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Journal articles on the topic 'Astrocyte neurodegeneration'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Amuti, T., I. Ouko, S. Mukonjia, et al. "Role of heterogeneous astrocyte receptor expression in determining astrocytic response to neuronal disorders." Anatomy Journal of Africa 7, no. 1 (2018): 1169–74. http://dx.doi.org/10.4314/aja.v7i1.169490.

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Following neuronal disorders, astrocytes carry out either neuroprotection or neurodegeneration. Previous authors suggest that favoring of neurodegeneration or neuroprotection by astrocytes can be due to many factors such as the influence of cytokines following their binding on their receptors on astrocytes. These receptors have however been shown to be region specific and heterogeneous. Further, research exploiting their role and influence in determining astrocytic response remains partly elucidated. A review of previous and ongoing research on these receptors would be helpful in the disclosur

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Sulimai, Nurul, Jason Brown, and David Lominadze. "Fibrinogen Interaction with Astrocyte ICAM-1 and PrPC Results in the Generation of ROS and Neuronal Death." International Journal of Molecular Sciences 22, no. 5 (2021): 2391. http://dx.doi.org/10.3390/ijms22052391.

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Many neuroinflammatory diseases, like traumatic brain injury (TBI), are associated with an elevated level of fibrinogen and short-term memory (STM) impairment. We found that during TBI, extravasated fibrinogen deposited in vasculo-astrocyte interfaces, which was associated with neurodegeneration and STM reduction. The mechanisms of this fibrinogen-astrocyte interaction and its functional role in neurodegeneration are still unclear. Cultured mouse brain astrocytes were treated with fibrinogen in the presence or absence of function-blocking antibody or peptide against its astrocyte receptors int

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Miyazaki, Ikuko, and Masato Asanuma. "Neuron-Astrocyte Interactions in Parkinson’s Disease." Cells 9, no. 12 (2020): 2623. http://dx.doi.org/10.3390/cells9122623.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease. PD patients exhibit motor symptoms such as akinesia/bradykinesia, tremor, rigidity, and postural instability due to a loss of nigrostriatal dopaminergic neurons. Although the pathogenesis in sporadic PD remains unknown, there is a consensus on the involvement of non-neuronal cells in the progression of PD pathology. Astrocytes are the most numerous glial cells in the central nervous system. Normally, astrocytes protect neurons by releasing neurotrophic factors, producing antioxidants, and disposing of neuronal waste

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Mitroshina, Elena, Elizaveta Kalinina, and Maria Vedunova. "Optogenetics in Alzheimer’s Disease: Focus on Astrocytes." Antioxidants 12, no. 10 (2023): 1856. http://dx.doi.org/10.3390/antiox12101856.

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Alzheimer’s disease (AD) is the most common form of dementia, resulting in disability and mortality. The global incidence of AD is consistently surging. Although numerous therapeutic agents with promising potential have been developed, none have successfully treated AD to date. Consequently, the pursuit of novel methodologies to address neurodegenerative processes in AD remains a paramount endeavor. A particularly promising avenue in this search is optogenetics, enabling the manipulation of neuronal activity. In recent years, research attention has pivoted from neurons to glial cells. This rev

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Mohn, Tal C., and Andrew O. Koob. "Adult Astrogenesis and the Etiology of Cortical Neurodegeneration." Journal of Experimental Neuroscience 9s2 (January 2015): JEN.S25520. http://dx.doi.org/10.4137/jen.s25520.

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As more evidence points to a clear role for astrocytes in synaptic processing, synaptogenesis and cognition, continuing research on astrocytic function could lead to strategies for neurodegenerative disease prevention. Reactive astrogliosis results in astrocyte proliferation early in injury and disease states and is considered neuroprotective, indicating a role for astrocytes in disease etiology. This review describes the different types of human cortical astrocytes and the current evidence regarding adult cortical astrogenesis in injury and degenerative disease. A role for disrupted astrogene

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Vicente-Acosta, Andrés, Alfredo Giménez-Cassina, Javier Díaz-Nido, and Frida Loria. "THE SONIC HEDGEHOG AGONIST SAG ATTENUATES MITOCHONDRIAL DYSFUNCTION AND DECREASES THE NEUROTOXOCITY INDUCED BY FRATAXIN-DEFICIENT ASTROCYTES." IBJ Plus 1, s5 (2022): 47. http://dx.doi.org/10.24217/2531-0151.22v1s5.00047.

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Friedreich’s ataxia (FRDA) is predominantly a neurodegenerative disease caused by the deficiency of a protein called frataxin (FXN). Although the main pathological alterations are observed in neurons, it is becoming clear that other non-neuronal cells such as astrocytes may be actively involved in the neurodegenerative process associated with the disease. Depending on the stimuli they respond to, astrocytes acquire different activation states in a process called astrogliosis. Neuroinflammatory stimuli induce the formation of A1 reactive astrocytes, which upregulate proinflammatory genes, being

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Preato, André Maciel, Ester da Silva Pinheiro, Tatiana Rosado Rosenstock, and Isaias Glezer. "The Relevance of Astrocytic Cell Culture Models for Neuroinflammation in Neurodegeneration Research." Neuroglia 5, no. 1 (2024): 27–49. http://dx.doi.org/10.3390/neuroglia5010003.

