Epileptic activity in Alzheimer's disease: causes and clinical relevance
暂无分享,去创建一个
K. Vossel | A. Zeman | M. Tartaglia | Bruce L Miller | Keith A Vossel | Maria C Tartaglia | Haakon B Nygaard | Adam Z Zeman | H. Nygaard | B. Miller | B. Miller
[1] B. Cretin,et al. Epileptic Prodromal Alzheimer's Disease, a Retrospective Study of 13 New Cases: Expanding the Spectrum of Alzheimer's Disease to an Epileptic Variant? , 2016, Journal of Alzheimer's disease : JAD.
[2] N. Krogan,et al. Critical Role of Acetylation in Tau-Mediated Neurodegeneration and Cognitive Deficits , 2015, Nature Medicine.
[3] Brivaracetam, but not ethosuximide, reverses memory impairments in an Alzheimer’s disease mouse model , 2015, Alzheimer's Research & Therapy.
[4] A. Vortmeyer,et al. Alzheimer Amyloid-β Oligomer Bound to Post-Synaptic Prion Protein Activates Fyn to Impair Neurons , 2012, Nature Neuroscience.
[5] Kai Zhang,et al. Tau Reduction Prevents Aβ-Induced Defects in Axonal Transport , 2010, Science.
[6] Lief E. Fenno,et al. Chronic optogenetic activation augments Aβ pathology in a mouse model of Alzheimer disease , 2022 .
[7] S. Younkin,et al. Tau Loss Attenuates Neuronal Network Hyperexcitability in Mouse and Drosophila Genetic Models of Epilepsy , 2013, The Journal of Neuroscience.
[8] E. Mandelkow,et al. Amyloid‐β oligomers induce synaptic damage via Tau‐dependent microtubule severing by TTLL6 and spastin , 2013, The EMBO journal.
[9] Shagufta Ahmad,et al. Lamotrigine, carbamazepine and phenytoin differentially alter extracellular levels of 5-hydroxytryptamine, dopamine and amino acids , 2005, Epilepsy Research.
[10] L. Willmore,et al. Effect of levetiracetam on molecular regulation of hippocampal glutamate and GABA transporters in rats with chronic seizures induced by amygdalar FeCl3 injection , 2007, Brain Research.
[11] Shaomin Li,et al. Soluble Aβ oligomers impair hippocampal LTP by disrupting glutamatergic/GABAergic balance , 2016, Neurobiology of Disease.
[12] Zeina N Chemali,et al. Clinical and Neurophysiologic Characteristics of Unprovoked Seizures in Patients Diagnosed With Dementia. , 2015, The Journal of neuropsychiatry and clinical neurosciences.
[13] Shaomin Li,et al. Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate Uptake , 2009, Neuron.
[14] T. Golde,et al. Genetic Suppression of Transgenic APP Rescues Hypersynchronous Network Activity in a Mouse Model of Alzeimer's Disease , 2014, The Journal of Neuroscience.
[15] E. Cumbo,et al. Levetiracetam, lamotrigine, and phenobarbital in patients with epileptic seizures and Alzheimer’s disease , 2010, Epilepsy & Behavior.
[16] Hwamee Oh,et al. Frontotemporal Network Connectivity during Memory Encoding Is Increased with Aging and Disrupted by Beta-Amyloid , 2013, The Journal of Neuroscience.
[17] Maria Thom,et al. Neurofibrillary tangle pathology and Braak staging in chronic epilepsy in relation to traumatic brain injury and hippocampal sclerosis: a post-mortem study. , 2011, Brain : a journal of neurology.
[18] 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.
[19] Chia-Hsiung Cheng,et al. Antiepileptic effects of low frequency repetitive transcranial magnetic stimulation: A meta-analysis , 2011, Epilepsy Research.
[20] A Hofman,et al. Clinical features and mortality in patients with early-onset Alzheimer's disease. , 1996, European neurology.
[21] E. Marsh,et al. Corticothalamic network dysfunction and behavioral deficits in a mouse model of Alzheimer's disease , 2016, Neurobiology of Aging.
[22] K Patterson,et al. Focal cortical presentations of Alzheimer's disease. , 2007, Brain : a journal of neurology.
[23] S. Rothman,et al. Levetiracetam has a time- and stimulation-dependent effect on synaptic transmission , 2009, Seizure.
