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Neddylation-dependent protein degradation is a nexus between synaptic insulin resistance,neuroinflammation and Alzheimer’s disease

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Translational Neurodegeneration 2022年第1期11卷 931-948页

作者： Alessandro Dario Confettura Eleonora Cuboni Mohamed Rafeet Ammar Shaobo Jia Guilherme M.Gomes pingan yuanxiang Rajeev Raman Tingting Li Katarzyna M.Grochowska Robert Ahrends Anna Karpova Alexander Dityatev Michael R.Kreutz RG Neuroplasticity Leibniz-Institute for Neurobiology39118 Magde-burgGermany German Center for Neurodegenerative Diseases(DZNE) 39120 MagdeburgGermany Center for Behavioral Brain Sciences Otto Von Guericke University39120 MagdeburgGermany Leibniz-Institut Für Analytische Wissenschaften-ISAS-e.V. 44227 DortmundGermany Leibniz Group‘Dendritic Organelles and Synaptic Function’ Center for Molecular NeurobiologyZMNHUniversity Medical Center Hamburg-Eppendorf20251 Ham-burgGermany Department of Analytical Chemistry Faculty of ChemistryUniversity of Vienna1090 WienAustria Medical Faculty Otto-von-Guericke University39120 MagdeburgGermany.

Background:The metabolic syndrome is a consequence of modern lifestyle that causes synaptic insulin resistance and cognitive deficits and that in interaction with a high amyloid load is an important risk factor for Alzheimer’s *** has been proposed that neuroinflammation might be an intervening variable,but the underlying mechanisms are currently ***:We utilized primary neurons to induce synaptic insulin resistance as well as a mouse model of high-risk aging that includes a high amyloid load,neuroinflammation,and diet-induced obesity to test hypotheses on underly-ing ***:We found that neddylation and subsequent activation of cullin-RING ligase complexes induced synaptic insulin resistance through ubiquitylation and degradation of the insulin-receptor substrate IRS1 that organizes synap-tic insulin ***,inhibition of neddylation preserved synaptic insulin signaling and rescued memory deficits in mice with a high amyloid load,which were fed with a’western diet’.Conclusions:Collectively,the data suggest that neddylation and degradation of the insulin-receptor substrate is a nodal point that links high amyloid load,neuroinflammation,and synaptic insulin resistance to cognitive decline and impaired synaptic plasticity in high-risk aging.

关键词： Metabolic syndrome Alzheimer’s disease Neddylation Cullins MLN-4924 Insulin IRS1 Amyloid-β TNFα

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Role of Jacob in synapto-nuclear communication of activity-dependent synaptic plasticity in hippocampus

Role of Jacob in synapto-nuclear communication of activity-d...

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中国神经科学学会第十届全国学术会议

作者： Ying CHEN Weiguang WENG pingan yuanxiang Yinghan ZHUANG Yuqing CHEN Thomas BEHNISCH Institutes of Brain Science and State Key Laboratory of Medical Neurobiology Fudan University

It is generally believed that synapse-to-nucleus communication plays an important role for long-term memory ***,the control of activity-dependent gene expression by synaptic signals is still far from being *** potential synapto-nuclear protein messengers have been characterized that are thought to be involved in regulation of gene expression after induction of activity-dependent synaptic ***,there is a surprising lack of demonstrations visualizing the nuclear import of such proteins in response to activity-dependent synaptic *** could show that two major forms of NMDA-receptor dependent synaptic plasticity,long-term potentiation（LTP） and long-term depression（LTD） have different impact on the nuclear transition of the putative synapto-nuclear protein messenger Jacob using lifetime imaging of overexpressed Jacob and *** found that electrical and chemical LTP induction induces an enrichment of nuclear Jacob in hippocampal ***,in both investigated systems LTD induction does not cause nuclear transition of ***,even a nuclear Jacob translocation was not detectable after induction of LTD;the Jacob knockdown mouse experiments indicate an involvement of Jacob in synaptic depression and also in activity-dependent synaptic *** finding that overexpression of wild type Jacob does not alter LTP,might point towards its efficiency to interfere with plasticity related processes at endogenous protein levels *** experiments show that Jacob is involved in mechanism underlying formation of activity-dependent synaptic plasticity in hippocampus.

关键词： Jacob synaptic plasticity hippocampus long-term memory formation

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