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Astrocytes are the predominant glial cells that provide essential support to neurons and promote microenvironment changes in neuropathological states. Astrocyte and astrocytic-like cell culture have substantially contributed to elucidating the molecular pathways involved in key glial roles, including those relevant to neurodevelopment, brain physiology and metabolism, which are not readily accessible with traditional approaches. The in vitro methodology has also been applied to neuroinflammatory and neurodegeneration contexts, revealing cellular changes involved in brain dysfunction. Astrocyte

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8

Sun, Yuanhong, Ali Winters, Linshu Wang, et al. "Metabolic Heterogeneity of Cerebral Cortical and Cerebellar Astrocytes." Life 13, no. 1 (2023): 184. http://dx.doi.org/10.3390/life13010184.

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Astrocytes play critical roles in regulating neuronal synaptogenesis, maintaining blood–brain barrier integrity, and recycling neurotransmitters. Increasing numbers of studies have suggested astrocyte heterogeneity in morphology, gene profile, and function. However, metabolic phenotype of astrocytes in different brain regions have not been explored. In this paper, we investigated the metabolic signature of cortical and cerebellar astrocytes using primary astrocyte cultures. We observed that cortical astrocytes were larger than cerebellar astrocytes, whereas cerebellar astrocytes had more and l

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9

Nassar, Ajmal, Triveni Kodi, Sairaj Satarker, et al. "Astrocytic MicroRNAs and Transcription Factors in Alzheimer’s Disease and Therapeutic Interventions." Cells 11, no. 24 (2022): 4111. http://dx.doi.org/10.3390/cells11244111.

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Astrocytes are important for maintaining cholesterol metabolism, glutamate uptake, and neurotransmission. Indeed, inflammatory processes and neurodegeneration contribute to the altered morphology, gene expression, and function of astrocytes. Astrocytes, in collaboration with numerous microRNAs, regulate brain cholesterol levels as well as glutamatergic and inflammatory signaling, all of which contribute to general brain homeostasis. Neural electrical activity, synaptic plasticity processes, learning, and memory are dependent on the astrocyte–neuron crosstalk. Here, we review the involvement of

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Valori, Chiara F., Agostino Possenti, Liliana Brambilla, and Daniela Rossi. "Challenges and Opportunities of Targeting Astrocytes to Halt Neurodegenerative Disorders." Cells 10, no. 8 (2021): 2019. http://dx.doi.org/10.3390/cells10082019.

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Neurodegenerative diseases are a heterogeneous group of disorders whose incidence is likely to duplicate in the next 30 years along with the progressive aging of the western population. Non-cell-specific therapeutics or therapeutics designed to tackle aberrant pathways within neurons failed to slow down or halt neurodegeneration. Yet, in the last few years, our knowledge of the importance of glial cells to maintain the central nervous system homeostasis in health conditions has increased exponentially, along with our awareness of their fundamental and multifaced role in pathological conditions

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Boal, Andrew M., Michael L. Risner, Melissa L. Cooper, Lauren K. Wareham, and David J. Calkins. "Astrocyte Networks as Therapeutic Targets in Glaucomatous Neurodegeneration." Cells 10, no. 6 (2021): 1368. http://dx.doi.org/10.3390/cells10061368.

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Astrocytes are intimately involved in the response to neurodegenerative stress and have become an attractive target for the development of neuroprotective therapies. However, studies often focus on astrocytes as single-cell units. Astrocytes are densely interconnected by gap junctions that are composed primarily of the protein connexin-43 (Cx43) and can function as a broader network of cells. Such networks contribute to a number of important processes, including metabolite distribution and extracellular ionic buffering, and are likely to play an important role in the progression of neurodegene

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Phillips, Emma C., Cara L. Croft, Ksenia Kurbatskaya, et al. "Astrocytes and neuroinflammation in Alzheimer's disease." Biochemical Society Transactions 42, no. 5 (2014): 1321–25. http://dx.doi.org/10.1042/bst20140155.

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Increased production of amyloid β-peptide (Aβ) and altered processing of tau in Alzheimer's disease (AD) are associated with synaptic dysfunction, neuronal death and cognitive and behavioural deficits. Neuroinflammation is also a prominent feature of AD brain and considerable evidence indicates that inflammatory events play a significant role in modulating the progression of AD. The role of microglia in AD inflammation has long been acknowledged. Substantial evidence now demonstrates that astrocyte-mediated inflammatory responses also influence pathology development, synapse health and neurode

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Morita, Mitsuhiro, Hiroko Ikeshima-Kataoka, Marko Kreft, Nina Vardjan, Robert Zorec, and Mami Noda. "Metabolic Plasticity of Astrocytes and Aging of the Brain." International Journal of Molecular Sciences 20, no. 4 (2019): 941. http://dx.doi.org/10.3390/ijms20040941.

