12 results on '"Quinn, Joseph"'
Search Results
2. Incidence of New-Onset Seizures in Mild to Moderate Alzheimer Disease
- Author
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Irizarry, Michael C., Jin, Shelia, He, Feng, Emond, Jennifer A., Raman, Rema, Thomas, Ronald G., Sano, Mary, Quinn, Joseph F., Tariot, Pierre N., Galasko, Douglas R., Ishihara, Lianna S., Weil, John G., and Aisen, Paul S.
- Published
- 2012
- Full Text
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3. SNCA Variant Associated With Parkinson Disease and Plasma α-Synuclein Level
- Author
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Mata, Ignacio F., Shi, Min, Agarwal, Pinky, Chung, Kathryn A., Edwards, Karen L., Factor, Stewart A., Galasko, Douglas R., Ginghina, Carmen, Griffith, Alida, Higgins, Donald S., Kay, Denise M., Kim, Hojoong, Leverenz, James B., Quinn, Joseph F., Roberts, John W., Samii, Ali, Snapinn, Katherine W., Tsuang, Debby W., Yearout, Dora, Zhang, Jing, Payami, Haydeh, and Zabetian, Cyrus P.
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- 2010
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4. Phase 2 Safety Trial Targeting Amyloid β Production With a γ-Secretase Inhibitor in Alzheimer Disease
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Fleisher, Adam S., Raman, Rema, Siemers, Eric R., Becerra, Lida, Clark, Christopher M., Dean, Robert A., Farlow, Martin R., Galvin, James E., Peskind, Elaine R., Quinn, Joseph F., Sherzai, Abdullah, Sowell, B. Brooke, Aisen, Paul S., and Thal, Leon J.
- Published
- 2008
5. Age and Apolipoprotein E*4 Allele Effects on Cerebrospinal Fluid β-Amyloid 42 in Adults With Normal Cognition
- Author
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Peskind, Elaine R., Li, Ge, Shofer, Jane, Quinn, Joseph F., Kaye, Jeffrey A., Clark, Chris M., Farlow, Martin R., DeCarli, Charles, Raskind, Murray A., Schellenberg, Gerard D., Lee, Virginia M.-Y., and Galasko, Douglas R.
- Published
- 2006
6. Cerebrospinal Fluid Tau and β-Amyloid: How Well Do These Biomarkers Reflect Autopsy-Confirmed Dementia Diagnoses?
- Author
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Clark, Christopher M., Xie, Sharon, Chittams, Jesse, Ewbank, Douglas, Peskind, Elaine, Galasko, Douglas, Morris, John C., McKeel, Daniel W., Jr, Farlow, Martin, Weitlauf, Sharon L., Quinn, Joseph, Kaye, Jeffrey, Knopman, David, Arai, Hiroyuki, Doody, Rachelle S., DeCarli, Charles, Leight, Susan, Lee, Virginia M.-Y., and Trojanowski, John Q.
- Published
- 2003
7. Age and Apolipoprotein E*4 Allele Effects on Cerebrospinal Fluid α-Amyloid 42 in Adults With Normal Cognition.
- Author
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Peskind, Elaine R., Ge Li, Shofer, Jane, Quinn, Joseph F., Kaye, Jeffrey A., Clark, Chris M., Farlow, Martin R., DeCarli, Charles, Raskind, Murray A., Schellenberg, Gerard D., Lee, Virginia M. -Y., and Galasko, Douglas R.
