Seizure activity triggers tau hyperphosphorylation and amyloidogenic pathways

Although epilepsies and neurodegenerative disorders show pathophysiological similarities, their direct functional associations are unclear. Here, we tested the hypothesis that experimental seizures can induce tau hyperphosphorylation and amyloidogenic modifications over time, with intersections with neuroinflammation.

[1]  N. Marchi,et al.  Chronic Glucocorticoids Consumption Triggers and Worsens Experimental Alzheimer’s Disease-Like Pathology by Detrimental Immune Modulations , 2021, Neuroendocrinology.

[2]  P. Kwan,et al.  Low prevalence of amyloid and tau pathology in drug‐resistant temporal lobe epilepsy , 2021, Epilepsia.

[3]  P. Calabresi,et al.  Amyloid-β: a potential link between epilepsy and cognitive decline , 2021, Nature Reviews Neurology.

[4]  R. Citraro,et al.  Epidemiology and Outcomes of Status Epilepticus , 2021, International journal of general medicine.

[5]  F. Forbes,et al.  Neurovascular multiparametric MRI defines epileptogenic and seizure propagation regions in experimental mesiotemporal lobe epilepsy , 2021, Epilepsia.

[6]  C. Bernard,et al.  The Kainic Acid Models of Temporal Lobe Epilepsy , 2021, eNeuro.

[7]  L. Buée,et al.  Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer’s disease models and human brains , 2020, Acta Neuropathologica.

[8]  A. Obenaus,et al.  Early cerebrovascular and long-term neurological modifications ensue following juvenile mild traumatic brain injury in male mice , 2020, Neurobiology of Disease.

[9]  Pablo M. Casillas-Espinosa,et al.  Neurodegenerative pathways as targets for acquired epilepsy therapy development , 2020, Epilepsia open.

[10]  O. Meijer,et al.  Glucocorticoid receptors signaling impairment potentiates amyloid‐β oligomers‐induced pathology in an acute model of Alzheimer’s disease , 2020, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[11]  T. Lucas,et al.  Alzheimer-like amyloid and tau alterations associated with cognitive deficit in temporal lobe epilepsy. , 2019, Brain : a journal of neurology.

[12]  Caroline L C Neely,et al.  Nest Building Behavior as an Early Indicator of Behavioral Deficits in Mice. , 2019, Journal of visualized experiments : JoVE.

[13]  E. Audinat,et al.  The GR‐ANXA1 pathway is a pathological player and a candidate target in epilepsy , 2019, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[14]  Emmanuel L. Barbier,et al.  A pericyte‐glia scarring develops at the leaky capillaries in the hippocampus during seizure activity , 2019, Epilepsia.

[15]  A. Vezzani,et al.  Neuroinflammatory pathways as treatment targets and biomarkers in epilepsy , 2019, Nature Reviews Neurology.

[16]  I. Fekete,et al.  The Outcome of Status Epilepticus and Long-Term Follow-Up , 2019, Front. Neurol..

[17]  Mayuren Candasamy,et al.  Emerging pathways to neurodegeneration: Dissecting the critical molecular mechanisms in Alzheimer's disease, Parkinson's disease. , 2019, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.

[18]  L. Givalois,et al.  Central Role of Glucocorticoid Receptors in Alzheimer’s Disease and Depression , 2018, Front. Neurosci..

[19]  L. Petrucelli,et al.  Converging pathways in neurodegeneration, from genetics to mechanisms , 2018, Nature Neuroscience.

[20]  T. Loddenkemper,et al.  Long‐term outcomes of status epilepticus: A critical assessment , 2018, Epilepsia.

[21]  Arthur W Toga,et al.  The role of brain vasculature in neurodegenerative disorders , 2018, Nature Neuroscience.

[22]  S. Kar,et al.  A role for astrocyte‐derived amyloid β peptides in the degeneration of neurons in an animal model of temporal lobe epilepsy , 2018, Brain pathology.

[23]  O. Meijer,et al.  Glucocorticoid receptor modulators. , 2018, Annales d'endocrinologie.

[24]  R. Garbelli,et al.  Seizure progression and inflammatory mediators promote pericytosis and pericyte-microglia clustering at the cerebrovasculature , 2018, Neurobiology of Disease.

[25]  P. Fontanaud,et al.  Topographic Reorganization of Cerebrovascular Mural Cells under Seizure Conditions. , 2018, Cell reports.

