Ann C McKee

Summary

Affiliation: Boston University
Country: USA

Publications

  1. pmc Ibuprofen reduces Abeta, hyperphosphorylated tau and memory deficits in Alzheimer mice
    Ann C McKee
    Department of Neurology, Boston University School of Medicine, Boston, MA, USA
    Brain Res 1207:225-36. 2008
  2. pmc Helmets and mouth guards: the role of personal equipment in preventing sport-related concussions
    Daniel 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
  3. pmc Acyl peptide hydrolase degrades monomeric and oligomeric amyloid-beta peptide
    Rina Yamin
    Department of Biochemistry, Boston University School of Medicine, 72 East Concord Street, Boston, K620, MA 02118, USA
    Mol Neurodegener 4:33. 2009
  4. pmc TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathy
    Ann C McKee
    Geriatric Research Education Clinical Center, Bedford Veterans Administration Hospital, Bedford, Massachusetts 01730, USA
    J Neuropathol Exp Neurol 69:918-29. 2010
  5. ncbi request reprint Visual association pathology in preclinical Alzheimer disease
    Ann 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
  6. pmc Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury
    Ann 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
  7. pmc The spectrum of disease in chronic traumatic encephalopathy
    Ann C McKee
    United States Department of Veterans Affairs, VA Boston Healthcare System, Boston, MA 02130, USA
    Brain 136:43-64. 2013
  8. doi request reprint Long-term consequences of repetitive brain trauma: chronic traumatic encephalopathy
    Robert 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
  9. pmc The Framingham Brain Donation Program: neuropathology along the cognitive continuum
    Rhoda Au
    Department of Neurology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA
    Curr Alzheimer Res 9:673-86. 2012
  10. pmc Long-term consequences: effects on normal development profile after concussion
    Daniel 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

Detail Information

Publications32

  1. pmc Ibuprofen reduces Abeta, hyperphosphorylated tau and memory deficits in Alzheimer mice
    Ann 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...
  2. pmc Helmets and mouth guards: the role of personal equipment in preventing sport-related concussions
    Daniel 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...
  3. pmc Acyl peptide hydrolase degrades monomeric and oligomeric amyloid-beta peptide
    Rina Yamin
    Department of Biochemistry, Boston University School of Medicine, 72 East Concord Street, Boston, K620, MA 02118, USA
    Mol Neurodegener 4:33. 2009
    ..abstract:..
  4. pmc TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathy
    Ann 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...
  5. ncbi request reprint Visual association pathology in preclinical Alzheimer disease
    Ann 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...
  6. pmc Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury
    Ann 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...
  7. pmc The spectrum of disease in chronic traumatic encephalopathy
    Ann C McKee
    United States Department of Veterans Affairs, VA Boston Healthcare System, Boston, MA 02130, USA
    Brain 136:43-64. 2013
    ....
  8. doi request reprint Long-term consequences of repetitive brain trauma: chronic traumatic encephalopathy
    Robert 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...
  9. pmc The Framingham Brain Donation Program: neuropathology along the cognitive continuum
    Rhoda 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...
  10. pmc Long-term consequences: effects on normal development profile after concussion
    Daniel 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...
  11. doi request reprint Chronic traumatic encephalopathy: neurodegeneration following repetitive concussive and subconcussive brain trauma
    Christine 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...
  12. doi request reprint Clinical appraisal of chronic traumatic encephalopathy: current perspectives and future directions
    Brandon 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...
  13. pmc Increased expression of TrkB and Capzb2 accompanies preserved cognitive status in early Alzheimer disease pathology
    Patricia 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...
  14. pmc Profile of self-reported problems with executive functioning in college and professional football players
    Daniel R Seichepine
    Boston University Alzheimer s Disease Center, Boston University School of Medicine, Boston University, Boston, Massachusetts, USA
    J Neurotrauma 30:1299-304. 2013
    ..The findings are in accord with a growing body of evidence that participation in football is associated with the development of cognitive changes and dementia as observed in CTE...
  15. pmc Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head trauma
    Brandon 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...
  16. pmc R-flurbiprofen improves tau, but not Aß pathology in a triple transgenic model of Alzheimer's disease
    Isabel Carreras
    Research GRECC, VA Boston Healthcare System, Boston, MA, USA Department of Biochemistry, Boston University School of Medicine, Boston, MA, USA
    Brain Res 1541:115-27. 2013
    ..Glutamine and glutamate, neurochemicals that shuttles between neurons and astrocytes to maintain glutamate homeostasis in the synapses, deserve further attention as MR markers of cognitive function. ..
  17. pmc Mild traumatic brain injury: a risk factor for neurodegeneration
    Brandon 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
    ....
  18. doi request reprint The neuropathology of sport
    Ann C McKee
    VA Boston Healthcare System, 150 South Huntington Ave, Boston, MA, 02130, USA
    Acta Neuropathol 127:29-51. 2014
    ..Other sports associated with CTE include ice hockey, professional wrestling, soccer, rugby, and baseball. ..
  19. pmc Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model
    Lee E Goldstein
    Molecular Aging and Development Laboratory, Boston University School of Medicine, Boston, MA 02118, USA
    Sci Transl Med 4:134ra60. 2012
    ....
  20. pmc Association of distinct variants in SORL1 with cerebrovascular and neurodegenerative changes related to Alzheimer disease
    Karen 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
    ....
  21. ncbi request reprint Dementia severity and Lewy bodies affect circadian rhythms in Alzheimer disease
    David G Harper
    Geriatric Psychiatric Program, Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA
    Neurobiol Aging 25:771-81. 2004
    ....
  22. pmc The epidemiology of sport-related concussion
    Daniel 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...
  23. pmc δ-Catenin is genetically and biologically associated with cortical cataract and future Alzheimer-related structural and functional brain changes
    Gyungah 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...
  24. ncbi request reprint Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons
    Yevgenya 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...
  25. ncbi request reprint Scattering differentiates Alzheimer disease in vitro
    Eugene 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...
  26. pmc Early-life sodium exposure unmasks susceptibility to stroke in hyperlipidemic, hypertensive heterozygous Tg25 rats transgenic for human cholesteryl ester transfer protein
    Julius 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...
  27. doi request reprint Chronic traumatic encephalopathy: where are we and where are we going?
    Jesse Mez
    Boston University Alzheimer s Disease Center, Boston University School of Medicine, 72 E Concord Street, Suite 7800, Boston, MA, 02118, USA
    Curr Neurol Neurosci Rep 13:407. 2013
    ..We conclude by suggesting seven essential areas for future CTE research. ..
  28. doi request reprint 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...
  29. pmc Pyroglutamate-Aβ 3 and 11 colocalize in amyloid plaques in Alzheimer's disease cerebral cortex with pyroglutamate-Aβ 11 forming the central core
    Christopher 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...
  30. pmc Sepiapterin reductase expression is increased in Parkinson's disease brain tissue
    Jennifer 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...
  31. ncbi request reprint Disturbance of endogenous circadian rhythm in aging and Alzheimer disease
    David 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...
  32. pmc Dorsomedial SCN neuronal subpopulations subserve different functions in human dementia
    David G Harper
    Geriatric Psychiatry Program, McLean Hospital, 115 Mill Street, Belmont, MA 02478, USA
    Brain 131:1609-17. 2008
    ....