Targeting hyperphosphorylated tau with sodium selenate suppresses seizures in rodent models

Neurobiology of Disease

Volumn 45, Issue 3, 2012, Pages 897-901

  Jones, Nigel C ^a   Nguyen, Thanh ^a   Corcoran, Niall M ^a   Velakoulis, Dennis ^a   Chen, Tracy ^b   Grundy, Robert ^c   O'Brien, Terence J ^a   Hovens, Christopher M ^a  

^a UNIVERSITY OF MELBOURNE   (Australia)

^b NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE   (United States)

^c Cerebricon Limited   (Finland)

Author keywords

Epilepsy models; Hyperphosphorylated tau; Seizure; Sodium selenate; Therapy

Indexed keywords

DRINKING WATER; OKADAIC ACID; PENTETRAZOLE; PHOSPHOPROTEIN PHOSPHATASE 2A; SELENATE; TAU PROTEIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTISEIZURE ACTIVITY; ARTICLE; COMBINATION CHEMOTHERAPY; CONTROLLED STUDY; CORNEA; DISEASE DURATION; DISEASE SEVERITY; DOSE RESPONSE; DRUG ACTIVITY; DRUG EFFECT; ELECTRICAL CORNEAL STIMULATION; ELECTROSTIMULATION; EVOKED CORTICAL RESPONSE; HUMAN; HUMAN CELL; IN VITRO STUDY; IN VIVO STUDY; MALE; MONOTHERAPY; MOUSE; NEUROPROTECTION; NONHUMAN; PRIORITY JOURNAL; PROTEIN HYPERPHOSPHORYLATION; PROTEIN PHOSPHORYLATION; PROTEIN TARGETING; RAT; SEIZURE; TREATMENT DURATION;

AMYGDALA; ANALYSIS OF VARIANCE; ANIMALS; ANTIOXIDANTS; CELL LINE, TUMOR; CONVULSANTS; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; ELECTRIC STIMULATION; ENZYME INHIBITORS; GENE EXPRESSION REGULATION; HUMANS; LEUCINE; MALE; MUTATION; NEUROBLASTOMA; OKADAIC ACID; PENTYLENETETRAZOLE; PHOSPHORYLATION; PROLINE; RATS; RATS, SPRAGUE-DAWLEY; RATS, WISTAR; SEIZURES; SELENIUM COMPOUNDS; TAU PROTEINS; TIME FACTORS; TRANSFECTION;

EID: 84856561031     PISSN: 09699961     EISSN: 1095953X     Source Type: Journal    
DOI: 10.1016/j.nbd.2011.12.005     Document Type: Article

References (24)

1. Amatniek J.C., et al. Incidence and predictors of seizures in patients with Alzheimer's disease. Epilepsia 2006, 47:867-872.
2. Activating PP2A as a therapeutic intervention strategy in Alzheimer's disease. Royal Society of Chemistry 2010, N. Corcoran, C. Hovens (Eds.).
3. Corcoran N.M., et al. Open-label, phase I dose-escalation study of sodium selenate, a novel activator of PP2A, in patients with castration-resistant prostate cancer. Br. J. Cancer 2010, 103:462-468.
4. Corcoran N.M., et al. Sodium selenate specifically activates PP2A phosphatase, dephosphorylates tau and reverses memory deficits in an Alzheimer's disease model. J. Clin. Neurosci. 2010, 17:1025-1033.
5. Crespo-Biel N., et al. Kainate induces AKT, ERK and cdk5/GSK3beta pathway deregulation, phosphorylates tau protein in mouse hippocampus. Neurochem. Int. 2007, 50:435-442.
6. D'Ambrosio R., et al. Progression from frontal-parietal to mesial-temporal epilepsy after fluid percussion injury in the rat. Brain 2005, 128:174-188.
7. Del Vecchio R.A., et al. Increased seizure threshold and severity in young transgenic CRND8 mice. Neurosci. Lett. 2004, 367:164-167.
8. Deters N., et al. Substrate-specific reduction of PP2A activity exaggerates tau pathology. Biochem. Biophys. Res. Commun. 2009, 379:400-405.
9. Galimberti D., Scarpini E. Alzheimer's disease: from pathogenesis to disease-modifying approaches. CNS Neurol. Disord. Drug Targets 2011, 10:163-174.
10. Ittner L.M., et al. Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models. Cell 2010, 142:387-397.
11. Jellinger Head injury and dementia. Curr. Opin. Neurol. 2005, 17:719-723.
12. Liang Z., et al. Dysregulation of tau phosphorylation in mouse brain during excitotoxic damage. J. Alzheimers Dis. 2009, 17:531-539.
13. Liu F., et al. Contributions of protein phosphatases PP1, PP2A, PP2B and PP5 to the regulation of tau phosphorylation. Eur. J. Neurosci. 2005, 22:1942-1950.
14. Marks D.A., et al. Seizure localization and pathology following head injury in patients with uncontrolled epilepsy. Neurology 1995, 45:2051-2057.
15. Mendez M.F., et al. Seizures in Alzheimer's disease: clinicopathologic study. J. Geriatr. Psychiatry Neurol. 1994, 7:230-233.
16. Morimoto K., et al. Kindling and status epilepticus models of epilepsy: rewiring the brain. Prog. Neurobiol. 2004, 73:1-60.
17. Palop J.J., Mucke L. Epilepsy and cognitive impairments in Alzheimer disease. Arch. Neurol. 2009, 66:435-440.
18. Racine R., et al. Modification of seizure activity by electrical stimulation. 3. Mechanisms. Electroencephalogr. Clin. Neurophysiol. 1972, 32:295-299.
19. Roberson E.D., et al. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model. Science 2007, 316:750-754.
20. Salzberg M., et al. Early postnatal stress confers enduring vulnerability to limbic epileptogenesis. Epilepsia 2007, 48:2079-2085.
21. Sen A., et al. Pathological tau tangles localize to focal cortical dysplasia in older patients. Epilepsia 2007, 48:1447-1454.
22. Tian F.F., et al. Potential roles of Cdk5/p35 and tau protein in hippocampal mossy fiber sprouting in the PTZ kindling model. Clin. Lab. 2010, 56:127-136.
23. van Eersel J., et al. Sodium selenate mitigates tau pathology, neurodegeneration, and functional deficits in Alzheimer's disease models. Proc. Natl. Acad. Sci. U.S.A. 2010, 107:13888-13893.
24. White H.S. Preclinical development of antiepileptic drugs: past, present, and future directions. Epilepsia 2003, 44(Suppl 7):2-8.