- Abstract
Background: Decreased cerebrospinal fluid (CSF) β-amyloid 42 (Aβ
42 ) concentration, but not Aβ40 concentration, is a biomarker for Alzheimer disease. This Aβ42 concentration decrease in CSF likely reflects precipitation of Aβ42 in amyloid plaques in brain parenchyma. This pathogenic plaque deposition begins years before the clinical expression of dementia in Alzheimer disease. Normal aging and the presence of the apolipoprotein E (APOE*4) allele are the most important known risk factors for Alzheimer disease. Objective: To estimate the interactive effects of normal aging and presence of the APOE*4 allele on CSF Aβ42 concentration in adults with normal cognition across the life span. Design: The CSF was collected in the morning after an overnight fast using Sprotte 24-g atraumatic spinal needles. The CSF Aβ42 and Aβ40 concentrations were measured in the 10th milliliter of CSF collected by sandwich enzyme-linked immunosorbent assay. The APOE genotype was determined by a restriction digest method. Subjects: One hundred eighty-four community volunteers with normal cognition aged 21 to 88 years. Results: The CSF Aβ42 , but not the Aβ40 , concentration decreased significantly with age. There was a sharp decrease in CSF Aβ42 concentration beginning in the sixth decade in subjects with the APOE*4 allele. This age-associated decrease in CSF Aβ42 concentration was significantly and substantially greater in subjects with the APOE*4 allele compared with those without the APOE*4 allele. Conclusion: These CSF Aβ42 findings are consistent with acceleration by the APOE*4 allele of pathogenic Aβ42 brain deposition starting in later middle age in persons with normal cognition. [ABSTRACT FROM AUTHOR]- Published
- 2006
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8. Meta-analysis Confirms CR1, CLU, and PICALM as Alzheimer Disease Risk Loci and Reveals Interactions With APOE GenotypesCR1, CLU, and PICALM as AD Susceptibility Loci
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Jun, Gyungah, Naj, Adam C., Beecham, Gary W., Wang, Li-San, Buros, Jacqueline, Gallins, Paul J., Buxbaum, Joseph D., Ertekin-Taner, Nilufer, Fallin, M. Daniele, Friedland, Robert, Inzelberg, Rivka, Kramer, Patricia, Rogaeva, Ekaterina, St. George-Hyslop, Peter, Arnold, Steven E., Baldwin, Clinton T., Barber, Robert, Beach, Thomas, Bigio, Eileen H., Bird, Thomas D., Boxer, Adam, Burke, James R., Cairns, Nigel, Carroll, Steven L., Chui, Helena C., Clark, David G., Cotman, Carl W., Cummings, Jeffrey L., DeCarli, Charles, Diaz-Arrastia, Ramon, Dick, Malcolm, Dickson, Dennis W., Ellis, William G., Fallon, Kenneth B., Farlow, Martin R., Ferris, Steven, Frosch, Matthew P., Galasko, Douglas R., Gearing, Marla, Geschwind, Daniel H., Ghetti, Bernardino, Gilman, Sid, Giordani, Bruno, Glass, Jonathan, Graff-Radford, Neill R., Green, Robert C., Growdon, John H., Hamilton, Ronald L., Harrell, Lindy E., Head, Elizabeth, Honig, Lawrence S., Hulette, Christine M., Hyman, Bradley T., Jicha, Gregory A., Jin, Lee-Way, Johnson, Nancy, Karlawish, Jason, Karydas, Anna, Kaye, Jeffrey A., Kim, Ronald, Koo, Edward H., Kowall, Neil W., Lah, James J., Levey, Allan I., Lieberman, Andrew, Lopez, Oscar L., Mack, Wendy J., Markesbery, William, Marson, Daniel C., Martiniuk, Frank, Masliah, Eliezer, McKee, Ann C., Mesulam, Marsel, Miller, Joshua W., Miller, Bruce L., Miller, Carol A., Parisi, Joseph E., Perl, Daniel P., Peskind, Elaine, Petersen, Ronald C., Poon, Wayne, Quinn, Joseph F., Raskind, Murray, Reisberg, Barry, Ringman, John M., Roberson, Erik D., Rosenberg, Roger N., Sano, Mary, Schneider, Julie A., Schneider, Lon S., Seeley, William, Shelanski, Michael L., Smith, Charles D., Spina, Salvatore, Stern, Robert A., Tanzi, Rudolph E., Trojanowski, John Q., Troncoso, Juan C., Van Deerlin, Vivianna M., Vinters, Harry V., Vonsattel, Jean Paul, Weintraub, Sandra, Welsh-Bohmer, Kathleen A., Woltjer, Randall L., Younkin, Steven G., Cantwell, Laura B., Dombroski, Beth A., Saykin, Andrew J., Reiman, Eric M., Bennett, David A., Morris, John C., Lunetta, Kathryn L., Martin, Eden R., Montine, Thomas J., Goate, Alison M., Blacker, Deborah, Tsuang, Debby W., Beekly, Duane, Cupples, L. Adrienne, Hakonarson, Hakon, Kukull, Walter, Foroud, Tatiana M., Haines, Jonathan, Mayeux, Richard, Farrer, Lindsay A., Pericak-Vance, Margaret A., and Schellenberg, Gerard D.
