AQP4 ELISA kit
- Known as:
- AQP4 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-AQP4-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- AQP4 ELISA kit
Related genes to: AQP4 ELISA kit
- Gene:
- AQP4 NIH gene
- Name:
- aquaporin 4
- Previous symbol:
- -
- Synonyms:
- MIWC
- Chromosome:
- 18q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-25
- Date modifiied:
- 2016-10-05
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- Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune astrocytopathy frequently complicated by neuropathic pain. Paroxysmal symptoms likely arise from ephaptic transmission within demyelinated spinal cord tracts and are underdescribed when presenting as isolated sensory phenomena, unlike the well-characterized tonic spasms. We report a 76-year-old woman with aquaporin-4 (AQP4) antibody-positive NMOSD recovering from her first disease flare, which initially manifested as longitudinally extensive transverse myelitis (LETM). Weeks later, she developed sudden, excruciating, movement-provoked paroxysmal burning pain in the lower extremities. Episodes lasted 4-8 seconds and occurred approximately 20 times daily. Serial neurologic examinations revealed no new deficits suggestive of relapse, and repeat MRI was deferred as relapse was considered clinically unlikely. Symptoms were refractory to gabapentin but improved dramatically within 24 hours of initiating oxcarbazepine 300 mg twice daily. The clinical phenotype and rapid response to sodium channel blockade support a sodium channel-mediated mechanism, most likely ephaptic transmission, rather than trigger-independent ectopic firing, which remains sparsely described in the literature. Recognition of this phenomenon is crucial to avoid misclassification as relapse, unnecessary imaging, and unwarranted escalation of immunotherapy. - Source: PubMed
Publication date: 2026/08/02
Philips AngelaSosa De La Cruz JohanUngerer RobertBetha Prudvi Tarun - Accumulation of amyloid-beta (Aβ) deposits is one of the neuropathological hallmarks of Alzheimer's disease (AD), the most frequent neurodegenerative disease in all age groups. While decades of research have focused on the production and aggregation of Aβ peptides, mounting evidence implicate impaired brain fluid dynamics and protein waste clearance as critical contributors to AD pathogenesis. The aquaporin family of water channels, particularly aquaporin-4 (AQP4) and AQP1, has emerged as central regulators of brain interstitial fluid (ISF) homeostasis and Aβ clearance. AQP4, expressed at the perivascular endfeet of astrocytes, is the principal water channel driving fluid convection exchange, acting as a brain-wide network in which ISF and solutes are cleared via venous, paravenous and periarterial routes, as well as through dural lymphatic vessels and along perineural spaces. AQP1, expressed predominantly in the choroid plexus epithelium, governs cerebrospinal fluid (CSF) secretion and thereby modulates the pressure gradients that sustain this convective flow. This review provides an integrated overview of the molecular pathology of AD, the physiological roles of AQP4 and AQP1, together with the major anatomical pathways of ISF and CSF drainage from the brain. We next address to the genetic and pharmacological modulation of AQP4 and AQP1 in transgenic AD mouse models and describe the resulting pathological changes. AQP4 knockout consistently exacerbates Aβ pathology and cognitive deficits, with the abnormal distribution of AQP4 within the astrocyte being sufficient to impair clearance, and these data highlight the critical importance of polarized expression versus bulk expression levels. AQP1 modulation, though less studied, alters CSF dynamics and may influence Aβ clearance indirectly through changes in CSF turnover. Pharmacological agents targeting AQP4 and AQP1 offer promising avenues for therapeutic intervention. Understanding the distinct and intersecting roles of aquaporins in brain fluid homeostasis may yield novel strategies for restoring protein clearance in AD. - Source: PubMed
Publication date: 2026/08/18
Manescu Marina DanielaMinca TeodoraPirici IonicaBusuioc Cristina JanaMateescu Valentin OctavianPirici Daniel - Acute brain injury (ABI) frequently precipitates severe extracranial target-organ complications, with the lungs being the most directly and fatally affected distant organs. Traditionally, the rapid onset of pulmonary dysfunction following brain injury has been attributed to the "massive catecholamine release"-a massive, dysregulated release of catecholamines leading to intense systemic vasoconstriction, elevated pulmonary capillary hydrostatic pressure, and subsequent neurogenic pulmonary edema. However, this purely neuro-hemodynamic model falls short of explaining the delayed onset and highly inflammatory nature of acute respiratory distress syndrome that persists during the later stages of injury. Recently, the discovery of the glymphatic system has provided a groundbreaking molecular and anatomical framework for understanding the pathological crosstalk within the "brain-lung axis." As a macroscopic waste clearance network within the central nervous system highly dependent on the polarized expression of aquaporin-4 (AQP4), the glymphatic system undergoes structural and functional severe impairment following ABI. The loss of AQP4 polarization, coupled with reactive astrogliosis, halts cerebrospinal fluid-interstitial fluid exchange. This drainage failure not only forces the massive accumulation of damage-associated molecular patterns and pro-inflammatory cytokines within the brain parenchyma but also drives the systemic "spillover" of high-concentration neurogenic toxins through enzymatic disruption of the blood-brain barrier and the hijacked meningeal lymphatics. These brain-derived mediators-whether circulating freely or encapsulated within extracellular vesicles-travel via the systemic circulation to the pulmonary capillary bed. Upon reaching the lungs, they specifically target pulmonary microvascular endothelial cells by binding to TLR4 and RAGE receptors, triggering the phosphorylation and internalization of vascular endothelial cadherin, and thus completely dismantling the endothelial barrier. Concurrently, these signals drive the M1 polarization of alveolar macrophages, eliciting destructive neutrophil infiltration and parenchymal damage. Crucially, this pulmonary dysfunction generates severe hypoxemia and releases lung-derived inflammatory mediators that feed back to the central nervous system, establishing a fatal bidirectional vicious cycle. This narrative conceptual review aims to comprehensively dissect the bidirectional immune-inflammatory cascade network of the brain-lung axis triggered by glymphatic collapse and systematically evaluate the latest therapeutic prospects, considering the impact of pre-morbid systemic stressors and mechanical ventilation, while targeting AQP4 modulation, lymphangiogenesis, and systemic inflammation blockade. - Source: PubMed
Publication date: 2026/08/18
Mao LielongYang ZhiweiJiang Feijun - Autoimmune disorders are characterized by impaired immune tolerance, largely mediated by CD4⁺ regulatory T cells (Tregs), whose function depends on the transcription factor FOXP3. - Source: PubMed
Publication date: 2026/08/11
Lago JulianaNarvaéz Diana MVillanueva Sara ValentinaGaitán JairoNoriega Juan PabloRodriguez DanielaIbarra Luis FelipeCortés-Muñoz FabianReyes SaúlGroot HelenaToro Jaime - Pediatric-onset multiple sclerosis (POMS) is uncommon but clinically relevant, as inflammatory demyelination occurs during brain maturation. Compared with adult-onset MS, POMS is characterized by higher early relapse rate and MRI inflammatory activity, better recovery from individual relapses, yet disability milestones are reached at a younger age. Early identification is essential to avoid treatment delays, while preventing misdiagnosis of mimics. - Source: PubMed
Publication date: 2026/09/01
Margoni MonicaFilippi MassimoRocca Maria A