A M Fagan

Summary

Affiliation: Washington University School of Medicine
Country: USA

Publications

  1. pmc Multiple γ-secretase product peptides are coordinately increased in concentration in the cerebrospinal fluid of a subpopulation of sporadic Alzheimer's disease subjects
    Saori Hata
    Laboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan
    Mol Neurodegener 7:16. 2012
  2. pmc Upcoming candidate cerebrospinal fluid biomarkers of Alzheimer's disease
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Ave, St Louis, MO 63110, USA
    Biomark Med 6:455-76. 2012
  3. pmc ApoAI deficiency results in marked reductions in plasma cholesterol but no alterations in amyloid-beta pathology in a mouse model of Alzheimer's disease-like cerebral amyloidosis
    Anne M Fagan
    Department of Neurology and Center for the Study of Nervous System Injury, Alzheimer s Disease Research Center, Washington University School of Medicine, 660 S Euclid Ave, Box 8111, St Louis, MO 63110, USA
    Am J Pathol 165:1413-22. 2004
  4. ncbi request reprint Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 59:512-9. 2006
  5. ncbi request reprint The search for antecedent biomarkers of Alzheimer's disease
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Alzheimers Dis 8:347-58. 2005
  6. ncbi request reprint Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, 660 S Euclid Ave, Box 8111, St Louis, MO 63110, USA
    Arch Neurol 64:343-9. 2007
  7. pmc Decreased cerebrospinal fluid Abeta(42) correlates with brain atrophy in cognitively normal elderly
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 65:176-83. 2009
  8. pmc Cerebrospinal fluid tau and ptau(181) increase with cortical amyloid deposition in cognitively normal individuals: implications for future clinical trials of Alzheimer's disease
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    EMBO Mol Med 1:371-80. 2009
  9. pmc Cerebrospinal fluid biomarkers of Alzheimer's disease
    Anne M Fagan
    Department of Neurology, Hope Center for Neuological Disorder, Washington University, School of Medicine, St Louis, MO 63110, USA
    Biomark Med 4:51-63. 2010
  10. pmc Comparison of analytical platforms for cerebrospinal fluid measures of β-amyloid 1-42, total tau, and p-tau181 for identifying Alzheimer disease amyloid plaque pathology
    Anne M Fagan
    Knight Alzheimer s Disease Research Center, St Louis, Missouri, USA
    Arch Neurol 68:1137-44. 2011

