Traumatic brain injury: A risk factor for Alzheimer's disease
暂无分享,去创建一个
[1] K. Kosik,et al. Overexpression of tau in a nonneuronal cell induces long cellular processes , 1991, The Journal of cell biology.
[2] J. Povlishock,et al. Pathobiology of traumatically induced axonal injury in animals and man. , 1993, Annals of emergency medicine.
[3] D. Graham,et al. β-Amyloid precursor protein (βAPP) as a marker for axonal injury after head injury , 1993, Neuroscience Letters.
[4] D. Graham,et al. Beta-amyloid precursor protein (beta APP) as a marker for axonal injury after head injury. , 1993, Neuroscience letters.
[5] J. Povlishock,et al. A mechanistic analysis of nondisruptive axonal injury: a review. , 1997, Journal of neurotrauma.
[6] W. H. Hall,et al. Rehabilitation of persons with traumatic brain injury. , 1999, NIH consensus statement.
[7] S. Gottlieb. Head injury doubles the risk of Alzheimer's disease , 2000, BMJ : British Medical Journal.
[8] D. Meaney,et al. Axonal Damage in Traumatic Brain Injury , 2000 .
[9] T. Mcintosh,et al. Models of Traumatic Brain Injury , 2000, European Journal of Trauma.
[10] J. Guralnik,et al. Documented head injury in early adulthood and risk of Alzheimer’s disease and other dementias , 2000, Neurology.
[11] Y. Orihara,et al. Induction of apolipoprotein E after traumatic brain injury in forensic autopsy cases , 2002, International Journal of Legal Medicine.
[12] A. Cronin,et al. Traumatic brain injury in children: issues in community function. , 2001, The American journal of occupational therapy : official publication of the American Occupational Therapy Association.
[13] Douglas H. Smith,et al. Long‐Term Accumulation of Amyloid‐β in Axons Following Brain Trauma Without Persistent Upregulation of Amyloid Precursor Protein Genes , 2002, Journal of neuropathology and experimental neurology.
[14] D. Okonkwo,et al. Caspase-3-mediated cleavage of amyloid precursor protein and formation of amyloid Beta peptide in traumatic axonal injury. , 2002, Journal of neurotrauma.
[15] L. Serpell,et al. Proteasomal degradation of tau protein , 2002, Journal of neurochemistry.
[16] O. Alonso,et al. Monoubiquitination and Cellular Distribution of XIAP in Neurons after Traumatic Brain Injury , 2003, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[17] E. Hogan,et al. Calpain in the pathophysiology of spinal cord injury: neuroprotection with calpain inhibitors , 2003, Brain Research Reviews.
[18] R. Mayeux,et al. Stroke and the risk of Alzheimer disease. , 2003, Archives of neurology.
[19] S Rabe-Hesketh,et al. Head injury as a risk factor for Alzheimer’s disease: the evidence 10 years on; a partial replication , 2003, Journal of neurology, neurosurgery, and psychiatry.
[20] E. Thompson,et al. Cerebrospinal fluid apolipoprotein E concentration decreases after traumatic brain injury. , 2003, Journal of neurotrauma.
[21] J. Fins,et al. Constructing an ethical stereotaxy for severe brain injury: balancing risks, benefits and access , 2003, Nature Reviews Neuroscience.
[22] John Q. Trojanowski,et al. Alzheimer's pathology in human temporal cortex surgically excised after severe brain injury , 2004, Experimental Neurology.
[23] J. Trojanowski,et al. Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury , 2004, Journal of neurochemistry.
[24] J. Simpkins,et al. Increased β-secretase activity and expression in rats following transient cerebral ischemia , 2004, Brain Research.
[25] J. Trojanowski,et al. Long-Term Accumulation of Amyloid-β, β-Secretase, Presenilin-1, and Caspase-3 in Damaged Axons Following Brain Trauma , 2004 .
[26] W. Strittmatter,et al. Apolipoprotein E and brain injury: implications for children , 2005, Developmental medicine and child neurology.
[27] D. Holtzman,et al. Human Apolipoprotein E4 Alters the Amyloid-β 40:42 Ratio and Promotes the Formation of Cerebral Amyloid Angiopathy in an Amyloid Precursor Protein Transgenic Model , 2005, The Journal of Neuroscience.
[28] W. Strittmatter,et al. Apolipoprotein E and brain injury: implications for children. , 2005 .
[29] S. Scheff,et al. Cleaved-tau: a biomarker of neuronal damage after traumatic brain injury. , 2005, Journal of neurotrauma.
[30] P. Falkai,et al. Traumatic brain injury: cause or risk of Alzheimer’s disease? A review of experimental studies , 2005, Journal of Neural Transmission.
[31] Alexander Sasha Rabchevsky,et al. Mitochondrial permeability transition in CNS trauma: Cause or effect of neuronal cell death? , 2005, Journal of neuroscience research.
[32] M. Thakur,et al. Estradiol regulates APP mRNA alternative splicing in the mice brain cortex , 2005, Neuroscience Letters.
[33] L. Goldstein,et al. Axonal transport and Alzheimer's disease. , 2006, Annual review of biochemistry.
