S G Younkin

Summary

Affiliation: Mayo Clinic
Country: USA

Publications

  1. pmc Concordant association of insulin degrading enzyme gene (IDE) variants with IDE mRNA, Abeta, and Alzheimer's disease
    Minerva M Carrasquillo
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, Florida, United States of America
    PLoS ONE 5:e8764. 2010
  2. pmc Linking protective GAB2 variants, increased cortical GAB2 expression and decreased Alzheimer's disease pathology
    Fanggeng Zou
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, Florida, United States of America
    PLoS ONE 8:e64802. 2013
  3. pmc TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson's disease
    Sruti Rayaprolu
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
    Mol Neurodegener 8:19. 2013
  4. pmc Replication of EPHA1 and CD33 associations with late-onset Alzheimer's disease: a multi-centre case-control study
    Minerva M Carrasquillo
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Mol Neurodegener 6:54. 2011
  5. pmc Glutathione S-transferase omega genes in Alzheimer and Parkinson disease risk, age-at-diagnosis and brain gene expression: an association study with mechanistic implications
    Mariet Allen
    Mayo Clinic Florida, Department of Neuroscience, Jacksonville, FL, USA
    Mol Neurodegener 7:13. 2012
  6. pmc Evaluation of the global association between cholesterol-associated polymorphisms and Alzheimer's disease suggests a role for rs3846662 and HMGCR splicing in disease risk
    Christopher R Simmons
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
    Mol Neurodegener 6:62. 2011
  7. pmc Rheumatoid arthritis-associated polymorphisms are not protective against Alzheimer's disease
    Christopher R Simmons
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
    Mol Neurodegener 6:33. 2011
  8. pmc Expression of SORL1 and a novel SORL1 splice variant in normal and Alzheimers disease brain
    Karrie E Grear
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
    Mol Neurodegener 4:46. 2009
  9. pmc Investigation of 15 of the top candidate genes for late-onset Alzheimer's disease
    Olivia Belbin
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Hum Genet 129:273-82. 2011
  10. ncbi request reprint Amyloid beta vaccination: reduced plaques and improved cognition
    S G Younkin
    Center for Neuroscience, Mayo Clinic Jacksonville, Jacksonville, Florida, USA
    Nat Med 7:18-9. 2001

Detail Information

Publications52

  1. pmc Concordant association of insulin degrading enzyme gene (IDE) variants with IDE mRNA, Abeta, and Alzheimer's disease
    Minerva M Carrasquillo
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, Florida, United States of America
    PLoS ONE 5:e8764. 2010
    ..The insulin-degrading enzyme gene (IDE) is a strong functional and positional candidate for late onset Alzheimer's disease (LOAD)...
  2. pmc Linking protective GAB2 variants, increased cortical GAB2 expression and decreased Alzheimer's disease pathology
    Fanggeng Zou
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, Florida, United States of America
    PLoS ONE 8:e64802. 2013
    ..These findings support the hypothesis that Gab2 may protect neurons against LOAD but due to significant population heterogeneity, it is still unclear whether this protection is detectable at the genetic level...
  3. pmc TREM2 in neurodegeneration: evidence for association of the p.R47H variant with frontotemporal dementia and Parkinson's disease
    Sruti Rayaprolu
    Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
    Mol Neurodegener 8:19. 2013
    ..With this in mind we set out to assess the genetic association of the Alzheimer's disease-related risk variant in TREM2 (rs75932628, p.R47H) with other related neurodegenerative disorders...
  4. pmc Replication of EPHA1 and CD33 associations with late-onset Alzheimer's disease: a multi-centre case-control study
    Minerva M Carrasquillo
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Mol Neurodegener 6:54. 2011
    ..abstract:..
  5. pmc Glutathione S-transferase omega genes in Alzheimer and Parkinson disease risk, age-at-diagnosis and brain gene expression: an association study with mechanistic implications
    Mariet Allen
    Mayo Clinic Florida, Department of Neuroscience, Jacksonville, FL, USA
    Mol Neurodegener 7:13. 2012
    ..4,617 controls) and PD (678 PDs vs. 712 controls) for association with disease risk (case-controls), age-at-diagnosis (cases) and brain gene expression levels (autopsied subjects)...