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As part of the blood-brain-barrier, astrocytes are ideally positioned between cerebral vasculature and neuronal synapses to mediate nutrient uptake from the systemic circulation. In addition, astrocytes have a robust enzymatic capacity of glycolysis, glycogenesis and lipid metabolism, managing nutrient support in the brain parenchyma for neuronal consumption. Here, we review the plasticity of astrocyte energy metabolism under physiologic and pathologic conditions, highlighting age-dependent brain dysfunctions. In astrocytes, glycolysis and glycogenesis are regulated by noradrenaline and insuli

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Cooper, Melissa L., Silvia Pasini, Wendi S. Lambert, et al. "Redistribution of metabolic resources through astrocyte networks mitigates neurodegenerative stress." Proceedings of the National Academy of Sciences 117, no. 31 (2020): 18810–21. http://dx.doi.org/10.1073/pnas.2009425117.

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In the central nervous system, glycogen-derived bioenergetic resources in astrocytes help promote tissue survival in response to focal neuronal stress. However, our understanding of the extent to which these resources are mobilized and utilized during neurodegeneration, especially in nearby regions that are not actively degenerating, remains incomplete. Here we modeled neurodegeneration in glaucoma, the world’s leading cause of irreversible blindness, and measured how metabolites mobilize through astrocyte gap junctions composed of connexin 43 (Cx43). We elevated intraocular pressure in one ey

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Colombo, Emanuela, Rosaria Pascente, Daniela Triolo, et al. "Laquinimod Modulates Human Astrocyte Function and Dampens Astrocyte-Induced Neurotoxicity during Inflammation." Molecules 25, no. 22 (2020): 5403. http://dx.doi.org/10.3390/molecules25225403.

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Astrocytes greatly participate to inflammatory and neurotoxic reactions occurring in neurodegenerative diseases and are valuable pharmacological targets to support neuroprotection. Here we used human astrocytes generated from reprogrammed fibroblasts as a cellular model to study the effect of the compound Laquinimod and its active metabolite de-Laquinimod on astrocyte functions and the astrocyte–neuron interaction. We show that human iAstrocytes expressed the receptor for the inflammatory mediator IL1 and responded to it via nuclear translocation of NFκB, an event that did not occur if cells w

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Cunha-Garcia, Daniela, Daniela Monteiro-Fernandes, Joana Sofia Correia, et al. "Genetic Ablation of Inositol 1,4,5-Trisphosphate Receptor Type 2 (IP3R2) Fails to Modify Disease Progression in a Mouse Model of Spinocerebellar Ataxia Type 3." International Journal of Molecular Sciences 24, no. 13 (2023): 10606. http://dx.doi.org/10.3390/ijms241310606.

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Spinocerebellar ataxia type 3 (SCA3) is a rare neurodegenerative disease caused by an abnormal polyglutamine expansion within the ataxin-3 protein (ATXN3). This leads to neurodegeneration of specific brain and spinal cord regions, resulting in a progressive loss of motor function. Despite neuronal death, non-neuronal cells, including astrocytes, are also involved in SCA3 pathogenesis. Astrogliosis is a common pathological feature in SCA3 patients and animal models of the disease. However, the contribution of astrocytes to SCA3 is not clearly defined. Inositol 1,4,5-trisphosphate receptor type

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Brambilla, Liliana, Francesca Martorana, and Daniela Rossi. "Astrocyte signaling and neurodegeneration." Prion 7, no. 1 (2013): 28–36. http://dx.doi.org/10.4161/pri.22512.

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Moro, Andrea Stefano, Chiara Balestrucci, Anna Cozzi, Paolo Santambrogio, and Sonia Levi. "Neuroferritinopathy Human-Induced Pluripotent Stem Cell-Derived Astrocytes Reveal an Active Role of Free Intracellular Iron in Astrocyte Reactivity." International Journal of Molecular Sciences 26, no. 13 (2025): 6197. https://doi.org/10.3390/ijms26136197.

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Increased iron levels, common in neurodegenerative diseases, correlate with disease severity, suggesting a role in the pathological process. Recently, efforts have been made to understand the role of iron in cerebral inflammatory processes. Employing astrocyte cell models of genetic neurodegenerative pathologies characterized by iron imbalance, such as the neurodegeneration with brain iron accumulation disorders, can provide valuable insights into astrocytes reactivity, a pivotal process in brain inflammation. Specifically, we employed human-induced pluripotent stem cell-derived astrocytes fro

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Charkviani, Mariam, Nino Muradashvili, Nurul Sulimai, and David Lominadze. "Fibrinogen-cellular prion protein complex formation on astrocytes." Journal of Neurophysiology 124, no. 2 (2020): 536–43. http://dx.doi.org/10.1152/jn.00224.2020.

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For the first time we showed that fibrinogen (Fg) can associate with cellular prion protein (PrPC) on the surface of cultured mouse brain astrocytes. At high levels, Fg causes upregulation of astrocyte PrPC and astrocyte activation accompanied with overexpression of tyrosine receptor kinase B (TrkB), which results in nitric oxide (NO) production and generation of reactive oxygen species (ROS). Fg/PrPC interaction can be a triggering mechanism for TrkB-NO-ROS axis activation and the resultant astrocyte-mediated neurodegeneration.

