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Genomes and Genes | Ann C McKeeSummaryAffiliation: Boston University Country: USA Publications
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Publications
Ibuprofen reduces Abeta, hyperphosphorylated tau and memory deficits in Alzheimer miceAnn C McKee
Department of Neurology, Boston University School of Medicine, Boston, MA, USA
Brain Res 1207:225-36. 2008..These findings provide further support for intraneuronal Abeta as a cause of cognitive impairment, and suggest that pathological alterations of tau are associated with intraneuronal oligomeric Abeta accumulation...
Helmets and mouth guards: the role of personal equipment in preventing sport-related concussionsDaniel H Daneshvar
Department of Neurology, Boston University School of Medicine, Center for the Study of Traumatic Encephalopathy, 72 East Concord Street, B7800, Boston, MA 02118, USA
Clin Sports Med 30:145-63, x. 2011..Improving coach and player education about proper concussion management, encouraging neck-strengthening exercises, and minimizing high-risk impacts may reduce concussions in sports...
Acyl peptide hydrolase degrades monomeric and oligomeric amyloid-beta peptideRina Yamin
Department of Biochemistry, Boston University School of Medicine, 72 East Concord Street, Boston, K620, MA 02118, USA
Mol Neurodegener 4:33. 2009..abstract:..
TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathyAnn C McKee
Geriatric Research Education Clinical Center, Bedford Veterans Administration Hospital, Bedford, Massachusetts 01730, USA
J Neuropathol Exp Neurol 69:918-29. 2010..This is the first pathological evidence that repetitive head trauma experienced in collision sports might be associated with the development of a motor neuron disease...
Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injuryAnn C McKee
Department of Neurology, Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, MA, USA
J Neuropathol Exp Neurol 68:709-35. 2009..Deposition of beta-amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases. Chronic traumatic encephalopathy is a neuropathologically distinct slowly progressive tauopathy with a clear environmental etiology...
Visual association pathology in preclinical Alzheimer diseaseAnn C McKee
Department of Neurology and Pathology, Boston University School of Medicine, Bedford Veterans Administration Medical Center, MA 01730, USA
J Neuropathol Exp Neurol 65:621-30. 2006..Dense AD pathology in area 19 is present in some cognitively intact subjects with preclinical AD. The unique metabolic, connectional, and vascular features of this region may confer enhanced vulnerability to neurodegeneration...
The spectrum of disease in chronic traumatic encephalopathyAnn C McKee
United States Department of Veterans Affairs, VA Boston Healthcare System, Boston, MA 02130, USA
Brain 136:43-64. 2013....
Long-term consequences of repetitive brain trauma: chronic traumatic encephalopathyRobert A Stern
Center for Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston University, 72 East Concord St, 7380, Boston, MA 02118, USA
PM R 3:S460-7. 2011..Research also will provide policy makers with the scientific knowledge to make appropriate guidelines regarding the prevention and treatment of brain trauma in all levels of athletic involvement as well as the military theater...
The Framingham Brain Donation Program: neuropathology along the cognitive continuumRhoda Au
Department of Neurology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA
Curr Alzheimer Res 9:673-86. 2012..We observed that an aggregate ischemic injury score was significantly higher in persons with a CDR score of 0.5 than in normal controls...
Long-term consequences: effects on normal development profile after concussionDaniel H Daneshvar
Department of Neurology, Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston 02118, MA, USA
Phys Med Rehabil Clin N Am 22:683-700, ix. 2011..Effective diagnoses, treatments, and education plans are required to reduce the future burden and incidence of long-term effects of head injuries...
Chronic traumatic encephalopathy: neurodegeneration following repetitive concussive and subconcussive brain traumaChristine M Baugh
Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, MA 02118, USA
Brain Imaging Behav 6:244-54. 2012..This review examines research to date and suggests future directions worthy of exploration...
Clinical appraisal of chronic traumatic encephalopathy: current perspectives and future directionsBrandon E Gavett
Center for the Study of Traumatic Encephalopathy, Boston University, and Brigham and Women s Hospital, Boston, Massachusetts 02118, USA
Curr Opin Neurol 24:525-31. 2011..This review provides an update on recent literature pertaining to clinically relevant procedures that--presently or in the future--may be useful for the in-vivo detection, characterization, and/or prediction of CTE...
Increased expression of TrkB and Capzb2 accompanies preserved cognitive status in early Alzheimer disease pathologyPatricia F Kao
Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA
J Neuropathol Exp Neurol 71:654-64. 2012..In subsequent stages of AD, the higher levels of TrkB and Capzb2 expression achieved may not be sufficient to prevent cognitive decline...
Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head traumaBrandon E Gavett
Center for the Study of Traumatic Encephalopathy and Alzheimer s Disease Center, Boston University School of Medicine, 72 East Concord Street, B 7800, Boston, MA 02118, USA
Clin Sports Med 30:179-88, xi. 2011..No formal clinical or pathologic diagnostic criteria for CTE currently exist, but the distinctive neuropathologic profile of the disorder lends promise for future research into its prevention, diagnosis, and treatment...