  6. pmc Evaluation of the global association between cholesterol-associated polymorphisms and Alzheimer's disease suggests a role for rs3846662 and HMGCR splicing in disease risk
    Christopher R Simmons
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
    Mol Neurodegener 6:62. 2011
    ..abstract:..
  7. pmc Rheumatoid arthritis-associated polymorphisms are not protective against Alzheimer's disease
    Christopher R Simmons
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
    Mol Neurodegener 6:33. 2011
    ..abstract:..
  8. pmc Expression of SORL1 and a novel SORL1 splice variant in normal and Alzheimers disease brain
    Karrie E Grear
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
    Mol Neurodegener 4:46. 2009
    ..abstract:..
  9. pmc Investigation of 15 of the top candidate genes for late-onset Alzheimer's disease
    Olivia Belbin
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Hum Genet 129:273-82. 2011
    ..Overall, this large, independent follow-up study for 15 of the top LOAD candidate genes provides support for GAB2 and LOC651924 (6q24.1) as risk modifiers of LOAD and novel associations between PGBD1 and EBF3 with age-at-onset...
  10. ncbi request reprint Amyloid beta vaccination: reduced plaques and improved cognition
    S G Younkin
    Center for Neuroscience, Mayo Clinic Jacksonville, Jacksonville, Florida, USA
    Nat Med 7:18-9. 2001
    ..Immunization with an amyloid beta-peptide fragment reduces learning and memory impairments in mice, and this approach may eventually be used to prevent and/or treat this disease in people...
  11. ncbi request reprint Linkage of plasma Abeta42 to a quantitative locus on chromosome 10 in late-onset Alzheimer's disease pedigrees
    N Ertekin-Taner
    Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA
    Science 290:2303-4. 2000
    ..Remarkably, linkage to the same region was obtained independently in a genome-wide screen of LOAD sibling pairs. These results provide strong evidence for a novel LOAD locus on chromosome 10 that acts to increase Abeta...
  12. ncbi request reprint Reduction of Abeta accumulation in the Tg2576 animal model of Alzheimer's disease after oral administration of the phosphatidyl-inositol kinase inhibitor wortmannin
    S J Haugabook
    Mayo Clinic Jacksonville, Jacksonville, Florida 32224, USA
    FASEB J 15:16-18. 2001
    ....
  13. ncbi request reprint Heritability of plasma amyloid beta in typical late-onset Alzheimer's disease pedigrees
    N Ertekin-Taner
    Mayo Clinic Jacksonville, Jacksonville, Florida, 32224, USA
    Genet Epidemiol 21:19-30. 2001
    ..Thus, we suggest that plasma Abeta levels are quantitative traits that may be excellent surrogate markers for use in linkage analysis to identify loci that are important in typical LOAD...
  14. ncbi request reprint Biochemical detection of Abeta isoforms: implications for pathogenesis, diagnosis, and treatment of Alzheimer's disease
    T E Golde
    Department of Pharmacology, Mayo Clinic Jacksonville, FL 32224, USA
    Biochim Biophys Acta 1502:172-87. 2000
    ..This review will highlight those aspects of Abeta biology that have led to our increased understanding of the pathogenesis of AD as well as areas which warrant additional study...
  15. ncbi request reprint Reduced effectiveness of Abeta1-42 immunization in APP transgenic mice with significant amyloid deposition
    P Das
    Department of Neurosciences, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, Florida 32224, USA
    Neurobiol Aging 22:721-7. 2001
    ..These results indicate that in Tg2576 mice, Abeta1-42 immunization is more effective at preventing additional Abeta accumulation and does not result in significant clearance of pre-existing Abeta deposits...
  16. ncbi request reprint Age-dependent changes in brain, CSF, and plasma amyloid (beta) protein in the Tg2576 transgenic mouse model of Alzheimer's disease
    T Kawarabayashi
    Mayo Clinic Jacksonville, Jacksonville, Florida 32224, USA
    J Neurosci 21:372-81. 2001
    ..If a similar decline occurs in human plasma, it is possible that measurement of plasma Abeta may be useful as a premorbid biomarker for AD...
  17. ncbi request reprint High throughput screens for the identification of compounds that alter the accumulation of the Alzheimer's amyloid beta peptide (Abeta)
    S J Haugabook
    Mayo Clinic Jacksonville, Birdsall Building Room 253, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    J Neurosci Methods 108:171-9. 2001
    ..If compounds such as these can be identified that lower Abeta in the brain, they may represent one of the fastest and most cost effective methods to therapy...