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Ramírez, Angelica E., Natalia Gil-Jaramillo, María Alejandra Tapias, et al. "MicroRNA: A Linking between Astrocyte Dysfunction, Mild Cognitive Impairment, and Neurodegenerative Diseases." Life 12, no. 9 (2022): 1439. http://dx.doi.org/10.3390/life12091439.

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The importance of miRNAs in cellular processes and their dysregulation has taken significant importance in understanding different pathologies. Due to the constant increase in the prevalence of neurodegenerative diseases (ND) worldwide and their economic impact, mild cognitive impairment (MCI), considered a prodromal phase, is a logical starting point to study this public health problem. Multiple studies have established the importance of miRNAs in MCI, including astrocyte regulation during stressful conditions. Additionally, the protection mechanisms exerted by astrocytes against some damage

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Stoklund Dittlau, Katarina, and Kristine Freude. "Astrocytes: The Stars in Neurodegeneration?" Biomolecules 14, no. 3 (2024): 289. http://dx.doi.org/10.3390/biom14030289.

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Today, neurodegenerative disorders like Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) affect millions of people worldwide, and as the average human lifespan increases, similarly grows the number of patients. For many decades, cognitive and motoric decline has been explained by the very apparent deterioration of neurons in various regions of the brain and spinal cord. However, more recent studies show that disease progression is greatly influenced by the vast population of glial cells. Astrocytes are traditionally consi

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Serrano, Geidy E., Sidra Aslam, Jessica E. Walker, et al. "Characterization of Isolated Human Astrocytes from Aging Brain." International Journal of Molecular Sciences 26, no. 7 (2025): 3416. https://doi.org/10.3390/ijms26073416.

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Astrocytes have multiple crucial roles, including maintaining brain homeostasis and synaptic function, performing phagocytic clearance, and responding to injury and repair. It has been suggested that astrocyte performance is progressively impaired with aging, leading to imbalances in the brain’s internal milieu that eventually impact neuronal function and lead to neurodegeneration. Until now, most evidence of astrocytic dysfunction in aging has come from experiments done with whole tissue homogenates, astrocytes collected by laser capture, or cell cultures derived from animal models or cell li

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Udovin, Lucas, Cecilia Quarracino, María I. Herrera, Francisco Capani, Matilde Otero-Losada, and Santiago Perez-Lloret. "Role of Astrocytic Dysfunction in the Pathogenesis of Parkinson’s Disease Animal Models from a Molecular Signaling Perspective." Neural Plasticity 2020 (February 7, 2020): 1–10. http://dx.doi.org/10.1155/2020/1859431.

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Despite the fact that astrocytes are the most abundant glial cells, critical for brain function, few studies have dealt with their possible role in neurodegenerative diseases like Parkinson’s disease (PD). This article explores relevant evidence on the involvement of astrocytes in experimental PD neurodegeneration from a molecular signaling perspective. For a long time, astrocytic proliferation was merely considered a byproduct of neuroinflammation, but by the time being, it is clear that astrocytic dysfunction plays a far more important role in PD pathophysiology. Indeed, ongoing experimental

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Colombo, Emanuela, Chiara Cordiglieri, Giorgia Melli, et al. "Stimulation of the neurotrophin receptor TrkB on astrocytes drives nitric oxide production and neurodegeneration." Journal of Experimental Medicine 209, no. 3 (2012): 521–35. http://dx.doi.org/10.1084/jem.20110698.

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Neurotrophin growth factors support neuronal survival and function. In this study, we show that the expression of the neurotrophin receptor TrkB is induced on astrocytes in white matter lesions in multiple sclerosis (MS) patients and mice with experimental autoimmune encephalomyelitis (EAE). Surprisingly, mice lacking TrkB specifically in astrocytes were protected from EAE-induced neurodegeneration. In an in vitro assay, astrocytes stimulated with the TrkB agonist brain-derived neurotrophic factor (BDNF) released nitric oxide (NO), and conditioned medium from activated astrocytes had detriment

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Mayo, Lior, Sunia Trauger, Manon Blain, et al. "B4GALT6 regulates astrocyte activation during CNS inflammation (INM8P.360)." Journal of Immunology 194, no. 1_Supplement (2015): 195.4. http://dx.doi.org/10.4049/jimmunol.194.supp.195.4.

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Abstract Astrocytes play complex roles in neuroinflammation. Thus, it is important to characterize the mechanisms regulating astrocyte function, as well as potential targets for the therapeutic modulation of astrocyte activity. Here we report that during the chronic-progressive phase of EAE, astrocytes promote disease pathogenesis by a lipid-dependent signaling pathway. In line with previous studies, depletion of reactive astrocytes during the acute phase of chronic-progressive EAE exacerbated disease. However, depletion of astrocytes in the chronic phase ameliorated the disease. Hence, to und

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Dejanovic, Borislav, Tiffany Wu, Ming-Chi Tsai, et al. "Complement C1q-dependent excitatory and inhibitory synapse elimination by astrocytes and microglia in Alzheimer’s disease mouse models." Nature Aging 2, no. 9 (2022): 837–50. http://dx.doi.org/10.1038/s43587-022-00281-1.

