Pathological phenotypes of astrocytes in Alzheimer’s disease
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Astrocytes are involved in various processes in the central nervous system (CNS). As the most abundant cell type in the CNS, astrocytes play an essential role in neuronal maintenance and support, synaptic activity, neuronal metabolism, and amyloid-beta (Aβ) clearance. Alzheimer’s disease (AD) is a neurodegenerative disorder associated with cognitive and behavioral impairment. The transformation of astrocytes is involved in various neurodegenerative diseases, such as AD. Since astrocytes have functional diversity and morphological and physiological heterogeneity in the CNS, AD-related astrocytes might show various pathological phenotypes during AD. Astrocytes developing pathological phenotypes could contribute to AD progression. In this review, we provide an overview of the pathological phenotypes of astrocytes in the context of AD, highlighting recent findings in human and mouse AD.
Abstract
Astrocytes are involved in various processes in the central nervous system (CNS). As the most abundant cell type in the CNS, astrocytes play an essential role in neuronal maintenance and support, synaptic activity, neuronal metabolism, and amyloid-beta (Aβ) clearance. Alzheimer’s disease (AD) is a neurodegenerative disorder associated with cognitive and behavioral impairment. The transformation of astrocytes is involved in various neurodegenerative diseases, such as AD. Since astrocytes have functional diversity and morphological and physiological heterogeneity in the CNS, AD-related astrocytes might show various pathological phenotypes during AD. Astrocytes developing pathological phenotypes could contribute to AD progression. In this review, we provide an overview of the pathological phenotypes of astrocytes in the context of AD, highlighting recent findings in human and mouse AD.
참고문헌 (75)
- Selkoe, D. J., "Alzheimer’s disease : genes, proteins, and therapy", Physiol. Rev, 81, pp.741~766 (2001)
- Holtzman, D. M., "Alzheimer’s disease: the challenge of the second century", Sci. Transl. Med, 3, pp.77sr1~ (2011)
- Gustavsson, A., "Global estimates on the number of persons across the Alzheimer’s disease continuum", Alzheimers Dement, 19, pp.658~670 (2023)
- Buckwalter, M. S., "Modelling neuroinflammatory phenotypes in vivo", J. Neuroinflammation, 1, pp.10~ (2004)
- Zhang, B., "Integrated systems approach identifies genetic nodes and net works in late-onset Alzheimer’s disease", Cell, 153, pp.707~720 (2013)
- Khakh, B. S., "The emerging nature of astrocyte diversity", Annu. Rev. Neurosci, 42, pp.187~207 (2019)
- Saunders, A., "Molecular diversity and specializations among the cells of the adult mouse brain", Cell, 174, pp.1015~1030 (2018)
- Khakh, B. S., "Diversity of astrocyte functions and phenotypes in neural circuits", Nat. Neurosci, 18, pp.942~952 (2015)
- Ben Haim, L., "Functional diversity of astrocytes in neural circuit regulation", Nat. Rev. Neurosci, 18, pp.31~41 (2017)
- Cahoy, J. D., "A transcriptome database for astrocytes, neurons, and oligo dendrocytes : a new resource for understanding brain development and function", J. Neurosci, 28, pp.264~278 (2008)
- Lanjakornsiripan, D., "Layer-specific morphological and molecular differences in neocortical astrocytes and their dependence on neuronal layers", Nat. Commun, 9, pp.1623~ (2018)
- Chai, H., "Neural circuit-specialized astrocytes: transcriptomic, proteomic, morphological, and functional evidence", Neuron, 95, pp.531~549 (2017)
- Morel, L., "Molecular and functional properties of regional astrocytes in the adult brain", J. Neurosci, 37, pp.8706~8717 (2017)
- Acosta, C., "Astrocyte dysfunction in Alzheimer", Dis. J. Neurosci. Res, 95, pp.2430~2447 (2017)
- Gonzalez-Reyes, R. E., "Involvement of astrocytes in alzheimer’s disease from a neu roinflammatory and oxidative stress perspective", Front. Mol. Neurosci, 10, pp.427~ (2017)
- Ricci, G., "Astrocyte-neuron inter actions in neurological disorders", J. Biol. Phys, 35, pp.317~336 (2009)
