Physiology of Astroglia

Verkhratsky, Alexei; Nedergaard, Maiken

doi:10.1152/physrev.00042.2016

Cited by 1,678Neuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration MechanismsBarrier Structure and Function Studies

Physiology of Astroglia

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Verkhratsky, Alexei, Nedergaard, Maiken·2018·Physiological Reviews

DOI 10.1152/physrev.00042.2016PMC PMC6050349

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Abstract

Astrocytes are neural cells of ectodermal, neuroepithelial origin that provide for homeostasis and defense of the central nervous system (CNS). Astrocytes are highly heterogeneous in morphological appearance; they express a multitude of receptors, channels, and membrane transporters. This complement underlies their remarkable adaptive plasticity that defines the functional maintenance of the CNS in development and aging. Astrocytes are tightly integrated into neural networks and act within the context of neural tissue; astrocytes control homeostasis of the CNS at all levels of organization from molecular to the whole organ.

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Reactive morphological changes are driven by an increase of intermediate filament proteins such as GFAP and vimentin.
“Finely tuned morphological changes are driven by an increase of intermediate filament proteins, such as GFAP and vimentin [15, 38, 41, 42, 43], which not only provide mechanical sustenance for the maintenance of astrocyte shape, but also support the functional profile of reactive astrocytes through transcriptional modulation of target genes involved in astroglial and microglial responsiveness [44,”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [15]
In “Major Findings from Transcriptional Studies” (page not available), the paper says GFAP and vimentin genes are highly upregulated in reactive astrocytes, reflecting morphological changes. Its GFAP discussion also says deleting these proteins impairs reactivity. These passages support their involvement, but do not establish that increased filament proteins drive the morphological changes. (LLM, conf=0.82)
Experimental — accuracy not yet measured
The astroglial reactive response is a context-specific reaction influenced by brain region, pathology, disease stage, genetics, age, and comorbidities, and is characteristic of multiple brain pathologies including Alzheimer's disease.
“The astroglial reactive response is far from a uniform process. Rather, it is a context‐specific reaction influenced by brain region, pathology, disease stage, genetics, age, and comorbidities [15, 43, 45, 52], and it is characteristic of multiple brain pathologies, including Alzheimer's disease (AD).”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [15]
The section “Major Findings From Transcriptional Studies” (page unavailable) says reactive astrogliosis is common in brain injury and disease and that responses in two injury models were not uniform but depended on pathology. The GFAP discussion also reports that genetic deletion impairs reactivity. The passages found do not establish that the reactive response varies with brain region, disease stage, age, or comorbidities, or that it is characteristic of Alzheimer’s disease specifically. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Through the reactive response, astrocytes aim to restore regional homeostasis by gradually modifying their transcriptional profile and adapting their cell morphology and activity.
“Through the reactive response, astrocytes aim to restore regional homeostasis gradually modifying their transcriptional profile and adapting their cell morphology and activity [15, 38].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [15]
The ‘Major Findings from Transcriptional Studies’ section reports altered transcriptional profiles and morphological changes in reactive astrocytes. The ‘Definition and Overview of Function’ section describes astrocytes’ homeostatic and defensive roles. Our copy does not establish that these reactive changes occur gradually or specifically restore regional homeostasis through adapted activity; no page numbers are available for these passages. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Hypertrophied astrocytes display thicker intermediate filament bundles, highly upregulate GFAP and are associated with neuroprotection and postlesion regeneration.
“hypertrophied astrocytes display thicker intermediate filament bundles, highly upregulate GFAP [45, 109] and are associated with neuroprotection and postlesion regeneration [28, 45, 46, 47].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [28]
The 'Major Findings from Transcriptional Studies' section says reactive astrocytes highly upregulate GFAP and other intermediate-filament genes, consistent with morphological changes. The available passages do not establish thicker filament bundles or associate hypertrophied astrocytes with postlesion regeneration; a cited study’s title instead says that preventing astrocytic-process hypertrophy improves post-traumatic regeneration. The GFAP section links impaired astrocyte reactivity to worsened neuropathology, offering indirect support for neuroprotection. Page numbers are unavailable in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Astrocyte reactivity is tightly linked to endothelial, which are in turn associated with loss of vascular structural integrity and opening of the BBB.
“Astrocyte reactivity is tightly linked to endothelial [50], which are in turn associated with loss of vascular structural integrity and opening of the BBB [15, 28, 38, 45, 107, 109, 121].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [28]
The Aquaporins section (page unavailable) says astrocyte endfeet interact directly with endothelial cells, and the transcriptional-studies section describes reactive astrogliosis after injury. Neither passage establishes that astrocyte reactivity is tightly linked to endothelial cells. The vascular-integrity and BBB-opening clause is attributed to other citations, not this paper. (LLM, conf=0.78)
Experimental — accuracy not yet measured