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AbstractMicroglia and complement can mediate neurodegeneration in Alzheimer’s disease (AD). By integrative multi-omics analysis, here we show that astrocytic and microglial proteins are increased in TauP301S synapse fractions with age and in a C1q-dependent manner. In addition to microglia, we identified that astrocytes contribute substantially to synapse elimination in TauP301S hippocampi. Notably, we found relatively more excitatory synapse marker proteins in astrocytic lysosomes, whereas microglial lysosomes contained more inhibitory synapse material. C1q deletion reduced astrocyte–synapse

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Wolosker, Herman, and Inna Radzishevsky. "The serine shuttle between glia and neurons: implications for neurotransmission and neurodegeneration." Biochemical Society Transactions 41, no. 6 (2013): 1546–50. http://dx.doi.org/10.1042/bst20130220.

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D-Serine is a physiological co-agonist of NMDARs (N-methyl-D-aspartate receptors) required for neurotransmission, synaptic plasticity and neurotoxicity. There is no consensus, however, on the relative roles of neurons and astrocytes in D-serine signalling. The effects of D-serine had been attributed to its role as a gliotransmitter specifically produced and released by astrocytes. In contrast, recent studies indicate that neurons regulate their own NMDARs by releasing D-serine via plasma membrane transporters and depolarization-sensitive pathways. Only a minority of astrocytes contain authenti

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Rodrigues, Ricardo J., Ana S. Figueira, and Joana M. Marques. "P2Y1 Receptor as a Catalyst of Brain Neurodegeneration." NeuroSci 3, no. 4 (2022): 604–15. http://dx.doi.org/10.3390/neurosci3040043.

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Different brain disorders display distinctive etiologies and pathogenic mechanisms. However, they also share pathogenic events. One event systematically occurring in different brain disorders, both acute and chronic, is the increase of the extracellular ATP levels. Accordingly, several P2 (ATP/ADP) and P1 (adenosine) receptors, as well as the ectoenzymes involved in the extracellular catabolism of ATP, have been associated to different brain pathologies, either with a neuroprotective or neurodegenerative action. The P2Y1 receptor (P2Y1R) is one of the purinergic receptors associated to differe

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Ma, Bochao, Jifeng Ren, and Xiuqing Qian. "Study on the Polarization of Astrocytes in the Optic Nerve Head of Rats Under High Intraocular Pressure: In Vitro." Bioengineering 12, no. 2 (2025): 104. https://doi.org/10.3390/bioengineering12020104.

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Astrocytes, the most common glial cells in the optic nerve head (ONH), provide support and nutrition to retinal ganglion cells. This study aims to investigate the polarization types of astrocytes in the ONH of rats under high intraocular pressure (IOP) and explore signaling pathways potentially associated with different types of polarized astrocytes. The rat models with chronic high IOP were established. High IOP lasted for 2, 4, 6, and 8 weeks. Astrocytes were extracted from the ONH of rats using the tissue block cultivation method. Western blot was used to detect the expression of proteins a

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Luo, Jian. "TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications". Biomedicines 10, № 5 (2022): 1206. http://dx.doi.org/10.3390/biomedicines10051206.

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Astrocytes are essential for normal brain development and functioning. They respond to brain injury and disease through a process referred to as reactive astrogliosis, where the reactivity is highly heterogenous and context-dependent. Reactive astrocytes are active contributors to brain pathology and can exert beneficial, detrimental, or mixed effects following brain insults. Transforming growth factor-β (TGF-β) has been identified as one of the key factors regulating astrocyte reactivity. The genetic and pharmacological manipulation of the TGF-β signaling pathway in animal models of central n

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Prunell, Giselle, and Silvia Olivera-Bravo. "A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology." Biomolecules 12, no. 12 (2022): 1745. http://dx.doi.org/10.3390/biom12121745.

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Parkinson’s disease (PD) is an incurable neurodegenerative disease of high prevalence, characterized by the prominent death of dopaminergic neurons in the substantia nigra pars compacta, which produces dopamine deficiency, leading to classic motor symptoms. Although PD has traditionally been considered as a neuronal cell autonomous pathology, in which the damage of vulnerable neurons is responsible for the disease, growing evidence strongly suggests that astrocytes might have an active role in the neurodegeneration observed. In the present review, we discuss several studies evidencing astrocyt

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Tyurikova, Olga, Thomas Jensen, and Dmitri Rusakov. "Exploring astrocyte structure and function in live human brain tissue." Ageing & Longevity, no. 3.2025 (June 25, 2025): 194–98. https://doi.org/10.47855/jal9020-2025-3-3.