[34] Hong Qing,et al. Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression , 2006, Proceedings of the National Academy of Sciences.
[35] R. Portin,et al. Outcome of traumatic brain injury after three decades--relationship to ApoE genotype. , 2006, Journal of neurotrauma.
[36] T. Kuroiwa,et al. Transient cognitive deficits are associated with the reversible accumulation of amyloid precursor protein after mild traumatic brain injury , 2006, Neuroscience Letters.
[37] S. DeKosky,et al. Caspase inhibition therapy abolishes brain trauma-induced increases in Aβ peptide: Implications for clinical outcome , 2006, Experimental Neurology.
[38] R. Tanzi,et al. Depletion of GGA3 Stabilizes BACE and Enhances β-Secretase Activity , 2007, Neuron.
[39] S. Knuutila,et al. Impairment of the Ubiquitin-Proteasome Pathway Is a Downstream Endoplasmic Reticulum Stress Response Induced by Extracellular Human Islet Amyloid Polypeptide and Contributes to Pancreatic β-Cell Apoptosis , 2007, Diabetes.
[40] R. Vink,et al. Traumatic brain injury and Alzheimer's disease: a review. , 2007, Progress in brain research.
[41] T. Kurki,et al. MRI changes and ApoE genotype, a prospective 1-year follow-up of traumatic brain injury: A pilot study , 2007, Brain injury.
[42] M. Vitek,et al. An apolipoprotein E-based therapeutic improves outcome and reduces Alzheimer’s disease pathology following closed head injury: Evidence of pharmacogenomic interaction , 2007, Neuroscience.
[43] J. McCabe,et al. Ubiquitin and ubiquitin-conjugated protein expression in the rat cerebral cortex and hippocampus following traumatic brain injury (TBI) , 2007, Brain Research.
[44] Bingren Hu,et al. Protein Aggregation and Proteasome Dysfunction After Brain Ischemia , 2007, Stroke.
[45] D. Selkoe,et al. A Critical Function for β-Amyloid Precursor Protein in Neuronal Migration Revealed by In Utero RNA Interference , 2007, The Journal of Neuroscience.
[46] C. Werner,et al. Pathophysiology of traumatic brain injury. , 2007, British journal of anaesthesia.
[47] Jiankun Cui,et al. Hypoxia-inducible Factor 1 (HIF-1 )-mediated Hypoxia Increases BACE1 Expression and -Amyloid Generation* , 2007 .
[48] Drug Therapies for the Neurobehavioral Sequelae of Traumatic Brain Injury , 2007 .
[49] D. Graham,et al. Multiple proteins implicated in neurodegenerative diseases accumulate in axons after brain trauma in humans , 2007, Experimental Neurology.
[50] C. Colton,et al. Human Apolipoprotein E Redistributes Fibrillar Amyloid Deposition in Tg-SwDI Mice , 2008, The Journal of Neuroscience.
[51] J. Jia,et al. Meta-analysis of APOE4 allele and outcome after traumatic brain injury. , 2008, Journal of neurotrauma.
[52] A. Kiss,et al. Traumatic brain injury, Apolipoprotein E-epsilon4, and cognition in older adults: a two-year longitudinal study. , 2008, The Journal of neuropsychiatry and clinical neurosciences.
[53] Rachel P Berger,et al. Biomarkers of primary and evolving damage in traumatic and ischemic brain injury: diagnosis, prognosis, probing mechanisms, and therapeutic decision making , 2008, Current opinion in critical care.
[54] K. Blennow,et al. Apolipoprotein E polymorphism and gender difference in outcome after severe traumatic brain injury , 2008, Acta anaesthesiologica Scandinavica.
[55] N. Grigoriadis,et al. Increased expression of the γ‐secretase components presenilin‐1 and nicastrin in activated astrocytes and microglia following traumatic brain injury , 2008, Glia.
[56] M. Shigemori,et al. Age-associated increases in poor outcomes after traumatic brain injury: a report from the Japan Neurotrauma Data Bank. , 2008, Journal of neurotrauma.
[57] Tzong-Shiue Yu,et al. Traumatic Brain Injury-Induced Hippocampal Neurogenesis Requires Activation of Early Nestin-Expressing Progenitors , 2008, The Journal of Neuroscience.
[58] T. Dóczi,et al. Traumatic axonal injury in the spinal cord evoked by traumatic brain injury. , 2008, Journal of neurotrauma.
[59] Firas H Kobeissy,et al. Neuroproteomics and systems biology‐based discovery of protein biomarkers for traumatic brain injury and clinical validation , 2008, Proteomics. Clinical applications.
[60] D. Graham,et al. A Neprilysin Polymorphism and Amyloid-β Plaques after Traumatic Brain Injury , 2009 .
[61] Per Enblad,et al. Monitoring of brain interstitial total tau and beta amyloid proteins by microdialysis in patients with traumatic brain injury. , 2009, Journal of neurosurgery.
[62] B. Zink,et al. Pathophysiology of traumatic brain injury. , 2009, The Mount Sinai journal of medicine, New York.
[63] Orsolya Farkas,et al. Update on protein biomarkers in traumatic brain injury with emphasis on clinical use in adults and pediatrics , 2009, Acta Neurochirurgica.