  18. ncbi request reprint Amyloid beta protein starting pyroglutamate at position 3 is a major component of the amyloid deposits in the Alzheimer's disease brain
    Y Harigaya
    Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, Florida 32224, USA
    Biochem Biophys Res Commun 276:422-7. 2000
    ..In vitro comparison of Abeta1-42 and Abeta3(pE)-42 showed that Abeta3(pE)-42 is highly prone to oligomerization. These findings suggest that Abeta3(pE)-42 may be particularly important in AD pathogenesis...
  19. ncbi request reprint Glycosylphosphatidylinositol-anchored proteins play an important role in the biogenesis of the Alzheimer's amyloid beta-protein
    K Sambamurti
    Mayo Clinic, Jacksonville, Florida 32224, USA
    J Biol Chem 274:26810-4. 1999
    ..The cell-surface GPI-anchored protein(s) involved in Abeta biogenesis may be excellent therapeutic target(s) in Alzheimer's disease...
  20. ncbi request reprint Association of low plasma Abeta42/Abeta40 ratios with increased imminent risk for mild cognitive impairment and Alzheimer disease
    Neill R Graff-Radford
    Department of Neuroscience, Mayo College of Medicine, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224, USA
    Arch Neurol 64:354-62. 2007
    ..To develop preventive therapy for Alzheimer disease (AD), it is essential to develop AD-related biomarkers that identify at-risk individuals in the same way that cholesterol levels identify persons at risk for heart disease...
  21. ncbi request reprint Presenilins as therapeutic targets for the treatment of Alzheimer's disease
    T E Golde
    Mayo Clinic Jacksonville, Dept of Neuroscience, 4500 San Pablo Road, 32224, Jacksonville, FL, USA
    Trends Mol Med 7:264-9. 2001
    ....
  22. pmc TMEM106B regulates progranulin levels and the penetrance of FTLD in GRN mutation carriers
    N Finch
    Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Neurology 76:467-74. 2011
    ....
  23. ncbi request reprint Decreased neprilysin immunoreactivity in Alzheimer disease, but not in pathological aging
    Deng Shun Wang
    Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    J Neuropathol Exp Neurol 64:378-85. 2005
    ..The results add further evidence that PA is distinct from AD and indicate that decreased Abeta degradation by NEP is unlikely to contribute significantly to amyloid deposition in PA or, in many cases, of AD...
  24. ncbi request reprint A new pathogenic mutation in the APP gene (I716V) increases the relative proportion of A beta 42(43)
    C B Eckman
    Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Hum Mol Genet 6:2087-9. 1997
    ....
  25. ncbi request reprint Plasma amyloid beta protein is elevated in late-onset Alzheimer disease families
    N Ertekin-Taner
    Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road South, Jacksonville, FL 32224, USA
    Neurology 70:596-606. 2008
    ..Plasma A beta levels are elevated in early-onset Alzheimer disease (AD) caused by autosomal dominant mutations. Our objective was to determine whether similar genetic elevations exist in late-onset AD (LOAD)...
  26. ncbi request reprint Elevated amyloid beta protein (Abeta42) and late onset Alzheimer's disease are associated with single nucleotide polymorphisms in the urokinase-type plasminogen activator gene
    Nilufer Ertekin-Taner
    Department of Neuroscience, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Hum Mol Genet 14:447-60. 2005
    ..PLAU_1 is a plausible pathogenic mutation that could act by increasing Abeta42, but additional biological experiments are required to show this definitively...
  27. ncbi request reprint Genetic variants in a haplotype block spanning IDE are significantly associated with plasma Abeta42 levels and risk for Alzheimer disease
    Nilufer Ertekin-Taner
    Mayo Clinic Jacksonville, Department of Neuroscience, Jacksonville, FL, USA
    Hum Mutat 23:334-42. 2004
    ..007) in our family series. These results provide strong evidence for pathogenic variant(s) in the 276-kb region harboring IDE that influence intermediate AD phenotypes and risk for AD...