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Astrocytes are essential regulators of neural function, yet their roles in brain ageing remain poorly understood. In this study, we present an optimized protocol for examining astrocyte structure and physiology in live human brain slices obtained from neurosurgical resections. This ex vivo approach preserves key human-specific cellular features and enables detailed analysis of astrocytic membrane properties, calcium dynamics, and structural morphology using electrophysiology and advanced imaging techniques. We outline key methodological considerations for tissue handling, slicing, and experime

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Picca, Anna, Evelyn Ferri, Riccardo Calvani, Hélio J. Coelho-Júnior, Emanuele Marzetti, and Beatrice Arosio. "Age-Associated Glia Remodeling and Mitochondrial Dysfunction in Neurodegeneration: Antioxidant Supplementation as a Possible Intervention." Nutrients 14, no. 12 (2022): 2406. http://dx.doi.org/10.3390/nu14122406.

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Aging induces substantial remodeling of glia, including density, morphology, cytokine expression, and phagocytic capacity. Alterations of glial cells, such as hypertrophy of lysosomes, endosomes and peroxisomes, and the progressive accumulation of lipofuscin, lipid droplets, and other debris have also been reported. These abnormalities have been associated with significant declines of microglial processes and reduced ability to survey the surrounding tissue, maintain synapses, and recover from injury. Similarly, aged astrocytes show reduced capacity to support metabolite transportation to neur

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Farmer, Brandon, Jude Kluemper, and Lance Johnson. "Apolipoprotein E4 Alters Astrocyte Fatty Acid Metabolism and Lipid Droplet Formation." Cells 8, no. 2 (2019): 182. http://dx.doi.org/10.3390/cells8020182.

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Lipid droplets (LDs) serve as energy rich reservoirs and have been associated with apolipoprotein E (APOE) and neurodegeneration. The E4 allele of APOE (E4) is the strongest genetic risk factor for the development of late onset Alzheimer’s disease (AD). Since both E4 carriers and individuals with AD exhibit a state of cerebral lipid dyshomeostasis, we hypothesized that APOE may play a role in regulating LD metabolism. We found that astrocytes expressing E4 accumulate significantly more and smaller LDs compared to E3 astrocytes. Accordingly, expression of perilipin-2, an essential LD protein co

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Szeky, Balazs, Veronika Jurakova, Eliska Fouskova, et al. "Efficient derivation of functional astrocytes from human induced pluripotent stem cells (hiPSCs)." PLOS ONE 19, no. 12 (2024): e0313514. https://doi.org/10.1371/journal.pone.0313514.

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Astrocytes are specialized glial cell types of the central nervous system (CNS) with remarkably high abundance, morphological and functional diversity. Astrocytes maintain neural metabolic support, synapse regulation, blood-brain barrier integrity and immunological homeostasis through intricate interactions with other cells, including neurons, microglia, pericytes and lymphocytes. Due to their extensive intercellular crosstalks, astrocytes are also implicated in the pathogenesis of CNS disorders, such as ALS (amyotrophic lateral sclerosis), Parkinson’s disease and Alzheimer’s disease. Despite

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Firth, Wyn, Katherine R. Pye, and Paul G. Weightman Potter. "Astrocytes at the intersection of ageing, obesity, and neurodegeneration." Clinical Science 138, no. 8 (2024): 515–36. http://dx.doi.org/10.1042/cs20230148.

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Abstract Once considered passive cells of the central nervous system (CNS), glia are now known to actively maintain the CNS parenchyma; in recent years, the evidence for glial functions in CNS physiology and pathophysiology has only grown. Astrocytes, a heterogeneous group of glial cells, play key roles in regulating the metabolic and inflammatory landscape of the CNS and have emerged as potential therapeutic targets for a variety of disorders. This review will outline astrocyte functions in the CNS in healthy ageing, obesity, and neurodegeneration, with a focus on the inflammatory responses a

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Sobral, Ana Filipa, Inês Costa, Vanessa Teixeira, Renata Silva, and Daniel José Barbosa. "Molecular Motors in Blood–Brain Barrier Maintenance by Astrocytes." Brain Sciences 15, no. 3 (2025): 279. https://doi.org/10.3390/brainsci15030279.

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The blood–brain barrier (BBB) comprises distinct cell types, including endothelial cells, pericytes, and astrocytes, and is essential for central nervous system (CNS) homeostasis by selectively regulating molecular transport and maintaining integrity. In particular, astrocytes are essential for BBB function, as they maintain BBB integrity through their end-feet, which form a physical and biochemical interface that enhances endothelial cell function and barrier selectivity. Moreover, they secrete growth factors like vascular endothelial growth factor (VEGF) and transforming growth factor-beta (

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Vishnumukkala, Thirupathirao, Ravindra Kumar Boddeti, Prarthana Kalerammana Gopalakrishna, et al. "Neuroprotective Effects of Centella asiatica Against AlCl3 and D-Galactose-Induced Astrocyte Activation and Hippocampal Neurodegeneration in Male Albino Wistar Rats." International Journal of Anatomy and Research 13, no. 1 (2025): 9118–26. https://doi.org/10.16965/ijar.2024.246.