- Rocchi, A., "NMR metabolomic investigation of astrocytes interacted with Abeta(4)(2) or its complexes with either copper(II) or zinc(II.)", J. Inorg. Biochem, 117, pp.326~333 (2012)
- Figley, C. R., "The role(s)of astrocytes and astrocyte activity in neurometabolism, neurovascular coupling, and the production of functional neuroimaging signals", Eur. J. Neurosci, 33, pp.577~588 (2011)
- Ishibashi, T., "Astrocytes promote myelination in response to electrical impulses", Neuron, 49, pp.823~832 (2006)
- Phatnani, H., "Astrocytes in neurodegenerative disease", Cold Spring Harb. Perspect. Biol, 7, pp.a020628~ (2015)
- Habib, N., "Disease-associated astrocytes in Alzheimer’s disease and aging", Nat. Neurosci, 23, pp.701~706 (2020)
- Ben Haim, L., "Elusive roles for reactive astrocytes in neurodegenerative diseases", Front. Cell. Neurosci, 9, pp.278~ (2015)
- Escartin, C., "Questions and (some)answers on reactive astrocytes", Glia, 67, pp.2221~2247 (2019)
- Liddelow, S. A., "Reactive astrocytes: production, function, and therapeutic potential", Immunity, 46, pp.957~967 (2017)
- Hinkle, J. T., "The A1 astrocyte paradigm : new avenues for pharmacological intervention in neurodegeneration", Mov. Disord, 34, pp.959~969 (2019)
- Neal, M., "Prokineticin-2 promotes chemotaxis and alternative A2 reactivity of astrocytes", Glia, 66, pp.2137~2157 (2018)
- Dai, D. L., "Human Alzheimer’s disease reactive astrocytes exhibit a loss of homeostastic gene expression", Acta Neuropathol. Commun, 11, pp.127~ (2023)
- Liddelow, S. A., "Neurotoxic reactive astrocytes are induced by activated microglia", Nature, 541, pp.481~487 (2017)
- Zamanian, J. L., "Genomic analysis of reactive astrogliosis", J. Neurosci, 32, pp.6391~6410 (2012)
- Li, C., "Astrocytes : implications for neuroinflammatory pathogenesis of Alz heimer’s disease", Curr. Alzheimer Res, 8, pp.67~80 (2011)
- Patel, N. S., "Inflammatory cytokine levels correlate with amyloid load in transgenic mouse models of Alzheimer’s disease", J. Neuroinflammation, 2, pp.9~ (2005)
- Thompson, C. B., "Apoptosis in the pathogenesis and treatment of disease", Science, 267, pp.1456~1462 (1995)
- Shimohama, S., "Changes in caspase expression in Alz heimer’s disease : comparison with development and aging", Biochem. Biophys. Res. Commun, 256, pp.381~384 (1999)
- Lassmann, H., "Cell death in Alzheimer’s disease evaluated by DNA frag mentation in situ", Acta Neuropathol, 89, pp.35~41 (1995)
- Kobayashi, K., "Correlation between astrocyte apoptosis and Alzheimer changes in gray matter lesions in Alzheimer’s disease", J. Alzheimers Dis, 6, pp.623~632 (2004)
- Kobayashi, K., "Apoptosis of astrocytes with enhanced lysosomal activity and oligodendrocytes in white matter lesions in Alzheimer’s disease", Neuropathol. Appl. Neurobiol, 28, pp.238~251 (2002)
- Dixon, S. J., "Ferroptosis : an iron-dependent form of nonapoptotic cell death", Cell, 149, pp.1060~1072 (2012)
- Park, M. W., "NOX4 promotes ferroptosis of astrocytes by oxidative stress induced lipid peroxidation via the impairment of mitochondrial metabolism in Alzheimer’s diseases", Redox Biol, 41, pp.101947~ (2021)
- Bao, W. D., "Loss of ferroportin induces memory impairment by promoting ferroptosis in Alzheimer’s disease", Cell Death Differ, 28, pp.1548~1562 (2021)
- Hou, Y., "Ageing as a risk factor for neurodegenerative disease", Nat. Rev. Neurol, 15, pp.565~581 (2019)
- Guerrero, A., "Cellular senescence at the crossroads of inflammation and Alzheimer’sdisease", Trends Neurosci, 44, pp.714~727 (2021)
- Lopez-Otin, C., "The hallmarks of aging", Cell, 153, pp.1194~1217 (2013)
- Han, X., "Astrocyte senescence and Alzheimer’s disease : a review", Front. Aging Neurosci, 12, pp.148~ (2020)
- Bhat, R., "Astrocyte senescence as a component of Alzheimer’s disease", PLoS ONE, 7, pp.e45069~ (2012)
- Myung, N. H., "Evidence of DNA damage in Alzheimer disease: phosphor ylation of histone H2AX in astrocytes", Age (Dordr.), 30, pp.209~215 (2008)
