ArticleMolecular medicine reports2017
Alterations in AQP4 expression and polarization in the course of motor neuron degeneration in SOD1G93A mice.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Bridging the gap: neuroinflammation and the dawn of precision medicine in amyotrophic lateral sclerosis.Translational neurodegeneration · 2026Review
- Aquaporin dysfunction and impaired brain interstitial fluid clearance in Alzheimer's disease - an integrative review.Frontiers in cellular neuroscience · 2026Review
- Region-specific features of early glial activation and Aquaporin-4 dysregulation in conditional mouse models of TDP-43 proteinopathies.Discovery immunology · 2026Article
- Neurovascular Dysfunction and Glymphatic Impairment: An Unexplored Therapeutic Frontier in Neurodegeneration.International journal of molecular sciences · 2025Review
- The Fluidic Connectome in Brain Disease: Integrating Aquaporin-4 Polarity with Multisystem Pathways in Neurodegeneration.International journal of molecular sciences · 2025Review
- Glymphatic System Dysregulation as a Key Contributor to Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2025Review
- Non-coding RNAs and Aquaporin 4: Their Role in the Pathogenesis of Neurological Disorders.Neurochemical research · 2024Review
- Liquiritin ameliorates painful diabetic neuropathy in SD rats by inhibiting NLRP3-MMP-9-mediated reversal of aquaporin-4 polarity in the glymphatic system.Frontiers in pharmacology · 2024Article
- Exploring Astrocyte-Mediated Mechanisms in Sleep Disorders and Comorbidity.Biomedicines · 2023Review
- Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice.Acta neuropathologica communications · 2023Article
- Astrocytes: Dissecting Their Diverse Roles in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.Cells · 2023Review
- A Microfluidic Model of AQP4 Polarization Dynamics and Fluid Transport in the Healthy and Inflamed Human Brain: The First Step Towards Glymphatics-on-a-Chip.Advanced biology · 2022Article
- Research Evidence of the Role of the Glymphatic System and Its Potential Pharmacological Modulation in Neurodegenerative Diseases.Journal of clinical medicine · 2022Review
- Article
- Ion Channel Dysfunction in Astrocytes in Neurodegenerative Diseases.Frontiers in physiology · 2022Review
- Glymphatic System Dysfunction in Central Nervous System Diseases and Mood Disorders.Frontiers in aging neuroscience · 2022Review
- Blood-Brain Barrier Dysfunction in CNS Disorders and Putative Therapeutic Targets: An Overview.Pharmaceutics · 2021Review
- Attenuation of cerebral edema facilitates recovery of glymphatic system function after status epilepticus.JCI insight · 2021Article
- The Glymphatic System: A Novel Therapeutic Target for Stroke Treatment.Frontiers in aging neuroscience · 2021Review
- Defining novel functions for cerebrospinal fluid in ALS pathophysiology.Acta neuropathologica communications · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by selective degeneration of upper and lower motor neurons. The disease progression is associated with the astrocytic environment. Aquaporin-4 (AQP4) water channels are the most abundant AQPs expressed in astrocytes, exerting important influences on central nervous system homeostasis. The present study aimed to characterize the alterations in AQP4 expression and loca-lization in superoxide dismutase 1 (SOD1) G93A transgenic mice. SOD1G93A mice were sacrificed during the presymptomatic, disease onset and end stages and immunostaining was performed on spinal cord sections to investigate neuronal loss, glial activation and AQP4 expression in the spinal cord. It was observed that global AQP4 expression increased in the spinal cord of SOD1G93A mice as the disease progressed. However, AQP4 polarization decreased as the disease progressed, and AQP4 polarized localization at the endfeet of astrocytes was decreased in the spinal ventral horn of SOD1G93A mice at the disease onset and end stages. Meanwhile, motor neuron dege-neration and decreased glutamate transporter 1 expression in astrocytes in SOD1G93A mice were observed as the disease progressed. The results of the present study demonstrated that AQP4 depolarization is a widespread pathological condition and may contribute to motor neuron degeneration in ALS.
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