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Background: Alzheimer's disease (AD) a neurodegenerative disorder is a leading cause of dementia in the elderly population. The concurrent dosing of rats with aluminium chloride (AlCl3) and D-galactose (D-gal) is regarded an effective approach for developing an animal model to study AD. Centella asiatica (CA) demonstrates neuroprotective effects in both in vitro and in vivo studies. This research investigated the protective effects of CA against neurodegeneration of the hippocampus and activation of astrocytes in rats treated with AlCl3 and D-gal. Materials and methods: Rats received AlCl3 at

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Ugbode, Chris, Yuhan Hu, Benjamin Whalley, Chris Peers, Marcus Rattray, and Mark L. Dallas. "Astrocytic transporters in Alzheimer's disease." Biochemical Journal 474, no. 3 (2017): 333–55. http://dx.doi.org/10.1042/bcj20160505.

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Astrocytes play a fundamental role in maintaining the health and function of the central nervous system. Increasing evidence indicates that astrocytes undergo both cellular and molecular changes at an early stage in neurological diseases, including Alzheimer's disease (AD). These changes may reflect a change from a neuroprotective to a neurotoxic phenotype. Given the lack of current disease-modifying therapies for AD, astrocytes have become an interesting and viable target for therapeutic intervention. The astrocyte transport system covers a diverse array of proteins involved in metabolic supp

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Caruso, Carla, Lila Carniglia, Daniela Durand, Teresa N. Scimonelli, and Mercedes Lasaga. "Astrocytes: new targets of melanocortin 4 receptor actions." Journal of Molecular Endocrinology 51, no. 2 (2013): R33—R50. http://dx.doi.org/10.1530/jme-13-0064.

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Astrocytes exert a wide variety of functions with paramount importance in brain physiology. After injury or infection, astrocytes become reactive and they respond by producing a variety of inflammatory mediators that help maintain brain homeostasis. Loss of astrocyte functions as well as their excessive activation can contribute to disease processes; thus, it is important to modulate reactive astrocyte response. Melanocortins are peptides with well-recognized anti-inflammatory and neuroprotective activity. Although melanocortin efficacy was shown in systemic models of inflammatory disease, mec

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Mirzaei, Nazanin, Nicola Davis, Tsz Wing Chau, and Magdalena Sastre. "Astrocyte Reactivity in Alzheimer’s Disease: Therapeutic Opportunities to Promote Repair." Current Alzheimer Research 19, no. 1 (2022): 1–15. http://dx.doi.org/10.2174/1567205018666211029164106.

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: Astrocytes are fast climbing the ladder of importance in neurodegenerative disorders, particularly in Alzheimer’s disease (AD), with the prominent presence of reactive astrocytes sur- rounding amyloid β- plaques, together with activated microglia. Reactive astrogliosis, implying morphological and molecular transformations in astrocytes, seems to precede neurodegeneration, suggesting a role in the development of the disease. Single-cell transcriptomics has recently demon- strated that astrocytes from AD brains are different from “normal” healthy astrocytes, showing dys- regulations in areas s

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Nikonenko, A. G. "Astrocytes play critical roles in neuroinflammation and Parkinson’s disease." Fiziolohichnyĭ zhurnal 70, no. 6 (2024): 110–17. https://doi.org/10.15407/fz70.06.110.

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Parkinson’s disease (PD) is a multifactorial disorder characterized mainly by the loss of dopaminergic neurons in the substantia nigra of the brain. The pathogenesis of a spontaneous PD is suggested to be multifactorial, an aberrant immune function being one of the factors influencing PD-associated neurodegeneration. It was found that negrostriatal astrocytes get involved in this process. Astrocytes play vital roles in brain homeostasis as well as participate in the local innate immune response triggered by a variety of insults. Astrocytes are not immune cells, but when sensing injury-associat

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Wang, Min, Tian Tian, Hong Zhou, et al. "Metformin normalizes mitochondrial function to delay astrocyte senescence in a mouse model of Parkinson’s disease through Mfn2-cGAS signaling." Journal of Neuroinflammation 21, no. 1 (2024). http://dx.doi.org/10.1186/s12974-024-03072-0.

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Abstract Background Senescent astrocytes play crucial roles in age-associated neurodegenerative diseases, including Parkinson’s disease (PD). Metformin, a drug widely used for treating diabetes, exerts longevity effects and neuroprotective activities. However, its effect on astrocyte senescence in PD remains to be defined. Methods Long culture-induced replicative senescence model and 1-methyl-4-phenylpyridinium/α-synuclein aggregate-induced premature senescence model, and a mouse model of PD were used to investigate the effect of metformin on astrocyte senescence in vivo and in vitro. Immunofl

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Mockenhaupt, Karli, Masoumeh Zarei‐Kheirabadi, Alexandra K. Gonsiewski, et al. "Defective Astrocyte Maturation Drives Cerebellar Neuroinflammation and Degeneration." FASEB Journal 39, no. 14 (2025). https://doi.org/10.1096/fj.202501225rr.

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ABSTRACTWhile persistent neuroinflammation and neurodegeneration are hallmarks of many diseases, the exact mechanisms triggering neurodegeneration are not fully established. Neurodegeneration is accompanied by activation of astrocytes that can have both neuroprotective and neurotoxic functions. Much less is known about how intrinsic dysfunction of astrocytes can lead to neuroinflammation and neurodegeneration. To study astrocyte‐driven neurodegeneration, we examined aging cerebella of adult astrocyte‐specific Yin Yang1 (Yy1) conditional knockout mice that contain improperly matured dysfunction

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Huang, Jingxuan, Chunyu Li, and Huifang Shang. "Astrocytes in Neurodegeneration: Inspiration From Genetics." Frontiers in Neuroscience 16 (June 24, 2022). http://dx.doi.org/10.3389/fnins.2022.882316.