  28. pmc Plasma progranulin levels predict progranulin mutation status in frontotemporal dementia patients and asymptomatic family members
    NiCole Finch
    Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Brain 132:583-91. 2009
    ..We propose that plasma GRN levels could be used as a reliable and inexpensive tool to identify all GRN mutation carriers in early-onset dementia populations and asymptomatic at-risk individuals...
  29. ncbi request reprint Cholesterol-dependent gamma-secretase activity in buoyant cholesterol-rich membrane microdomains
    Suzanne Wahrle
    Department of Neuroscience and Pharmacology, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, Florida 32224, USA
    Neurobiol Dis 9:11-23. 2002
    ..Thus, altering cholesterol levels may influence the development of Alzheimer's disease (AD) by influencing production and deposition of Abeta within cholesterol rich membrane microdomains...
  30. pmc Replication of CLU, CR1, and PICALM associations with alzheimer disease
    Minerva M Carrasquillo
    Department of Neuroscience, Mayo Clinic, 4500 San Pablo Rd, Birdsall Building, Jacksonville, FL 32224, USA
    Arch Neurol 67:961-4. 2010
    ..To test for replication of the association between variants in the CLU, CR1, and PICALM genes with Alzheimer disease...
  31. pmc BRI2 (ITM2b) inhibits Abeta deposition in vivo
    Jungsu Kim
    Department of Neuroscience, Mayo Clinic College of Medicine, Mayo Clinic Jacksonville, Jacksonville, Florida 32224, USA
    J Neurosci 28:6030-6. 2008
    ..These studies demonstrate that BRI2 is a novel mediator of Abeta deposition in vivo...
  32. pmc Sex-dependent association of a common low-density lipoprotein receptor polymorphism with RNA splicing efficiency in the brain and Alzheimer's disease
    Fanggeng Zou
    Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Hum Mol Genet 17:929-35. 2008
    ..49, 95% confidence interval (CI) of 1.13-1.97, uncorrected P = 0.005], but not in females. In summary, these studies identify a functional apoE receptor SNP that is associated with AD in a sex-dependent fashion...
  33. pmc Gene expression levels as endophenotypes in genome-wide association studies of Alzheimer disease
    F Zou
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Neurology 74:480-6. 2010
    ..Late-onset Alzheimer disease (LOAD) is a common disorder with a substantial genetic component. We postulate that many disease susceptibility variants act by altering gene expression levels...
  34. pmc Genetic variation in PCDH11X is associated with susceptibility to late-onset Alzheimer's disease
    Minerva M Carrasquillo
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, Florida 32224, USA
    Nat Genet 41:192-8. 2009
    ..0 x 10(-7)) and 1.26 (95% CI = 1.05-1.51) for female heterozygotes (P = 0.01) compared to female noncarriers. For male hemizygotes (P = 0.07) compared to male noncarriers, the odds ratio was 1.18 (95% CI = 0.99-1.41)...
  35. ncbi request reprint Identification of loci determining susceptibility to the lethal effects of amyloid precursor protein transgene overexpression
    Joseph Krezowski
    McLaughlin Research Institute, 1520 23rd Street South, Great Falls, MT 59405, USA
    Hum Mol Genet 13:1989-97. 2004
    ....
  36. ncbi request reprint Serum creatinine levels correlate with plasma amyloid Beta protein
    Zoe Arvanitakis
    Rush University, Chicago, Illinois, USA
    Alzheimer Dis Assoc Disord 16:187-90. 2002
    ..01), accounting for 7.3% and 3.1% of shared variance, respectively. Significant associations were also present in NC and AD groups separately. These results indicate that it may be useful to consider Cr levels when measuring plasma Abeta...
  37. ncbi request reprint The presenilin-1 familial Alzheimer disease mutant P117L impairs neurogenesis in the hippocampus of adult mice
    Paul H Wen
    Department of Psychiatry, Mount Sinai School of Medicine, New York, NY 10029, USA
    Exp Neurol 188:224-37. 2004
    ..They also identify a new mechanism whereby PS1 FAD mutants may impair normal neuronal function and may have implications for the physiological functioning of the hippocampus in FAD...
  38. ncbi request reprint Genetic background regulates beta-amyloid precursor protein processing and beta-amyloid deposition in the mouse
    Emily J H Lehman
    Department of Genetics, Case Western Reserve University, and Center for Human Genetics, University Hospitals of Cleveland, OH 44106 4955, USA
    Hum Mol Genet 12:2949-56. 2003
    ....