Astrocyte reactivity is tightly linked to endothelial, which are in turn associated with loss of vascular structural integrity and opening of the BBB.
“Astrocyte reactivity is tightly linked to endothelial [50], which are in turn associated with loss of vascular structural integrity and opening of the BBB [15, 28, 38, 45, 107, 109, 121].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [15]
The Aquaporins section (page unavailable) describes direct interactions between astrocyte endfeet and endothelial cells, and the Definition and Overview section describes astrocytes mounting a reactive response. Neither passage says astrocyte reactivity is tightly linked to endothelial cells. The later claim about vascular integrity and BBB opening carries different citations and is not assessed here. (LLM, conf=0.77)
Experimental — accuracy not yet measured
Astrocytes are critical for maintaining brain homeostasis.
“Astrocytes are critical for maintaining brain homeostasis2”
From Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer’s disease (2024) · cites this paper as [2]
Astroglial cells are the main regulators of cerebral glutamate clearance and metabolism.
“The astroglial cells are the main regulators of cerebral glutamate clearance and metabolism [21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [28]
Together with microglia, astrocytes constitute the principal defensive system of the CNS and respond to damage-related stimuli including Aβ and glutamate overload in a process known as astrocyte reactivity.
“Together with microglia, astrocytes constitute the principal defensive system of the CNS [37], responding to numerous damage‐related stimuli [6, 7, 8, 9] including amyloid β peptides (Aβ) and glutamate overload, in a process known as astrocyte reactivity [15, 37, 38, 39, 40].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [15]
Alteration of cell shape is one of the changes associated with astroglial reactivity and modification of vimentin and GFAP.
“alteration of cell shape is one of the changes associated with astroglial reactivity and modification of vimentin and GFAP [15, 28, 42, 43, 91].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [28]
Fine‐tuned modification of astrocytic GFAP and vimentin expression is critical for the execution of the astrocyte reactive program.
“fine‐tuned modification of astrocytic GFAP and vimentin expression is critical for the execution of the astrocyte reactive program [28, 71, 91].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [28]
Alteration of cell shape is one of the changes associated with astroglial reactivity and modification of vimentin and GFAP.
“alteration of cell shape is one of the changes associated with astroglial reactivity and modification of vimentin and GFAP [15, 28, 42, 43, 91].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [15]
Atrophied astrocytes fail to maintain the glutamate‐glutamine shuttle and display insufficient glutamate clearance because of reduced synaptic coverage, contributing to synaptic extinction and cognitive deficiency.
“previous reports have shown that atrophied astrocytes fail to maintain the glutamate‐glutamine shuttle [28, 47] and display insufficient glutamate clearance [43] because of reduced synaptic coverage [45, 46, 47], contributing to synaptic extinction and cognitive deficiency [43].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [28]
The sections on glutamine transporters and glutamate transporters describe the normal shuttle and the role of perisynaptic astrocyte processes in buffering glutamate (page unavailable). The passages retrieved for astrocytic atrophy and reduced synaptic coverage do not say that atrophied astrocytes fail to maintain the shuttle or establish the claimed consequences; the decisive portion may also be absent from our truncated copy. (LLM, conf=0.68)
Experimental — accuracy not yet measured
Under this context, astroglial death increases.
“Under this context, astroglial death increases [28, 47].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [28]
The overview says the review does not discuss astrogliopathology. A passage on reactive astrogliosis after injury mentions cell death but does not identify it as astroglial death; the passages found by searching for astroglial death and astrocyte apoptosis likewise do not report an increase in astroglial death. The cited copy therefore does not establish the claim, and the preceding context is not provided. (LLM, conf=0.72)
Experimental — accuracy not yet measured
Ablation of reactive astrocytes prevents the reconstruction of injured blood-brain barrier (BBB).
“ablation of reactive astrocytes prevents the reconstruction of injured BBB [28, 38, 45]”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection (2023) · cites this paper as [28]
The overview (section I; page unavailable) says astrocytes control the blood-brain barrier and mount a defensive response, while the transcriptional-studies section describes reactive astrocytes after injury. Neither passage addresses whether ablating reactive astrocytes prevents reconstruction of an injured barrier. Searches for astrocyte ablation and blood-brain barrier repair found no decisive passage in our copy, whose end may be missing. (LLM, conf=0.68)
Experimental — accuracy not yet measured

