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000282297 1001_ $$00000-0001-8699-0794$$aHartmann, Christiane$$b0
000282297 245__ $$aPrematurely Aged Human Microglia Exhibit Impaired Stress Response and Defective Nucleocytoplasmic Shuttling of ALS Associated FUS.
000282297 260__ $$aOxford [u.a.]$$bWiley-Blackwell$$c2025
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000282297 520__ $$aMicroglia, the brain's resident immune cells, are crucial for maintaining healthy brain homeostasis. However, as the brain ages, microglia can shift from a neuroprotective to a neurotoxic phenotype, contributing to chronic inflammation and promoting neurodegenerative processes. Despite the importance of understanding microglial aging, there are currently few human in vitro models to study these processes. To address this gap, we have developed a model in which human microglia undergo accelerated aging through inducible progerin expression. HMC3-Progerin cells display key age-related markers such as activation of the senescence-associated secretory phenotype (SASP) as well as an increase in DNA damage. These prematurely aged HMC3 cells show a reduced response to LPS activation, exhibit impairments in essential microglial functions including decreased migration and phagocytosis as well as transcriptomic alterations including a shift observed in aging and neurodegeneration. Additionally, we observed an impaired stress response and a defect in nucleocytoplasmic transport, especially affecting the amyotrophic lateral sclerosis (ALS) associated protein FUS. This suggests that microglia play a contributory role in driving neurodegenerative processes in the aging brain. Our microglia aging model offers a valuable tool for exploring how aged microglia affect brain function, enhancing our understanding of their role in brain aging.
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000282297 650_7 $$2Other$$aFUS
000282297 650_7 $$2Other$$aaging
000282297 650_7 $$2Other$$aaging clock
000282297 650_7 $$2Other$$aamyotrophic lateral sclerosis
000282297 650_7 $$2Other$$amicroglia
000282297 650_7 $$2Other$$anucleocytoplasmic shuttling
000282297 650_7 $$2Other$$aprogerin
000282297 650_7 $$2Other$$asenolytics
000282297 650_7 $$2NLM Chemicals$$aRNA-Binding Protein FUS
000282297 650_2 $$2MeSH$$aHumans
000282297 650_2 $$2MeSH$$aMicroglia: metabolism
000282297 650_2 $$2MeSH$$aMicroglia: pathology
000282297 650_2 $$2MeSH$$aAmyotrophic Lateral Sclerosis: metabolism
000282297 650_2 $$2MeSH$$aAmyotrophic Lateral Sclerosis: pathology
000282297 650_2 $$2MeSH$$aAmyotrophic Lateral Sclerosis: genetics
000282297 650_2 $$2MeSH$$aRNA-Binding Protein FUS: metabolism
000282297 650_2 $$2MeSH$$aCellular Senescence
000282297 650_2 $$2MeSH$$aActive Transport, Cell Nucleus
000282297 650_2 $$2MeSH$$aStress, Physiological
000282297 650_2 $$2MeSH$$aPhagocytosis
000282297 7001_ $$aHaß, Christina$$b1
000282297 7001_ $$aKnobloch, Muriel$$b2
000282297 7001_ $$aBarrantes, Israel$$b3
000282297 7001_ $$00000-0002-9333-926X$$aFumagalli, Laura$$b4
000282297 7001_ $$aPremereur, Jessie$$b5
000282297 7001_ $$00000-0001-6502-2567$$aMarkert, Franz$$b6
000282297 7001_ $$aPeters, Maite$$b7
000282297 7001_ $$aKoromila, Georgia$$b8
000282297 7001_ $$aHartmann, Alexander$$b9
000282297 7001_ $$aJäger, Kathrin$$b10
000282297 7001_ $$aAbel, Jette$$b11
000282297 7001_ $$aMancuso, Renzo$$b12
000282297 7001_ $$0P:(DE-2719)9000306$$aStorch, Alexander$$b13
000282297 7001_ $$aWalter, Michael$$b14
000282297 7001_ $$aFuellen, Georg$$b15
000282297 7001_ $$0P:(DE-2719)2811732$$aHermann, Andreas$$b16$$eLast author$$udzne
000282297 773__ $$0PERI:(DE-600)2099130-7$$a10.1111/acel.70232$$gVol. 24, no. 11, p. e70232$$n11$$pe70232$$tAging cell$$v24$$x1474-9718$$y2025
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