[24] L. Hugonot-Diener,et al. Masitinib as an adjunct therapy for mild-to-moderate Alzheimer's disease: a randomised, placebo-controlled phase 2 trial , 2011, Alzheimer's Research & Therapy.
[25] D. Neary,et al. TDP-43 pathological changes in early onset familial and sporadic Alzheimer’s disease, late onset Alzheimer’s disease and Down’s Syndrome: association with age, hippocampal sclerosis and clinical phenotype , 2011, Acta Neuropathologica.
[26] J. Hodges,et al. The syndrome of transient epileptic amnesia , 2007, Annals of neurology.
[27] Jukka Peltola,et al. Immediate effects of deep brain stimulation of anterior thalamic nuclei on executive functions and emotion-attention interaction in humans , 2014, Journal of clinical and experimental neuropsychology.
[28] C. Jack,et al. Chronic divalproex sodium to attenuate agitation and clinical progression of Alzheimer disease. , 2011, Archives of general psychiatry.
[29] Q. Gong,et al. Altered functional connectivity in default mode network in absence epilepsy: A resting‐state fMRI study , 2011, Human brain mapping.
[30] J. McLaurin,et al. Hippocampal GABAergic neurons are susceptible to amyloid-β toxicity in vitro and are decreased in number in the Alzheimer's disease TgCRND8 mouse model. , 2012, Journal of Alzheimer's disease : JAD.
[31] Heidi E Kirsch,et al. Seizures and epileptiform activity in the early stages of Alzheimer disease. , 2013, JAMA neurology.
[32] V. Prasher,et al. Onset of seizures as a poor indicator of longevity in people with down syndrome and dementia , 1993 .
[33] Yadong Huang,et al. Apolipoprotein E4 Causes Age- and Tau-Dependent Impairment of GABAergic Interneurons, Leading to Learning and Memory Deficits in Mice , 2010, The Journal of Neuroscience.
[34] Keith A. Johnson,et al. Amyloid-β deposition in mild cognitive impairment is associated with increased hippocampal activity, atrophy and clinical progression. , 2015, Brain : a journal of neurology.
[35] Jeffrey Noebels,et al. A perfect storm: Converging paths of epilepsy and Alzheimer’s dementia intersect in the hippocampal formation , 2011, Epilepsia.
[36] R. S. Williams,et al. A prospective study of Alzheimer disease in Down syndrome. , 1989, Archives of neurology.
[37] S. Maeda,et al. Expression of A152T human tau causes age‐dependent neuronal dysfunction and loss in transgenic mice , 2016, EMBO reports.
[38] Edward O. Mann,et al. Inhibitory Interneuron Deficit Links Altered Network Activity and Cognitive Dysfunction in Alzheimer Model , 2012, Cell.
[39] S. A. Hussaini,et al. Neuronal activity enhances tau propagation and tau pathology in vivo , 2016, Nature Neuroscience.
[40] J. Ziburkus,et al. Inhibitory Neuron and Hippocampal Circuit Dysfunction in an Aged Mouse Model of Alzheimer's Disease , 2013, PloS one.
[41] L. Mucke,et al. Amyloid-β–induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks , 2010, Nature Neuroscience.
[42] H. Kim,et al. Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease , 2014, Scientific Reports.
[43] L. Hirsch,et al. A Randomized, Double‐Blind, Placebo‐Controlled Trial of Donepezil to Improve Memory in Epilepsy , 2007, Epilepsia.
[44] M. Gillard,et al. Binding characteristics of brivaracetam, a selective, high affinity SV2A ligand in rat, mouse and human brain: relationship to anti-convulsant properties. , 2011, European journal of pharmacology.
[45] W. M. van der Flier,et al. Prevalence and Clinical Significance of Epileptiform EEG Discharges in a Large Memory Clinic Cohort , 2010, Dementia and Geriatric Cognitive Disorders.
[46] R. Mayeux,et al. Cumulative risks of developing extrapyramidal signs, psychosis, or myoclonus in the course of Alzheimer's disease. , 1991, Archives of neurology.
[47] D. Y. Lee,et al. Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis. , 2015, JAMA.
[48] A. Pariente,et al. Benzodiazepine use and risk of Alzheimer’s disease: case-control study , 2014, BMJ : British Medical Journal.
[49] C. Rowe,et al. Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: a prospective cohort study , 2013, The Lancet Neurology.
[50] Jürgen Götz,et al. Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models , 2010, Cell.