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Identification of region-specific astrocyte subtypes at single cell resolution
Batiuk, M. Y., Martirosyan, A., Wahis, J., de Vin, F., Marneffe, C., Kusserow, C., Koeppen, J., Viana, J. F., Oliveira, J. F., Voet, T., et al. (2020) · Nature Communications · doi:10.1038/s41467-019-14198-8 · Cited by 805 · see citing works
Interaction between Aβ and Tau in the Pathogenesis of Alzheimer’s Disease
Zhang, H., Wei, W., Zhao, M., Ma, L., Jiang, X., Pei, H., Cao, Y., & Li, H. (2021) · International Journal of Biological Sciences · doi:10.7150/ijbs.57078 · Cited by 689 · see citing works
Markers of central inflammation in major depressive disorder: a systematic review and meta-analysis of studies examining cerebrospinal fluid, positron emission tomography and post-mortem brain tissue
Enache, D., Pariante, C. M., & Mondelli, V. (2019) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2019.06.015 · Cited by 615 · see citing works
“Astrocytes play a key role in maintaining the neurotransmitters homeostasis (glutamate and GABA), water transport homeostasis, ion homeostasis, metabolic support, synaptogenesis and synaptic plasticity, maintaining the integrity of the blood brain barrier (Verkhratsky and Nedergaard, 2018).”
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Astrocyte contribution to dysfunction, risk and progression in neurodegenerative disorders
Brandebura, A. N., Paumier, A., Onur, T. S., & Allen, N. J. (2023) · Nature Reviews Neuroscience · doi:10.1038/s41583-022-00641-1 · Cited by 427 · see citing works
Cell-cell communication: New insights and clinical implications
Su, J., Song, Y., Zhu, Z., Huang, X., Fan, J., Qiao, J., & Mao, F. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01888-z · Cited by 433 · see citing works
Neuroinfection may contribute to pathophysiology and clinical manifestations of COVID‐19
Steardo, L., Steardo, L., Zorec, R., & Verkhratsky, A. (2020) · Acta Physiologica · doi:10.1111/apha.13473 · Cited by 367 · see citing works
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Beyond the GFAP-Astrocyte Protein Markers in the Brain
Jurga, A. M., Paleczna, M., Kadluczka, J., & Kuter, K. Z. (2021) · Biomolecules · doi:10.3390/biom11091361 · Cited by 319 · see citing works
Astrocyte senescence: Evidence and significance
Cohen, J., & Torres, C. (2019) · Aging Cell · doi:10.1111/acel.12937 · Cited by 281 · see citing works
The contribution of astrocytes to the neuroinflammatory response in multiple sclerosis and experimental autoimmune encephalomyelitis
Brambilla, R. (2019) · Acta Neuropathologica · doi:10.1007/s00401-019-01980-7 · Cited by 246 · see citing works
Stratification of astrocytes in healthy and diseased brain
Verkhratsky, A., Zorec, R., & Parpura, V. (2017) · Brain Pathology · doi:10.1111/bpa.12537 · Cited by 236 · see citing works
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Lipid-accumulated reactive astrocytes promote disease progression in epilepsy
Chen, Z.-P., Wang, S., Zhao, X., Fang, W., Wang, Z., Ye, H., Wang, M.-J., Ke, L., Huang, T., Lv, P., et al. (2023) · Nature Neuroscience · doi:10.1038/s41593-023-01288-6 · Cited by 214 · see citing works
Loss of lamin‐B1 and defective nuclear morphology are hallmarks of astrocyte senescence in vitro and in the aging human hippocampus
Matias, I., Diniz, L. P., Damico, I. V., Araujo, A. P. B., Neves, L. D. S., Vargas, G., Leite, R. E. P., Suemoto, C. K., Nitrini, R., Jacob‐Filho, W., et al. (2022) · Aging Cell · doi:10.1111/acel.13521 · Cited by 183 · see citing works
Astrocyte Senescence and Alzheimer’s Disease: A Review
Han, X., Zhang, T., Liu, H., Mi, Y., & Gou, X. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00148 · Cited by 177 · see citing works
Neuropathobiology of COVID-19: The Role for Glia
Tremblay, M.-E., Madore, C., Bordeleau, M., Tian, L., & Verkhratsky, A. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.592214 · Cited by 159 · see citing works
“of reactive oxygen species (molecular level), regulation of neurogenesis, synapse formation, maintenance and elimination (cellular and network levels), regulation of blood flow, glycogen synthesis and storage (metabolic level), as well as control of the BBB and glymphatic clearance (whole brain level) (Hanisch and Ket…”