Mild traumatic brain injury: a risk factor for neurodegenerationBrandon E Gavett
Department of Neurology, Boston University School of Medicine, 72 East Concord St, B 7800, Boston, MA 02118, USA
Alzheimers Res Ther 2:18. 2010....
Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse modelLee E Goldstein
Molecular Aging and Development Laboratory, Boston University School of Medicine, Boston, MA 02118, USA
Sci Transl Med 4:134ra60. 2012....
Association of distinct variants in SORL1 with cerebrovascular and neurodegenerative changes related to Alzheimer diseaseKaren T Cuenco
Genetics Program, Department of Medicine, Room L320, Boston University School of Medicine, 715 Albany St, Boston, MA 02118, USA
Arch Neurol 65:1640-8. 2008....
Dementia severity and Lewy bodies affect circadian rhythms in Alzheimer diseaseDavid G Harper
Geriatric Psychiatric Program, Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA
Neurobiol Aging 25:771-81. 2004....
The epidemiology of sport-related concussionDaniel H Daneshvar
Department of Neurology, Boston University School of Medicine, Center for the Study of Traumatic Encephalopathy, 72 East Concord Street, B7800, Boston, MA 02118, USA
Clin Sports Med 30:1-17, vii. 2011..With this knowledge can come improved techniques and rule changes to minimize the rate and severity of concussions in sports. This article identifies the factors that affect concussion rate...
δ-Catenin is genetically and biologically associated with cortical cataract and future Alzheimer-related structural and functional brain changesGyungah Jun
Department of Medicine, Biomedical Genetics, Boston University Schools of Medicine and Public Health, Boston, Massachusetts, United States of America
PLoS ONE 7:e43728. 2012..Our findings suggest that genetic variation in delta catenin may underlie both cortical lens opacities in mid-life and subsequent MRI and cognitive changes that presage the development of AD...
Early-life sodium exposure unmasks susceptibility to stroke in hyperlipidemic, hypertensive heterozygous Tg25 rats transgenic for human cholesteryl ester transfer proteinJulius L Decano
Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA
Circulation 119:1501-9. 2009..Early-life risk factor exposure increases aortic atherosclerosis and blood pressure in humans and animal models; however, limited insight has been gained as to end-organ complications...
Scattering differentiates Alzheimer disease in vitroEugene B Hanlon
Department of Veterans Affairs, Office of Research and Development, and Geriatric Research, Education and Clinical Center, 200 Springs Road, Bedford, Massachusetts 01730, USA
Opt Lett 33:624-6. 2008..Diffuse reflectance spectra of gross brain tissue in vitro confirmed this observation. These results suggest a means for diagnosing and monitoring Alzheimer disease in vivo, using near-infrared optical spectroscopy...
Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neuronsYevgenya Kraytsberg
Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
Nat Genet 38:518-20. 2006..The fraction of mtDNA deletions is significantly higher in cytochrome c oxidase (COX)-deficient neurons than in COX-positive neurons, suggesting that mtDNA deletions may be directly responsible for impaired cellular respiration...
Response to comment on "chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model"Lee E Goldstein
College of Engineering and Photonics Center, Boston University Alzheimer s Disease Center, Boston University School of Medicine, Boston, MA 02118, USA
Sci Transl Med 4:157lr5. 2012..Goldstein and McKee respond to points raised in two letters about their study of tau neuropathology in postmortem brain tissue samples from blast-exposed military veterans with traumatic brain injury...
Pyroglutamate-Aβ 3 and 11 colocalize in amyloid plaques in Alzheimer's disease cerebral cortex with pyroglutamate-Aβ 11 forming the central coreChristopher P Sullivan
Geriatrics Research, Education and Clinical Center, Bedford Veterans Administration Medical Center, Bedford, MA 01730, USA
Neurosci Lett 505:109-12. 2011..In a majority of plaques examined, AβpE11 was observed to be the dominant form in the innermost core. These data suggest that AβpE11 may serve as a generating site for senile plaque formation...
Sepiapterin reductase expression is increased in Parkinson's disease brain tissueJennifer E Tobin
Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA 02118, USA
Brain Res 1139:42-7. 2007..While the association of SPR to PD is not strong enough to support that this is the PARK3 gene, this study further implicates a role for SPR in idiopathic PD...
Disturbance of endogenous circadian rhythm in aging and Alzheimer diseaseDavid G Harper
Department of Psychiatry, McLean Hospital, 115 Mill Street, Belmont, MA 02478, USA
Am J Geriatr Psychiatry 13:359-68. 2005..The authors evaluated the similarities and differences between the consequences of aging and AD on endogenous circadian rhythm...
Dorsomedial SCN neuronal subpopulations subserve different functions in human dementiaDavid G Harper
Geriatric Psychiatry Program, McLean Hospital, 115 Mill Street, Belmont, MA 02478, USA
Brain 131:1609-17. 2008....