[51] Laurie A. Miller,et al. Senile plaques in temporal lobe epilepsy , 1994, Acta Neuropathologica.
[52] Dietmar R. Thal,et al. Stages of the Pathologic Process in Alzheimer Disease: Age Categories From 1 to 100 Years , 2011, Journal of neuropathology and experimental neurology.
[53] S. Ferreira,et al. Taurine prevents the neurotoxicity of β‐amyloid and glutamate receptor agonists: activation of GABA receptors and possible implications for Alzheimer's disease and other neurological disorders , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[54] L. Volicer,et al. Effect of seizures on progression of dementia of the Alzheimer type. , 1995, Dementia.
[55] Daniel Friedman,et al. Seizures and Epilepsy in Alzheimer's Disease , 2012, CNS neuroscience & therapeutics.
[56] Vinh Q Nguyen,et al. Down syndrome and dementia: seizures and cognitive decline. , 2012, Journal of Alzheimer's disease : JAD.
[57] You-Qiang Song,et al. A systematic review of familial Alzheimer's disease: Differences in presentation of clinical features among three mutated genes and potential ethnic differences. , 2016, Journal of the Formosan Medical Association = Taiwan yi zhi.
[58] W. Löscher,et al. High doses of memantine (1-amino-3,5-dimethyladamantane) induce seizures in kindled but not in non-kindled rats , 1990, Naunyn-Schmiedeberg's Archives of Pharmacology.
[59] P. Calabresi,et al. Levetiracetam monotherapy in Alzheimer patients with late‐onset seizures: a prospective observational study , 2007, European journal of neurology.
[60] Keith A. Johnson,et al. Amyloid Deposition Is Associated with Impaired Default Network Function in Older Persons without Dementia , 2009, Neuron.
[61] S. Tekin,et al. Antiglutamatergic therapy in Alzheimer's disease – effects of lamotrigine , 1998, Journal of Neural Transmission.
[62] A. Palmeri,et al. Picomolar Amyloid-β Positively Modulates Synaptic Plasticity and Memory in Hippocampus , 2008, The Journal of Neuroscience.
[63] D. Hoffman,et al. Tau-Dependent Kv4.2 Depletion and Dendritic Hyperexcitability in a Mouse Model of Alzheimer's Disease , 2015, The Journal of Neuroscience.
[64] S. Strittmatter,et al. Fyn inhibition rescues established memory and synapse loss in Alzheimer mice , 2015, Annals of neurology.
[65] Caroline L. Speck,et al. Response of the medial temporal lobe network in amnestic mild cognitive impairment to therapeutic intervention assessed by fMRI and memory task performance , 2015, NeuroImage: Clinical.
[66] Arturo Alvarez-Buylla,et al. Inhibitory Interneuron Progenitor Transplantation Restores Normal Learning and Memory in ApoE4 Knock-In Mice without or with Aβ Accumulation , 2014, The Journal of Neuroscience.
[67] N. Muhlert,et al. Accelerated forgetting of real-life events in Transient Epileptic Amnesia , 2010, Neuropsychologia.
[68] J. Trojanowski,et al. Clinicopathological correlations in corticobasal degeneration , 2011, Annals of neurology.
[69] Keith A. Vossel,et al. Tau reduction prevents A-induced axonal transport deficits by blocking activation of GSK 3 , 2015 .
[70] L. Mucke,et al. Amyloid-β/Fyn–Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer's Disease , 2011, The Journal of Neuroscience.
[71] R. Gallassi. Epileptic Amnesic Syndrome: An Update and Further Considerations , 2006, Epilepsia.
[72] Karen M Rodrigue,et al. Prevalence of amyloid PET positivity in dementia syndromes: a meta-analysis. , 2015, JAMA.
[73] R. Petersen,et al. Recurrent seizures in patients with dementia: Frequency, seizure types, and treatment outcome , 2009, Epilepsy & Behavior.
[74] Y. Smith,et al. Mitochondrial biogenesis in the anticonvulsant mechanism of the ketogenic diet , 2006, Annals of neurology.
[75] Korey Kam,et al. Interictal spikes during sleep are an early defect in the Tg2576 mouse model of β-amyloid neuropathology , 2016, Scientific Reports.
[76] D. Bredesen,et al. Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain , 2011, Neurobiology of Aging.