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Despite the discovery of numerous molecules and pathologies, the pathophysiology of various neurodegenerative diseases remains unknown. Genetics participates in the pathogenesis of neurodegeneration. Neural dysfunction, which is thought to be a cell-autonomous mechanism, is insufficient to explain the development of neurodegenerative disease, implying that other cells surrounding or related to neurons, such as glial cells, are involved in the pathogenesis. As the primary component of glial cells, astrocytes play a variety of roles in the maintenance of physiological functions in neurons and ot

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Monterey, Michael D., Haichao Wei, Xizi Wu, and Jia Qian Wu. "The Many Faces of Astrocytes in Alzheimer's Disease." Frontiers in Neurology 12 (August 31, 2021). http://dx.doi.org/10.3389/fneur.2021.619626.

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Alzheimer's disease (AD) is a progressive neurodegenerative disease and is the most common cause of dementia in an aging population. The majority of research effort has focused on the role of neurons in neurodegeneration and current therapies have limited ability to slow disease progression. Recently more attention has been given to the role of astrocytes in the process of neurodegeneration. Specifically, reactive astrocytes have both advantageous and adverse effects during neurodegeneration. The ability to isolate and depict astrocyte phenotype has been challenging. However, with the recent d

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Han, Xiaojuan, Qing Lei, Huanhuan Liu, Tianying Zhang, and Xingchun Gou. "SerpinA3N regulates the secretory phenotype of mouse senescent astrocytes contributing to neurodegeneration." Journals of Gerontology, Series A: Biological Sciences and Medical Sciences, January 4, 2024. http://dx.doi.org/10.1093/gerona/glad278.

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Abstract Senescent astrocyte accumulation in the brain during normal aging is a driver of age-related neurodegenerative diseases such as Alzheimer's disease (AD). However, the molecular events underlying astrocyte senescence in AD are not fully understood. In this study, we demonstrated that senescent astrocytes display a secretory phenotype known as the senescence-associated secretory phenotype (SASP), which is associated with the upregulation of various proinflammatory factors and the downregulation of neurotrophic growth factors (e.g., NGF and BDNF), resulting in a decrease in astrocyte-med

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Mi, Yashi, Guoyuan Qi, Francesca Vitali, et al. "Loss of Fatty Acid Degradation by Astrocytic Mitochondria as a Mechanism of Neuroinflammation and Neurodegeneration." Alzheimer's & Dementia 19, S13 (2023). http://dx.doi.org/10.1002/alz.076572.

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AbstractBackgroundAstrocytes provide key neuronal support, and their phenotypic transformation is strongly implicated in neurodegenerative disorders including Alzheimer’s disease (AD). Metabolically, astrocytes possess modest mitochondrial oxidative phosphorylation (OxPhos) activity, yet the pathological role of astrocytic OxPhos in neurodegeneration remains to be defined.MethodWe generated the TfamAKO mice, in which the transcription factor A mitochondrial (Tfam) is deleted selectively in astrocytes. Behavioral, electrophysiological, immunostaining, transcriptomics, metabolomics, and magnetic

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Yang, Fangjia, Paula Beltran-Lobo, Katherine Sung, et al. "Reactive astrocytes secrete the chaperone HSPB1 to mediate neuroprotection." Science Advances 10, no. 12 (2024). http://dx.doi.org/10.1126/sciadv.adk9884.

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Molecular chaperones are protective in neurodegenerative diseases by preventing protein misfolding and aggregation, such as extracellular amyloid plaques and intracellular tau neurofibrillary tangles in Alzheimer’s disease (AD). In addition, AD is characterized by an increase in astrocyte reactivity. The chaperone HSPB1 has been proposed as a marker for reactive astrocytes; however, its astrocytic functions in neurodegeneration remain to be elucidated. Here, we identify that HSPB1 is secreted from astrocytes to exert non–cell-autonomous protective functions. We show that in human AD brain, HSP

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Chou, Tsui-Wen, Nydia P. Chang, Medha Krishnagiri та ін. "Fibrillar α-synuclein induces neurotoxic astrocyte activation via RIP kinase signaling and NF-κB". Cell Death & Disease 12, № 8 (2021). http://dx.doi.org/10.1038/s41419-021-04049-0.

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AbstractParkinson’s disease (PD) is a neurodegenerative disorder characterized by the death of midbrain dopamine neurons. The pathogenesis of PD is poorly understood, though misfolded and/or aggregated forms of the protein α-synuclein have been implicated in several neurodegenerative disease processes, including neuroinflammation and astrocyte activation. Astrocytes in the midbrain play complex roles during PD, initiating both harmful and protective processes that vary over the course of the disease. However, despite their significant regulatory roles during neurodegeneration, the cellular and

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