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Inflammatory pathways in Alzheimer’s disease mediated by gut microbiota
Qian, X.-H., Song, X.-X., Liu, X.-L., Chen, S.-D., & Tang, H.-D. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101317 · Cited by 153 · see citing works
Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer’s disease
Serrano-Pozo, A., Li, H., Li, Z., Muñoz-Castro, C., Jaisa-aad, M., Healey, M. A., Welikovitch, L. A., Jayakumar, R., Bryant, A. G., Noori, A., et al. (2024) · Nature Neuroscience · doi:10.1038/s41593-024-01791-4 · Cited by 140 · see citing works
Neuroinflammation in Huntington’s Disease: A Starring Role for Astrocyte and Microglia
Saba, J., Couselo, F. L., Bruno, J., Carniglia, L., Durand, D., Lasaga, M., & Caruso, C. (2022) · Current Neuropharmacology · doi:10.2174/1570159x19666211201094608 · Cited by 117 · see citing works
Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies
Gaikwad, S., Senapati, S., Haque, M. A., & Kayed, R. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.13490 · Cited by 117 · see citing works
Microglial autophagy is impaired by prolonged exposure to β-amyloid peptides: evidence from experimental models and Alzheimer’s disease patients
Pomilio, C., Gorojod, R. M., Riudavets, M., Vinuesa, A., Presa, J., Gregosa, A., Bentivegna, M., Alaimo, A., Alcon, S. P., Sevlever, G., et al. (2020) · GeroScience · doi:10.1007/s11357-020-00161-9 · Cited by 109 · see citing works
Electroacupuncture prevents astrocyte atrophy to alleviate depression
Lin, S.-S., Zhou, B., Chen, B.-J., Jiang, R.-T., Li, B., Illes, P., Semyanov, A., Tang, Y., & Verkhratsky, A. (2023) · Cell Death & Disease · doi:10.1038/s41419-023-05839-4 · Cited by 102 · see citing works
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Fluoxetine inhibited the activation of A1 reactive astrocyte in a mouse model of major depressive disorder through astrocytic 5-HT2BR/β-arrestin2 pathway
Fang, Y., Ding, X., Zhang, Y., Cai, L., Ge, Y., Ma, K., Xu, R., Li, S., Song, M., Zhu, H., et al. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02389-y · Cited by 96 · see citing works
Neuronal and astrocytic primary cilia in the mature brain
Sterpka, A., & Chen, X. (2018) · Pharmacological Research · doi:10.1016/j.phrs.2018.10.002 · Cited by 80 · see citing works
Cortical Interlaminar Astrocytes Are Generated Prenatally, Mature Postnatally, and Express Unique Markers in Human and Nonhuman Primates
Falcone, C., Penna, E., Hong, T., Tarantal, A. F., Hof, P. R., Hopkins, W. D., Sherwood, C. C., Noctor, S. C., & Martínez-Cerdeño, V. (2021) · Cerebral Cortex · doi:10.1093/cercor/bhaa231 · Cited by 72 · see citing works
Properties of human astrocytes and NG2 glia
Bedner, P., Jabs, R., & Steinhäuser, C. (2020) · Glia · doi:10.1002/glia.23725 · Cited by 71 · see citing works
Short-chain fatty acids: Important components of the gut-brain axis against AD
Huang, Y., Wang, Y. F., Miao, J., Zheng, R. F., & Li, J. Y. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.116601 · Cited by 70 · see citing works
GABA release from astrocytes in health and disease.
Kilb, W., & Kirischuk, S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232415859 · Cited by 66 · see citing works
Redefining varicose projection astrocytes in primates.
Falcone, C., McBride, E. L., Hopkins, W. D., Hof, P. R., Manger, P. R., Sherwood, C. C., Noctor, S. C., & Martínez‐Cerdeño, V. (2022) · Glia · doi:10.1002/glia.24093 · Cited by 56 · see citing works
Insulin action on astrocytes: From energy homeostasis to behaviour
González‐García, I., Gruber, T., & García‐Cáceres, C. (2021) · Journal of Neuroendocrinology · doi:10.1111/jne.12953 · Cited by 52 · see citing works
Noradrenergic Hypothesis Linking Neurodegeneration-Based Cognitive Decline and Astroglia
Leanza, G., Gulino, R., & Zorec, R. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00254 · Cited by 54 · see citing works
How expensive is the astrocyte?
Barros, L. (2022) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x221077343 · Cited by 51 · see citing works
Exacerbation of Epilepsy by Astrocyte Alkalization and Gap Junction Uncoupling
Onodera, M., Meyer, J., Furukawa, K., Hiraoka, Y., Aida, T., Tanaka, K., Tanaka, K. F., Rose, C. R., & Matsui, K. (2021) · The Journal of Neuroscience · doi:10.1523/jneurosci.2365-20.2020 · Cited by 50 · see citing works