  39. ncbi request reprint Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase
    Joanna L Jankowsky
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hum Mol Genet 13:159-70. 2004
    ..These data suggest that PS1 variants do not simply alter the preferred cleavage site for gamma-secretase, but rather that they have more complex effects on the regulation of gamma-secretase and its access to substrates...
  40. ncbi request reprint Dimeric amyloid beta protein rapidly accumulates in lipid rafts followed by apolipoprotein E and phosphorylated tau accumulation in the Tg2576 mouse model of Alzheimer's disease
    Takeshi Kawarabayashi
    Department of Neurology, Okayama University Graduate School of Medicine, Okayama, 700 8558, Japan
    J Neurosci 24:3801-9. 2004
    ..A similar increase in ApoE and a large increase in phosphorylated tau was observed in lipid rafts from AD brain. These findings suggest that lipid rafts may be an important site for interaction between dimeric Abeta, ApoE, and tau...
  41. ncbi request reprint Environmental enrichment mitigates cognitive deficits in a mouse model of Alzheimer's disease
    Joanna L Jankowsky
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 25:5217-24. 2005
    ..These results demonstrate that the generation of Abeta in vivo and its impact on the function of the nervous system can be strongly modulated by environmental factors...
  42. ncbi request reprint BACE1 deficiency rescues memory deficits and cholinergic dysfunction in a mouse model of Alzheimer's disease
    Masuo Ohno
    Department of Physiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
    Neuron 41:27-33. 2004
    ..Our gene-based approach demonstrates that lower Abeta levels are beneficial for AD-associated memory impairments, validating BACE1 as a therapeutic target for AD...
  43. ncbi request reprint Plasmin deficiency does not alter endogenous murine amyloid beta levels in mice
    H Michael Tucker
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, 800 S Limestone St, Lexington, KY 40536 0230, USA
    Neurosci Lett 368:285-9. 2004
    ..Hence, although plasmin is potentially important in the degradation of A beta aggregates, we interpret these data as suggesting that plasmin does not regulate steady-state A beta levels in non-pathologic conditions...
  44. ncbi request reprint Alterations in cerebral blood flow and glucose utilization in mice overexpressing the amyloid precursor protein
    Kiyoshi Niwa
    Center for Clinical and Molecular Neurobiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    Neurobiol Dis 9:61-8. 2002
    ..These observations support the hypothesis that cerebrovascular and metabolic abnormalities are early events in the pathogenesis of Alzheimer's disease...
  45. ncbi request reprint The relationship between Abeta and memory in the Tg2576 mouse model of Alzheimer's disease
    Marcus A Westerman
    Department of Neurology, Center for Clinical and Molecular Neurobiology, University of Minnesota, Minneapolis, Minnesota 55455, USA
    J Neurosci 22:1858-67. 2002
    ..These studies also provide a methodological framework within which to investigate these Abeta assemblies in vivo...
  46. ncbi request reprint Cerebrovascular autoregulation is profoundly impaired in mice overexpressing amyloid precursor protein
    Kiyoshi Niwa
    Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455, USA
    Am J Physiol Heart Circ Physiol 283:H315-23. 2002
    ..The resulting alterations in cerebral perfusion may play a role in the brain dysfunction and periventricular white-matter changes associated with Alzheimer's dementia...
  47. ncbi request reprint Type-specific evolution of amyloid plaque and angiopathy in APPsw mice
    Yasuo Harigaya
    Neurology Service, Maebashi Red Cross Hospital, 3 21 36 Asahi cho, Maebashi, Gunma 371 0014, Japan
    Neurosci Lett 395:37-41. 2006
    ....
  48. ncbi request reprint Rodent A beta modulates the solubility and distribution of amyloid deposits in transgenic mice
    Joanna L Jankowsky
    Division of Biology, California Institute of Technology, Pasadena, California 91125, USA
    J Biol Chem 282:22707-20. 2007
    ..These findings suggest that, although mouse A beta does not influence the rate of amyloid formation, the incorporation of A beta peptides with differing sequences alters the solubility and localization of the resulting aggregates...
  49. pmc Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease
    Joanna L Jankowsky
    Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS Med 2:e355. 2005
    ..However, no long-term studies using animal models of amyloid pathology have yet been performed to test this hypothesis...
