ArticleActa neuropathologica communications2020
Behavioral and electrophysiological evidence for a neuroprotective role of aquaporin-4 in the 5xFAD transgenic mice model.
Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- AQP4-dependent enhancement of glymphatic function attenuates tau pathology and neurodegeneration in PS19 mice.Molecular neurodegeneration · 2026Article
- Therapeutic targeting of fibrin-microglia interactions ameliorates Alzheimer's disease-related hyperexcitability and brain network dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Aquaporin dysfunction and impaired brain interstitial fluid clearance in Alzheimer's disease - an integrative review.Frontiers in cellular neuroscience · 2026Review
- Hyperactivity of subicular parvalbumin interneurons drives early amyloid pathology and cognitive deficits in Alzheimer's disease.Molecular psychiatry · 2025Article
- The Glymphatic System in Cerebrospinal Fluid Dynamics: Clinical Implications, Its Evaluation, and Application to Therapeutics.Neuro-degenerative diseases · 2025Review
- Behaviour Hallmarks in Alzheimer's Disease 5xFAD Mouse Model.International journal of molecular sciences · 2024Review
- Seizures exacerbate excitatory: inhibitory imbalance in Alzheimer's disease and 5XFAD mice.Brain : a journal of neurology · 2024Article
- Involvement of the glymphatic/meningeal lymphatic system in Alzheimer's disease: insights into proteostasis and future directions.Cellular and molecular life sciences : CMLS · 2024Review
- Investigating metabolic dysregulation in serum of triple transgenic Alzheimer's disease male mice: implications for pathogenesis and potential biomarkers.Amino acids · 2024Article
- Inflammatory signaling pathways in the treatment of Alzheimer's disease with inhibitors, natural products and metabolites (Review).International journal of molecular medicine · 2023Review
- The Expression of Major Facilitator Superfamily Domain-Containing Protein2a (Mfsd2a) and Aquaporin 4 Is Altered in the Retinas of a 5xFAD Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Multifaceted Roles of Aquaporins in the Pathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Levetiracetam modulates brain metabolic networks and transcriptomic signatures in the 5XFAD mouse model of Alzheimer's disease.Frontiers in neuroscience · 2023Article
- Preserved blood-brain barrier and neurovascular coupling in female 5xFAD model of Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- The Role of Glymphatic System in Alzheimer's and Parkinson's Disease Pathogenesis.Biomedicines · 2022Review
- The role of mTORC1 activation in seizure-induced exacerbation of Alzheimer's disease.Brain : a journal of neurology · 2022Article
- Glymphatic system clears extracellular tau and protects from tau aggregation and neurodegeneration.The Journal of experimental medicine · 2022Article
- Distribution of intraperitoneally administered deuterium-labeled water in aquaporin-4-knockout mouse brain after middle cerebral artery occlusion.Frontiers in neuroscience · 2022Article
- Sleep: The Tip of the Iceberg in the Bidirectional Link Between Alzheimer's Disease and Epilepsy.Frontiers in neurology · 2022Review
- Emerging Electroencephalographic Biomarkers to Improve Preclinical to Clinical Translation in Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
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Authors and funding
22 authors.
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Abstract
Aquaporin-4 (AQP4) has been suggested to be involved in the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD), which may be due to the modulation of neuroinflammation or the impairment of interstitial fluid bulk flow system in the central nervous system. Here, we show an age-dependent impairment of several behavioral outcomes in 5xFAD AQP4 null mice. Twenty-four-hour video recordings and computational analyses of their movement revealed that the nighttime motion of AQP4-deficient 5xFAD mice was progressively reduced between 20 and 36 weeks of age, with a sharp deterioration occurring between 30 and 32 weeks. This reduction in nighttime motion was accompanied by motor dysfunction and epileptiform neuronal activities, demonstrated by increased abnormal spikes by electroencephalography. In addition, all AQP4-deficient 5xFAD mice exhibited convulsions at least once during the period of the analysis. Interestingly, despite such obvious phenotypes, parenchymal amyloid β (Aβ) deposition, reactive astrocytosis, and activated microgliosis surrounding amyloid plaques were unchanged in the AQP4-deficient 5xFAD mice relative to 5xFAD mice. Taken together, our data indicate that AQP4 deficiency greatly accelerates an age-dependent deterioration of neuronal function in 5xFAD mice associated with epileptiform neuronal activity without significantly altering Aβ deposition or neuroinflammation in this mouse model. We therefore propose that there exists another pathophysiological phase in AD which follows amyloid plaque deposition and neuroinflammation and is sensitive to AQP4 deficiency.
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