Journal
NEUROPHARMACOLOGY
Volume 169, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2018.12.008
Keywords
Na+/K+-ATPase; neurodegeneration; Alzheimer's disease; Parkinson's disease; ATP1A3 disorders
Categories
Funding
- Centre National de la Recherche Scientifique
- Agence Nationale de la Recherche Scientifique
- EC Joint Programme on Neurodegenerative Diseases [JPND-NeuTARGETs-ANR-14-JPCD-0002-02, JPND-SYNACTION-ANR-15-JPWG-0012-03]
- Institut de FranceFondation Simone et Cino Del Duca
- Fondation Pour La Recherche Medicale [DEQ. 20160334896]
- Innovative Medicine Initiative 2 Joint grant [116060]
- European Union's Horizon 2020 research and innovation program
- EFPIA
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Neuronal Na+/K(+-)ATPase is responsible for the maintenance of ionic gradient across plasma membrane. In doing so, in a healthy brain, Na+/K+-ATPase activity accounts for nearly half of total brain energy consumption. The alpha 3-subunit containing Na+/K+-ATPase expression is restricted to neurons. Heterozygous mutations within alpha 3-subunit leads to Rapid-onset Dystonia Parkinsonism, Alternating Hemiplegia of Childhood and other neurological and neuropsychiatric disorders. Additionally, proteins such as alpha-synuclein, amyloid-beta, tau and SOD1 whose aggregation is associated to neurodegenerative diseases directly bind and impair alpha 3-Na+/K+-ATPase activity. The review will provide a summary of neuronal alpha 3-Na+/K+-ATPase functional properties, expression pattern, protein-protein interactions at the plasma membrane, biophysical properties (distribution and lateral diffusion). Lastly, the role of alpha 3-Na+/K+-ATPase in neurological and neurodegenerative disorders will be discussed. This article is part of the special issue entitled 'Mobility and trafficking of neuronal membrane proteins'.
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