Research Grants

  1. EFFECTS OF AGING & PGP ON AB EFFLUX FROM THE BRAIN
    ANNE FAGAN NIVEN; Fiscal Year: 2005

Collaborators

Detail Information

Publications26

  1. pmc Multiple γ-secretase product peptides are coordinately increased in concentration in the cerebrospinal fluid of a subpopulation of sporadic Alzheimer's disease subjects
    Saori Hata
    Laboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan
    Mol Neurodegener 7:16. 2012
    ..Aβ and p3-Alcα can be recovered from human cerebrospinal fluid (CSF). We have previously reported alternative processing of APP and Alcα in the CSF of some patients with sporadic mild cognitive impairment (MCI) and AD (SAD)...
  2. pmc Upcoming candidate cerebrospinal fluid biomarkers of Alzheimer's disease
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Ave, St Louis, MO 63110, USA
    Biomark Med 6:455-76. 2012
    ..This article discusses the potential of several promising novel cerebrospinal fluid analytes, highlights the next steps critical for advancement in the field, and provides a prediction on how the field may evolve in 5-10 years...
  3. pmc ApoAI deficiency results in marked reductions in plasma cholesterol but no alterations in amyloid-beta pathology in a mouse model of Alzheimer's disease-like cerebral amyloidosis
    Anne M Fagan
    Department of Neurology and Center for the Study of Nervous System Injury, Alzheimer s Disease Research Center, Washington University School of Medicine, 660 S Euclid Ave, Box 8111, St Louis, MO 63110, USA
    Am J Pathol 165:1413-22. 2004
    ..These and other data suggest that it is perhaps the level of brain apolipoprotein E, not cholesterol per se, that plays a primary role in brain Abeta metabolism...
  4. ncbi request reprint Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 59:512-9. 2006
    ..This decrease may reflect plaques acting as an Abeta(42) "sink," hindering transport of soluble Abeta(42) between brain and CSF. We investigated this hypothesis...
  5. ncbi request reprint The search for antecedent biomarkers of Alzheimer's disease
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Alzheimers Dis 8:347-58. 2005
    ..Louis. The Adult Children Study provides an opportunity to discuss the challenges and goals for investigations of antecedent AD biomarkers...
  6. ncbi request reprint Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, 660 S Euclid Ave, Box 8111, St Louis, MO 63110, USA
    Arch Neurol 64:343-9. 2007
    ....
  7. pmc Decreased cerebrospinal fluid Abeta(42) correlates with brain atrophy in cognitively normal elderly
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 65:176-83. 2009
    ..The objective of this study was to determine whether cerebrospinal fluid (CSF) biomarkers for AD suggest the presence of brain damage in the preclinical stage of AD...
  8. pmc Cerebrospinal fluid tau and ptau(181) increase with cortical amyloid deposition in cognitively normal individuals: implications for future clinical trials of Alzheimer's disease
    Anne M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    EMBO Mol Med 1:371-80. 2009
    ..These findings have important implications for preclinical AD diagnosis and treatment...
  9. pmc Cerebrospinal fluid biomarkers of Alzheimer's disease
    Anne M Fagan
    Department of Neurology, Hope Center for Neuological Disorder, Washington University, School of Medicine, St Louis, MO 63110, USA
    Biomark Med 4:51-63. 2010
    ..This article summarizes the most promising cerebrospinal fluid biomarkers, highlights novel applications and current challenges, and provides a prediction on how the field may evolve in 5-10 years...
  10. pmc Comparison of analytical platforms for cerebrospinal fluid measures of β-amyloid 1-42, total tau, and p-tau181 for identifying Alzheimer disease amyloid plaque pathology
    Anne M Fagan
    Knight Alzheimer s Disease Research Center, St Louis, Missouri, USA
    Arch Neurol 68:1137-44. 2011
    ..Cerebrospinal fluid (CSF) biomarkers of Alzheimer disease (AD) are currently being considered for inclusion in revised diagnostic criteria for research and/or clinical purposes to increase the certainty of antemortem diagnosis...
  11. ncbi request reprint Human and murine ApoE markedly alters A beta metabolism before and after plaque formation in a mouse model of Alzheimer's disease
    Anne M Fagan
    Center for the Study of Nervous System Injury, Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Neurobiol Dis 9:305-18. 2002
    ....
  12. ncbi request reprint Astrocyte lipoproteins, effects of apoE on neuronal function, and role of apoE in amyloid-beta deposition in vivo
    A M Fagan
    Center for the Study of Nervous System Injury, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Microsc Res Tech 50:297-304. 2000
    ..Together, these data have provided important clues as to possible mechanism(s) by which apoE genotype modifies AD risk...
  13. ncbi request reprint Unique lipoproteins secreted by primary astrocytes from wild type, apoE (-/-), and human apoE transgenic mice
    A M Fagan
    Center for the Study of Nervous System Injury, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 274:30001-7. 1999
    ..These studies suggest that apoE expression influences the unique structure of astrocyte lipoproteins, a process further modified by apoE species...
  14. ncbi request reprint Evidence for normal aging of the septo-hippocampal cholinergic system in apoE (-/-) mice but impaired clearance of axonal degeneration products following injury
    A M Fagan