  50. ncbi request reprint Bosentan preserves endothelial function in mice overexpressing APP
    Ahmad A Elesber
    Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    Neurobiol Aging 27:446-50. 2006
    ..The current study demonstrates the presence of endothelial dysfunction in both carotid and aortic arteries in mice overexpressing APP and suggests a pathophysiological role for the endogenous endothelin system in AD...
  51. pmc Cyclooxygenase-2 inhibition improves amyloid-beta-mediated suppression of memory and synaptic plasticity
    Linda A Kotilinek
    Department of Neurology, University of Minnesota, Minneapolis, MN 55455, USA
    Brain 131:651-64. 2008
    ..The results lead us to propose a third possible mechanism by which NSAIDs may protect against Alzheimer's disease, involving the blockade of a COX-2-mediated PGE2 response at synapses...
  52. pmc Lack of association of hepatic lipase polymorphisms with late-onset Alzheimer's disease
    Haiyan Zhu
    Department of Physiology and Sanders Brown Center on Aging, University of Kentucky, 800 S Limestone St, Lexington, KY 40536 0230, USA
    Neurobiol Aging 29:793-4. 2008
    ..However, this association was not confirmed in two subsequent series based at the University of Kentucky (UKY, p=0.15) or the Mayo Clinic in Jacksonville (MCJ, p=0.97). Hence, rs6084 is not consistently associated with LOAD...

Research Grants20

  1. ChAT, AChE, and Cholinergic Neurons in Aging and AD
    Steven Younkin; Fiscal Year: 2009
    ..The utility of these additional biomarkers will be evaluated singly as compared to plasma Aft and jointly with plasma AB. ..
  2. PLASMA A BETA AS A SURROGATE GENETIC MARKER FOR LOAD
    Steven Younkin; Fiscal Year: 2005
    ....
  3. ChAT, AChE, and Cholinergic Neurons in Aging and AD
    Steven Younkin; Fiscal Year: 2007
    ..The utility of these additional biomarkers will be evaluated singly as compared to plasma Aft and jointly with plasma AB. ..
  4. Plasma AB as a Surrogate Genetic Marker for LOAD
    Steven Younkin; Fiscal Year: 2009
    ....
  5. ChAT, AChE, and Cholinergic Neurons in Aging and AD
    Steven G Younkin; Fiscal Year: 2010
    ..The utility of these additional biomarkers will be evaluated singly as compared to plasma Aft and jointly with plasma AB. ..
  6. PLASMA A BETA AS A SURROGATE GENETIC MARKER FOR LOAD
    Steven Younkin; Fiscal Year: 2004
    ....
  7. CHAT, ACHE, AND CHOLINERGIC NEURONS IN AGING AND ALZHEIM
    Steven Younkin; Fiscal Year: 2004
    ..abstract_text> ..
  8. CHAT, ACHE, AND CHOLINERGIC NEURONS IN AGING AND ALZHEIM
    Steven Younkin; Fiscal Year: 2003
    ..abstract_text> ..
  9. PLASMA A BETA AS A SURROGATE GENETIC MARKER FOR LOAD
    Steven Younkin; Fiscal Year: 2003
    ....
  10. PLASMA A BETA AS A SURROGATE GENETIC MARKER FOR LOAD
    Steven Younkin; Fiscal Year: 2002
    ....
  11. CHAT, ACHE, AND CHOLINERGIC NEURONS IN AGING AND ALZHEIM
    Steven Younkin; Fiscal Year: 2002
    ..abstract_text> ..
  12. CHAT, ACHE, AND CHOLINERGIC NEURONS IN AGING AND ALZHEIM
    Steven Younkin; Fiscal Year: 2001
    ..abstract_text> ..
  13. PLASMA A BETA AS A SURROGATE GENETIC MARKER FOR LOAD
    Steven Younkin; Fiscal Year: 2001
    ....
  14. CHAT, ACHE, AND CHOLINERGIC NEURONS IN AGING AND ALZHEIM
    Steven Younkin; Fiscal Year: 2000
    ..abstract_text> ..
  15. Plasma AB as a Surrogate Genetic Marker for LOAD
    Steven G Younkin; Fiscal Year: 2010
    ....