- Burma, S., "ATM phosphorylates histone H2AX in response to DNA double-strand breaks", J. Biol. Chem, 276, pp.42462~42467 (2001)
- Rogakou, E. P., "DNA double stranded breaks induce histone H2AX phosphorylation on serine 139", J. Biol. Chem, 273, pp.5858~5868 (1998)
- Sedelnikova, O. A., "Histone H2AX in DNA damage and repair", Cancer Biol. Ther, 2, pp.233~235 (2003)
- Rogakou, E. P., "Initiation of DNA fragmentation during apoptosis induces phosphorylation of H2AX his tone at serine 139", J. Biol. Chem, 275, pp.9390~9395 (2000)
- Bussian, T. J., "Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline", Nature, 562, pp.578~582 (2018)
- Chang, J., "Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice", Nat. Med, 22, pp.78~83 (2016)
- Zhu, Y., "Identification of a novel senolytic agent, navitoclax, targeting the Bcl-2 family of anti-apoptotic factors", Aging Cell, 15, pp.428~435 (2016)
- Lines, J., "Astrocytes modulate sensory-evoked neuronal network activity", Nat. Commun, 11, pp.3689~ (2020)
- Guerra-Gomes, S., "Functional roles of astrocyte calcium elevations : from synapses to behavior", Front. Cell. Neurosci, 11, pp.427~ (2017)
- Shah, D., "Astrocyte calcium dysfunction causes early network hyperactivity in Alzheimer’s disease", Cell Rep, 40, pp.111280~ (2022)
- Saito, T., "Single App knock-in mouse models of Alzheimer’s disease", Nat. Neurosci, 17, pp.661~663 (2014)
- Abdul, H. M., "Cognitive decline in Alzheimer’s disease is associated with selective changes in calcineurin", NFAT signaling, 2009, pp.29, 12957~12969
- Blalock, E. M., "Incipient Alzheimer’s disease : microarray correlation analyses reveal major transcriptional and tumor suppressor responses", Proc. Natl Acad. Sci. USA, 101, pp.2173~2178 (2004)
- Gasic, G. P., "Molecular neurobiology of glutamate receptors", Annu. Rev. Physiol, 54, pp.507~536 (1992)
- Lipton, S. A., "Excitatory amino acids as a final common pathway for neurologic disorders", N. Engl. J. Med, 330, pp.613~622 (1994)
- Anderson, C. M., "Astrocyte glutamate transport : review of properties, regulation, and physiological functions", Glia, 32, pp.1~14 (2000)
- Bergles, D. E., "Synaptic activation of glutamate transporters in hip pocampal astrocytes", Neuron, 19, pp.1297~1308 (1997)
- Otis, T. S., "Postsynaptic glutamate transport at the climbing fiber-Purkinje cell synapse", Science, 277, pp.1515~1518 (1997)
- Bergles, D. E., "Glial contribution to glutamate uptake at Schaffer collateral commissural synapses in the hippocampus", J. Neurosci, 18, pp.7709~7716 (1998)
- Melone, M., "Synaptic localization of GLT-1a in the rat somatic sensory cortex", Glia, 57, pp.108~117 (2009)
- Rothstein, J. D., "Localization of neuronal and glial glutamate transporters", Neuron, 13, pp.713~725 (1994)
- Chaudhry, F. A., "Glutamate transporters in glial plasma membranes : highly differentiated localizations revealed by quantitative ultrastructural immunocy tochemistry", Neuron, 15, pp.711~720 (1995)
- Rimmele, T. S., "GLT-1 : The elusive presynaptic glutamate transporter", Neurochem. Int, 98, pp.19~28 (2016)
- Danbolt, N. C., "Neuronal vs glial glutamate uptake:resolving the conundrum", Neurochem. Int, 98, pp.29~45 (2016)
- Zhou, J., "Glutamate transporter cluster formation in astrocytic processes regulates glutamate uptake activity", J. Neurosci, 24, pp.6301~6306 (2004)
- Hynd, M. R., "Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer’s disease", Neurochem. Int, 45, pp.583~595 (2004)
- Masliah, E., "Deficient glutamate transport is associated with neurodegeneration in Alzheimer’s disease", Ann. Neurol, 40, pp.759~766 (1996)
- Li, S., "Glutamate transporter alterations in Alzheimer disease are possibly associated with abnormal APP expression", J. Neuropathol. Exp. Neurol, 56, pp.901~911 (1997)
- Mookherjee, P., "GLT-1 loss accelerates cognitive deficit onset in an Alzhei mer’s disease animal model", J. Alzheimers Dis, 26, pp.447~455 (2011)
- Takahashi, K., "Restored glial glutamate transporter EAAT2 function as a potential therapeutic approach for Alzheimer’s disease", J. Exp. Med, 212, pp.319~332 (2015)