    Center for the Study of Nervous System Injury, and, Washington University School of Medicine, St Louis, Missouri, 63110, USA
    Exp Neurol 151:314-25. 1998
    ..These data suggest that although apoE is not required for the maintenance of BFCNs in vivo, it may play a role in the clearance of cholesterol-laden neurodegeneration products following brain injury...
  15. ncbi request reprint Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model
    D M Holtzman
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 47:739-47. 2000
    ..These data demonstrate that ApoE facilitates the formation of both neuritic and cerebrovascular plaques, which are pathological hallmarks of AD and cerebral amyloid angiopathy...
  16. pmc Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease
    D M Holtzman
    Department of Neurology, Center for the Study of Nervous System Injury, Washington University School of Medicine, 660 South Euclid Avenue, Box 8111, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 97:2892-7. 2000
    ..Our data demonstrate a critical and isoform-specific role for apoE in neuritic plaque formation, a pathological hallmark of AD...
  17. pmc Expression of human apolipoprotein E reduces amyloid-beta deposition in a mouse model of Alzheimer's disease
    D M Holtzman
    Department of Neurology, Center for the Study of Nervous System Injury, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Clin Invest 103:R15-R21. 1999
    ..The results may have important implications for understanding mechanisms underlying the link between apo E and AD...
  18. pmc Improving CSF biomarker accuracy in predicting prevalent and incident Alzheimer disease
    C M Roe
    Knight Alzheimer s Disease Research Center, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 76:501-10. 2011
    ....
  19. ncbi request reprint A role for TrkA during maturation of striatal and basal forebrain cholinergic neurons in vivo
    A M Fagan
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 17:7644-54. 1997
    ..Our data suggest that, in the absence of NGF/TrkA signaling, striatal cholinergic neurons and BFCNs do not mature fully and that BFCNs begin to atrophy and/or die surrounding the time of target innervation...
  20. pmc Cognitively unimpaired HIV-positive subjects do not have increased 11C-PiB: a case-control study
    B M Ances
    Department of Neurology, Washington University, St Louis, MO 63110, USA
    Neurology 75:111-5. 2010
    ..We evaluated the amyloid-binding agent (11)C-Pittsburgh compound B ((11)C-PiB), a biomarker for Alphabeta42 deposition, in cognitively unimpaired HIV+ (n = 10) participants and matched community controls without dementia (n = 20)...
  21. ncbi request reprint Glial fibrillary acidic protein-apolipoprotein E (apoE) transgenic mice: astrocyte-specific expression and differing biological effects of astrocyte-secreted apoE3 and apoE4 lipoproteins
    Y Sun
    Department of Neurology and Center for the Study of Nervous System Injury, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 18:3261-72. 1998
    ..In addition to providing information regarding the role of astrocyte-secreted apoE lipoproteins in the normal brain, these animals will also be useful in models of both AD and CNS injury...
  22. ncbi request reprint Purification and characterization of astrocyte-secreted apolipoprotein E and J-containing lipoproteins from wild-type and human apoE transgenic mice
    R B DeMattos
    Center for the Study of Nervous System Injury, Washington University School of Medicine, 660 South Euclid Avenue, Box 8111, St Louis, MO 63110, USA
    Neurochem Int 39:415-25. 2001
    ..Further use of physiological preparations of CNS-derived lipoproteins may allow for a detailed understanding of the role of these molecules in the normal brain and in diseases such as AD...
  23. pmc CSF biomarkers of Alzheimer disease in HIV-associated neurologic disease
    D B Clifford
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 73:1982-7. 2009
    ..CSF amyloid measurements in HAND have been reported to be similar to those in dementia of the Alzheimer type (DAT). Confirmatory evaluation of this finding in carefully evaluated subjects is needed...
  24. ncbi request reprint Non-TrkA-expressing small DRG neurons are lost in TrkA deficient mice
    I Silos-Santiago
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 15:5929-42. 1995
    ..These neurons must either depend on NGF via a novel, indirect mechanism or alternatively, downregulate TrkA expression during development...
  25. ncbi request reprint Severe sensory deficits but normal CNS development in newborn mice lacking TrkB and TrkC tyrosine protein kinase receptors
    I Silos-Santiago
    Department of Molecular Oncology, Bristol Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543 4000, USA
    Eur J Neurosci 9:2045-56. 1997
    ....
  26. ncbi request reprint TrkA, but not TrkC, receptors are essential for survival of sympathetic neurons in vivo
    A M Fagan
    Department of Molecular Oncology, Bristol Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543, USA
    J Neurosci 16:6208-18. 1996
    ..Moreover, these observations raise the possibility that at least some SCG neurons become neurotrophin-dependent before complete target innervation...

Research Grants1

  1. EFFECTS OF AGING & PGP ON AB EFFLUX FROM THE BRAIN
    ANNE FAGAN NIVEN; Fiscal Year: 2005
    ..Support for the hypothesis would establish a role for age-dependent defects in A-beta clearance from the brain in the pathogenesis of AD and, importantly, provide a novel therapeutic target for treatment of the disease. ..