[77] Kewei Chen,et al. A phase Ib multiple ascending dose study of the safety, tolerability, and central nervous system availability of AZD0530 (saracatinib) in Alzheimer’s disease , 2015, Alzheimer's Research & Therapy.
[78] Bradley T. Hyman,et al. The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease , 2014, Neuron.
[79] Jason E Gestwicki,et al. Phenothiazine-mediated rescue of cognition in tau transgenic mice requires neuroprotection and reduced soluble tau burden , 2010, Molecular Neurodegeneration.
[80] G. Holmes,et al. Hippocampal interictal epileptiform activity disrupts cognition in humans , 2013, Neurology.
[81] Heidi E Kirsch,et al. Incidence and impact of subclinical epileptiform activity in Alzheimer's disease , 2016, Annals of neurology.
[82] C. Jack,et al. Chronic divalproex sodium use and brain atrophy in Alzheimer disease , 2011, Neurology.
[83] T. Losey,et al. Seizures and dementia in the elderly: Nationwide Inpatient Sample 1999–2008 , 2014, Epilepsy & Behavior.
[84] Julie Harris,et al. Reversing EphB2 depletion rescues cognitive functions in Alzheimer model , 2011, Nature.
[85] D. Holtzman,et al. Antisense Reduction of Tau in Adult Mice Protects against Seizures , 2013, The Journal of Neuroscience.
[86] J. Tsiouris,et al. Adverse effects of phenytoin given for late-onset seizures in adults with Down syndrome , 2002, Neurology.
[87] B. Uthman,et al. New onset geriatric epilepsy , 2005, Neurology.
[88] A. Cukiert,et al. Seizure outcome after hippocampal deep brain stimulation in a prospective cohort of patients with refractory temporal lobe epilepsy , 2014, Seizure.
[89] W. Hauser,et al. Seizures and myoclonus in patients with Alzheimer's disease , 1986, Neurology.
[90] E. Mandelkow,et al. The Tau/A152T mutation, a risk factor for frontotemporal‐spectrum disorders, leads to NR2B receptor‐mediated excitotoxicity , 2016, EMBO reports.
[91] Sylvain Rheims,et al. Amyloid β-Induced Neuronal Hyperexcitability Triggers Progressive Epilepsy , 2009, The Journal of Neuroscience.
[92] M. Romero-Acebal,et al. Calretinin interneurons are early targets of extracellular amyloid-beta pathology in PS1/AbetaPP Alzheimer mice hippocampus. , 2010, Journal of Alzheimer's disease : JAD.
[93] A. Hofman,et al. Risk of dementia in patients with Parkinson's disease, epilepsy, and severe head trauma: a register-based follow-up study. , 1995, American journal of epidemiology.
[94] Hong-Guang Xie,et al. Antiepileptics Topiramate and Levetiracetam Alleviate Behavioral Deficits and Reduce Neuropathology in APPswe/PS1dE9 Transgenic Mice , 2013, CNS neuroscience & therapeutics.
[95] Shao Li,et al. Lamotrigine attenuates deficits in synaptic plasticity and accumulation of amyloid plaques in APP/PS1 transgenic mice , 2014, Neurobiology of Aging.
[96] James T. Becker,et al. A multicenter study of the early detection of synaptic dysfunction in Mild Cognitive Impairment using Magnetoencephalography-derived functional connectivity , 2015, NeuroImage: Clinical.
[97] H. Tanila,et al. Spontaneous epileptiform discharges in a mouse model of Alzheimer's disease are suppressed by antiepileptic drugs that block sodium channels , 2011, Epilepsy Research.
[98] L. Costantini,et al. Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer's disease: a randomized, double-blind, placebo-controlled, multicenter trial , 2009, Nutrition & metabolism.
[99] Susanne Schoch,et al. Dendritic Structural Degeneration Is Functionally Linked to Cellular Hyperexcitability in a Mouse Model of Alzheimer’s Disease , 2014, Neuron.
[100] G. Landreth,et al. Bexarotene reduces network excitability in models of Alzheimer's disease and epilepsy , 2014, Neurobiology of Aging.
[101] M. Pangalos,et al. Sodium Channel Cleavage Is Associated with Aberrant Neuronal Activity and Cognitive Deficits in a Mouse Model of Alzheimer's Disease , 2013, The Journal of Neuroscience.
[102] Keith A. Vossel,et al. Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer’s disease model , 2012, Proceedings of the National Academy of Sciences.