Intestinal Permeability and Its Significance in Psychiatric Disorders—A Narrative Review and Future Perspectives
Wasiak, J., & Gawlik-Kotelnicka, O. (2023) · Behavioural Brain Research · doi:10.1016/j.bbr.2023.114459 · Cited by 47 · see citing works
Sodium Fluctuations in Astroglia and Their Potential Impact on Astrocyte Function
Felix, L., Delekate, A., Petzold, G. C., & Rose, C. R. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00871 · Cited by 38 · see citing works
Role of Glial Cells in Neuronal Function, Mood Disorders, and Drug Addiction
Tizabi, Y., Getachew, B., Hauser, S. R., Tsytsarev, V., Manhães, A. C., & da Silva, V. D. A. (2024) · Brain Sciences · doi:10.3390/brainsci14060558 · Cited by 27 · see citing works
In vivo evidence of microstructural hypo-connectivity of brain white matter in 22q11.2 deletion syndrome
Raven, E. P., Veraart, J., Kievit, R. A., Genc, S., Ward, I. L., Hall, J., Cunningham, A., Doherty, J., van den Bree, M. B. M., & Jones, D. K. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02178-w · Cited by 21 · see citing works
Astroglial Serotonin Receptors as the Central Target of Classic Antidepressants
Verkhratsky, A., Parpura, V., Scuderi, C., & Li, B. (2021) · Advances in Neurobiology · doi:10.1007/978-3-030-77375-5_13 · Cited by 19 · see citing works
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The Anemonia Sulcata Toxin BDS-I Protects Astrocytes Exposed to Aβ1-42 Oligomers by Restoring [Ca2+]i Transients and ER Ca2+ Signaling
Piccialli, I., Tedeschi, V., Boscia, F., Ciccone, R., Casamassa, A., de Rosa, V., Grieco, P., Secondo, A., & Pannaccione, A. (2020) · Toxins · doi:10.3390/toxins13010020 · Cited by 14 · see citing works
Interlaminar and varicose-projection astrocytes: toward a new understanding of the primate brain
Ciani, C., & Falcone, C. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1477753 · Cited by 11 · see citing works
Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp>APOE3</scp> Christchurch homozygote glioprotection
Henao‐Restrepo, J., López‐Murillo, C., Valderrama‐Carmona, P., Orozco‐Santa, N., Gomez, J., Gutiérrez‐Vargas, J., Moraga, R., Toledo, J., Littau, J. L., Härtel, S., et al. (2023) · Brain Pathology · doi:10.1111/bpa.13119 · Cited by 11 · see citing works
Gut Microbiota Metabolites Differentially Release Gliotransmitters from the Cultured Human Astrocytes: A Preliminary Report
Karbownik, M. S., Sokołowska, P., & Kowalczyk, E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076617 · Cited by 6 · see citing works
Classical-quantum interfaces in living neural tissue supporting conscious functions
(2020) · Advances in Quantum Chemistry · doi:10.1016/bs.aiq.2020.08.002 · Cited by 6 · see citing works
Chimeric brain models to study human glial-neuronal and macroglial-microglial interactions
Jin, M., Ma, Z., Zhang, H., Dang, R., Papetti, A. V., Stillitano, A. C., Zou, L., Goldman, S. A., & Jiang, P. (2026) · Cell Reports · doi:10.1016/j.celrep.2025.116794 · Cited by 6 · see citing works
Regulation of astrocyte metabolism by mitochondrial translocator protein <scp>18 kDa</scp>
Firth, W., Robb, J. L., Stewart, D., Pye, K. R., Bamford, R., Oguro‐Ando, A., Beall, C., & Ellacott, K. L. J. (2024) · Journal of Neurochemistry · doi:10.1111/jnc.16089 · Cited by 5 · see citing works
Varicose projection astrocytes: Conserved reactive cells in brain pathology
Ciani, C., Pistorio, G., Giancola, S., Mearelli, M., Mongelli, F. E., Forouzeh, D., Campos Soares, L., Gonzalez Martin, M., Lichtenstein, M. E., Mio, L., et al. (2026) · Science Advances · doi:10.1126/sciadv.ady8204 · Cited by 4 · see citing works
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Cell Adhesion Molecule Protocadherin-γC5 Ameliorates Aβ Plaque Pathogenesis by Modulating Astrocyte Function in Alzheimer's Disease
Sun, X., Pan, S., Li, D., Su, M., Zheng, H., Zhang, Y.-W., & Li, Y. (2025) · The Journal of Neuroscience · doi:10.1523/jneurosci.0967-24.2025 · Cited by 4 · see citing works
Multi-omics reveals changes in astrocyte fatty acid metabolism during early stages of Alzheimer's disease
Zhong, J., Li, M., Dai, Z., & Wan, J. (2025) · Neurochemistry International · doi:10.1016/j.neuint.2025.106049 · Cited by 3 · see citing works

