ReviewFrontiers in physiology2016
The Influence of Na(+), K(+)-ATPase on Glutamate Signaling in Neurodegenerative Diseases and Senescence.
Review in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 92 citations in OpenAlex.
- A randomized, controlled, double-blind, crossover trial of triheptanoin in alternating hemiplegia of childhood.Orphanet journal of rare diseases · 2017Trial
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- Identification of Copy Number Variations in Familial Hemiplegic Migraine Genes in Suspected Hemiplegic Migraine Patients.Biomedicines · 2026Article
- Personalizing treatment of pancreatitis-associated chronic pain: the need for an integrated omics approach.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Ouabain-induced hypertension in rats: Mechanisms, variability and translational implications.Experimental physiology · 2026Review
- Reconceptualizing bipolar disorder through an integrative biological lens: synthesis, convergence, and emerging directions.Frontiers in integrative neuroscience · 2026Review
- Cognitive impairment and risk of dementia in heart failure: the exuberating role of digoxin.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Unveiling the role of Na⁺/K⁺-ATPase pump: neurodegenerative mechanisms and therapeutic horizons.Pharmacological reports : PR · 2025Review
- Brain tissue electrical conductivity as a promising biomarker for dementia assessment using MRI.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Membrane ATPases and Mitochondrial Proteins in Fetal Cerebellum After Exposure to L-Glutamate During Gestation.Membranes · 2025Article
- Acyclic sesquiterpenes nerolidol and farnesol: mechanistic insights into their neuroprotective potential.Pharmacological reports : PR · 2025Review
- Insights into Vincristine-Induced Peripheral Neuropathy in Aged Rats: Wallerian Degeneration, Oxidative Damage, and Alterations in ATPase Enzymes.ACS chemical neuroscience · 2024Article
- Multigenerational, Indirect Exposure to Pyrethroids Demonstrates Potential Compensatory Response and Reduced Toxicity at Higher Salinity in Estuarine Fish.Environmental science & technology · 2024Article
- Shared Proteins and Pathways of Cardiovascular and Cognitive Diseases: Relation to Vascular Cognitive Impairment.Journal of proteome research · 2024Article
- Variable bioenergetic sensitivity of neurons and astrocytes to insulin and extracellular glucose.npj metabolic health and disease · 2024Article
- Ouabain Reverts CUS-Induced Disruption of the HPA Axis and Avoids Long-Term Spatial Memory Deficits.Biomedicines · 2023Article
- Effect of Ouabain on Glutamate Transport in the Hippocampus of Rats with LPS-Induced Neuroinflammation.Biomedicines · 2023Article
- The role ofFrontiers in cellular neuroscience · 2023Review
- Recent Advances in the Study of NaCells · 2022Review
- Continuous high-frequency deep brain stimulation of the anterior insula modulates autism-like behavior in a valproic acid-induced rat model.Journal of translational medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decreased Na(+), K(+)-ATPase (NKA) activity causes energy deficiency, which is commonly observed in neurodegenerative diseases. The NKA is constituted of three subunits: α, β, and γ, with four distinct isoforms of the catalytic α subunit (α1-4). Genetic mutations in the ATP1A2 gene and ATP1A3 gene, encoding the α2 and α3 subunit isoforms, respectively can cause distinct neurological disorders, concurrent to impaired NKA activity. Within the central nervous system (CNS), the α2 isoform is expressed mostly in glial cells and the α3 isoform is neuron-specific. Mutations in ATP1A2 gene can result in familial hemiplegic migraine (FHM2), while mutations in the ATP1A3 gene can cause Rapid-onset dystonia-Parkinsonism (RDP) and alternating hemiplegia of childhood (AHC), as well as the cerebellar ataxia, areflexia, pescavus, optic atrophy and sensorineural hearing loss (CAPOS) syndrome. Data indicates that the central glutamatergic system is affected by mutations in the α2 isoform, however further investigations are required to establish a connection to mutations in the α3 isoform, especially given the diagnostic confusion and overlap with glutamate transporter disease. The age-related decline in brain α2∕3 activity may arise from changes in the cyclic guanosine monophosphate (cGMP) and cGMP-dependent protein kinase (PKG) pathway. Glutamate, through nitric oxide synthase (NOS), cGMP and PKG, stimulates brain α2∕3 activity, with the glutamatergic N-methyl-D-aspartate (NMDA) receptor cascade able to drive an adaptive, neuroprotective response to inflammatory and challenging stimuli, including amyloid-β. Here we review the NKA, both as an ion pump as well as a receptor that interacts with NMDA, including the role of NKA subunits mutations. Failure of the NKA-associated adaptive response mechanisms may render neurons more susceptible to degeneration over the course of aging.
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