[26]  M. Vignes,et al.  Deletion of plasma Phospholipid Transfer Protein (PLTP) increases microglial phagocytosis and reduces cerebral amyloid-β deposition in the J20 mouse model of Alzheimer's disease , 2018, Oncotarget.

[27]  C. Libert,et al.  Therapeutic Mechanisms of Glucocorticoids , 2018, Trends in Endocrinology & Metabolism.

[28]  C. Marmar,et al.  Traumatic Brain Injury and Alzheimer's Disease: The Cerebrovascular Link , 2018, EBioMedicine.

[29]  J. Pascussi,et al.  Hepatic and hippocampal cytochrome P450 enzyme overexpression during spontaneous recurrent seizures , 2018, Epilepsia.

[30]  Ó. García-Leal,et al.  Behavioral changes in models of chemoconvulsant-induced epilepsy: A review , 2017, Neuroscience & Biobehavioral Reviews.

[31]  J. Rinne,et al.  Association Between Childhood-Onset Epilepsy and Amyloid Burden 5 Decades Later , 2017, JAMA neurology.

[32]  H. Hunt,et al.  New selective glucocorticoid receptor modulators reverse amyloid-β peptide–induced hippocampus toxicity , 2016, Neurobiology of Aging.

[33]  Nick C Fox,et al.  Hyperphosphorylated tau in patients with refractory epilepsy correlates with cognitive decline: a study of temporal lobe resections. , 2016, Brain : a journal of neurology.

[34]  David K. Wright,et al.  Sodium selenate retards epileptogenesis in acquired epilepsy models reversing changes in protein phosphatase 2A and hyperphosphorylated tau. , 2016, Brain : a journal of neurology.

[35]  S. A. Hussaini,et al.  Neuronal activity enhances tau propagation and tau pathology in vivo , 2016, Nature Neuroscience.

[36]  P. Nichelli,et al.  Cerebrospinal fluid tau proteins in status epilepticus , 2015, Epilepsy & Behavior.

[37]  N. Smith,et al.  Epilepsy in older people , 2015 .

[38]  K. Blennow,et al.  Cerebrospinal fluid biomarkers of β‐amyloid metabolism and neuronal damage in epileptic seizures , 2014, European journal of neurology.

[39]  D. Holtzman,et al.  Antisense Reduction of Tau in Adult Mice Protects against Seizures , 2013, The Journal of Neuroscience.

[40]  T. Maurice,et al.  Deregulation of hypothalamic-pituitary-adrenal axis functions in an Alzheimer's disease rat model , 2013, Neurobiology of Aging.

[41]  W. Löscher,et al.  The intrahippocampal kainate model of temporal lobe epilepsy revisited: Epileptogenesis, behavioral and cognitive alterations, pharmacological response, and hippoccampal damage in epileptic rats , 2013, Epilepsy Research.

[42]  S. Marchal,et al.  Alzheimer's Disease Related Markers, Cellular Toxicity and Behavioral Deficits Induced Six Weeks after Oligomeric Amyloid-β Peptide Injection in Rats , 2013, PloS one.

[43]  H. Cai,et al.  BACE1 elevation is associated with aberrant limbic axonal sprouting in epileptic CD1 mice , 2012, Experimental Neurology.

[44]  N. Corcoran,et al.  Targeting hyperphosphorylated tau with sodium selenate suppresses seizures in rodent models , 2012, Neurobiology of Disease.

[45]  K. Chapman,et al.  The anti-inflammatory and immunosuppressive effects of glucocorticoids, recent developments and mechanistic insights , 2011, Molecular and Cellular Endocrinology.

[46]  T. O'Leary,et al.  Learning, memory and search strategies of inbred mouse strains with different visual abilities in the Barnes maze , 2011, Behavioural Brain Research.

[47]  L. Mucke,et al.  Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.

[48]  R. Nelson,et al.  Anesthesia Leads to Tau Hyperphosphorylation through Inhibition of Phosphatase Activity by Hypothermia , 2007, The Journal of Neuroscience.

[49]  P. Davies,et al.  Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms , 2003, Journal of neurochemistry.

[50]  A. Depaulis,et al.  Evolution of hippocampal epileptic activity during the development of hippocampal sclerosis in a mouse model of temporal lobe epilepsy , 2002, Neuroscience.

[51]  Kang Hu,et al.  High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation , 2000, The Journal of Neuroscience.

[52]  I. Grundke‐Iqbal,et al.  Dysregulation of tau phosphorylation in mouse brain during excitotoxic damage. , 2009, Journal of Alzheimer's disease : JAD.