Authors: Verkhratsky, A., & Nedergaard, M.
Affiliations: Ikerbasque (ES)
ORCID: Verkhratsky, Alexei
Nedergaard, Maiken
Venue: Physiological Reviews
Publisher: American Physiological Society
Published: 2018-01-01
Volume: 98
Issue: 1
Pages: 239-389
ISSN: 0031-9333 (ISSN-L)
1522-1210
DOI: 10.1152/physrev.00042.2016
PMC: PMC6050349
OpenAlex: W2777525962
Cited by: 1,678
References: 93
Citations by year: 2026: 176 · 2025: 250 · 2024: 239 · 2023: 229 · 2022: 207 · 2021: 228 · 2020: 167 · 2019: 121 · 2018: 53 · 2017: 3 · 2013: 1
FWCI: 11.60
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Physiological Reviews (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, other-oa)
Research Explorer (The University of Manchester) (submittedVersion)
Funders: HHS | National Institutes of Health (NIH)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Keywords: astrocytes, CNS homeostasis, astrocyte heterogeneity, membrane transporters, astrocyte plasticity, central nervous system development, astrocyte-neuron interaction
MeSH terms: Animals, Astrocytes, Biological Evolution, Higher Nervous Activity, Homeostasis, Humans, Ion Channels, Membrane Potentials, Receptors, Cell Surface

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