?odowska-Curie Innovative Training Networks(ITN-ETN)[#642691]BBSRC China [BB/J020060/1] to HVWCorbel:EU-H2020 [PID 2354] to HVW and AMC
文摘The recognition that neurogenesis does not stop with adolescence has spun off research towards the reduction of brain disorders by enhancing brain regeneration. Adult neurogenesis is one of the tougher problems of developmental biology as it requires the generation of complex intracellular and pericellular anatomies, amidst the danger of neuroinflammation. We here review how a multitude of regulatory pathways optimized for early neurogenesis has to be revamped into a new choreography of time dependencies. Distinct pathways need to be regulated, ranging from neural growth factor induced differentiation to mitochondrial bioenergetics, reactive oxygen metabolism, and apoptosis. Requiring much Gibbs energy consumption, brain depends on aerobic energy metabolism, hence on mitochondrial activity. Mitochondrial fission and fusion, movement and perhaps even mitoptosis, thereby come into play. All these network processes are interlinked and involve a plethora of molecules. We recommend a deep thinking approach to adult neurobiology.
文摘Who drew the borders between central and peripheral nervous sys tem? A complex question but a simple answer. Human anatomy and clinical neurology need to differentiate peripheral nerves from central nervous system (CNS), peripheral or central disorders, respectively. However, there are no anatomical and functional clefts between peripheral axons and central synaps- es. There is a direct continuity from the periphery to the center, from the receptor to the sensory neuron, from the spinal motor neuron to the muscle, just the neuromuscular junction.