[64] M. Tabaton,et al. The up‐regulation of BACE1 mediated by hypoxia and ischemic injury: role of oxidative stress and HIF1α , 2009, Journal of neurochemistry.
[65] N. Berman,et al. Impaired expression of neuroprotective molecules in the HIF-1alpha pathway following traumatic brain injury in aged mice. , 2009, Journal of neurotrauma.
[66] S. Strittmatter,et al. Axon regeneration in the peripheral and central nervous systems. , 2009, Results and problems in cell differentiation.
[67] A. McKee,et al. Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy After Repetitive Head Injury , 2009, Journal of neuropathology and experimental neurology.
[68] B. Tang. Neuronal protein trafficking associated with Alzheimer disease , 2009, Cell adhesion & migration.
[69] H. Bramlett,et al. Deficits in ERK and CREB activation in the hippocampus after traumatic brain injury , 2009, Neuroscience Letters.
[70] Y. Matsuoka,et al. Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury , 2009, Nature Medicine.
[71] Douglas H. Smith,et al. Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease? , 2010, Nature Reviews Neuroscience.
[72] Silvana Riggio,et al. Traumatic brain injury and its neurobehavioral sequelae. , 2010, The Psychiatric clinics of North America.
[73] S. Scheff,et al. Age-related mitochondrial changes after traumatic brain injury. , 2010, Journal of neurotrauma.
[74] H. Weng,et al. Tau proteins in serum predict outcome after severe traumatic brain injury. , 2010, The Journal of surgical research.
[75] V. Mathura,et al. Apolipoprotein E genotype and oxidative stress response to traumatic brain injury , 2010, Neuroscience.
[76] F. Gomez-Pinilla,et al. Voluntary exercise may engage proteasome function to benefit the brain after trauma , 2010, Brain Research.
[77] Zong Zhuang,et al. Preliminary study on the effect of trauma-induced secondary cellular hypoxia in brain injury , 2010, Neuroscience Letters.
[78] E. Yan,et al. Post-traumatic hypoxia exacerbates brain tissue damage: analysis of axonal injury and glial responses. , 2010, Journal of neurotrauma.
[79] G. Pasinetti,et al. Personalized medicine in traumatic brain injury. , 2010, The Psychiatric clinics of North America.
[80] B. Masel,et al. Traumatic brain injury: a disease process, not an event. , 2010, Journal of neurotrauma.
[81] D. Holtzman,et al. Traumatic brain injury reduces soluble extracellular amyloid-β in mice: A methodologically novel combined microdialysis-controlled cortical impact study , 2010, Neurobiology of Disease.
[82] R. Stern,et al. Chronic Traumatic Encephalopathy , 2020, Seminars in Neurology.
[83] M. Thakur,et al. Age-Dependent Expression of Apolipoprotein E in Mouse Cerebral Cortex , 2011, Journal of Molecular Neuroscience.
[84] T. M. Sivanandam,et al. Amyloid Precursor Protein (APP) mRNA Level is Higher in the Old Mouse Cerebral Cortex and is Regulated by Sex Steroids , 2011, Journal of Molecular Neuroscience.
[85] W. Le,et al. Pathological role of hypoxia in Alzheimer's disease , 2010, Experimental Neurology.
[86] D. Brody,et al. New perspectives on amyloid-beta dynamics after acute brain injury: moving between experimental approaches and studies in the human brain. , 2010, Archives of neurology.
[87] C. Mclean,et al. In situ detection of inflammatory mediators in post mortem human brain tissue after traumatic injury. , 2010, Journal of neurotrauma.
[88] N. Berman,et al. Age-dependent response of CCAAT/enhancer binding proteins following traumatic brain injury in mice , 2010, Neurochemistry International.
[89] A. Faden,et al. Modulation of ABCA1 by an LXR agonist reduces β-amyloid levels and improves outcome after traumatic brain injury. , 2011, Journal of neurotrauma.
[90] M. Cekic,et al. Traumatic brain injury and aging: Is a combination of progesterone and vitamin D hormone a simple solution to a complex problem? , 2011, Neurotherapeutics.
[91] R. Raghupathi,et al. Calpain as a therapeutic target in traumatic brain injury , 2011, Neurotherapeutics.
[92] Sudarshan C. Upadhya,et al. Role of ubiquitin-proteasome-mediated proteolysis in nervous system disease. , 2011, Biochimica et biophysica acta.
[93] C. Thiel,et al. Amyloid Precursor Protein Is Trafficked and Secreted via Synaptic Vesicles , 2011, PloS one.
[94] D. Alkon,et al. PKC activator therapeutic for mild traumatic brain injury in mice , 2011, Neurobiology of Disease.
[95] J. Weber,et al. Animal Models of Traumatically-Induced Dementia , 2011 .
[96] B. Stoica,et al. Cell death mechanisms and modulation in traumatic brain injury , 2011, Neurotherapeutics.
[97] C. Masters,et al. The neuroprotective domains of the amyloid precursor protein, in traumatic brain injury, are located in the two growth factor domains , 2011, Brain Research.