- Published
- 2010
- Full Text
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9. SNCA variant associated with Parkinson disease and plasma alpha-synuclein level.
- Author
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Mata IF, Shi M, Agarwal P, Chung KA, Edwards KL, Factor SA, Galasko DR, Ginghina C, Griffith A, Higgins DS, Kay DM, Kim H, Leverenz JB, Quinn JF, Roberts JW, Samii A, Snapinn KW, Tsuang DW, Yearout D, Zhang J, Payami H, and Zabetian CP
- Subjects
- Alleles, Enzyme-Linked Immunosorbent Assay, Female, Genetic Association Studies, Genetic Heterogeneity, Genetic Linkage, Genetic Predisposition to Disease, Genotype, Haplotypes, Humans, Logistic Models, Male, Odds Ratio, Polymorphism, Single Nucleotide, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Parkinson Disease blood, Parkinson Disease genetics, Promoter Regions, Genetic, alpha-Synuclein blood, alpha-Synuclein genetics
- Abstract
Background: A functional repeat polymorphism in the SNCA promoter (REP1) conveys susceptibility for Parkinson disease (PD). There is also increasing evidence that single-nucleotide polymorphisms (SNPs) elsewhere in the gene are associated with PD risk., Objectives: To further explore the association of common SNCA SNPs with PD susceptibility, to determine whether evidence of allelic heterogeneity exists, and to examine the correlation between PD-associated variants and plasma α-synuclein levels., Design: Two-tiered analysis., Setting: Academic research., Patients: Patients and control subjects from the NeuroGenetics Research Consortium., Main Outcome Measures: We performed a 2-tiered analysis of 1956 patients with PD and 2112 controls from the NeuroGenetics Research Consortium using a comprehensive tag SNP approach. Previously published REP1 genotypes were also included. Plasma α-synuclein was assayed in 86 patients with PD and 78 controls using a highly sensitive Luminex assay., Results: Five of 15 SNPs genotyped were associated with PD under an additive model in tier 1 (α = .05). Of these, 4 were successfully replicated in tier 2. In the combined sample, the most significant marker was rs356219 (odds ratio, 1.41; 95% confidence interval, 1.28-1.55; P = 1.6 × 10(-12)), located approximately 9 kilobases downstream from the gene. A regression model containing rs356219 alone best fit the data. The linkage disequilibrium correlation coefficient between this SNP and REP1 was low (r(2) = 0.09). The risk-associated C allele of rs356219 was also correlated with higher transformed plasma α-synuclein levels in patients under an adjusted additive model (P = .005)., Conclusions: Our data suggest that 1 or more unidentified functional SNCA variants modify risk for PD and that the effect is larger than and independent of REP1. This variant(s), tagged by rs356219, might act by upregulating SNCA expression in a dose-dependent manner.
- Published
- 2010
- Full Text
- View/download PDF
10. Phase 2 safety trial targeting amyloid beta production with a gamma-secretase inhibitor in Alzheimer disease.
- Author
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Fleisher AS, Raman R, Siemers ER, Becerra L, Clark CM, Dean RA, Farlow MR, Galvin JE, Peskind ER, Quinn JF, Sherzai A, Sowell BB, Aisen PS, and Thal LJ
- Subjects
- Aged, Aged, 80 and over, Alanine administration & dosage, Alanine adverse effects, Alanine blood, Alzheimer Disease metabolism, Amnesia chemically induced, Amnesia enzymology, Amyloid Precursor Protein Secretases metabolism, Amyloid beta-Peptides biosynthesis, Amyloid beta-Peptides blood, Amyloid beta-Peptides cerebrospinal fluid, Azepines blood, Double-Blind Method, Female, Humans, Intestinal Obstruction chemically induced, Intestinal Obstruction enzymology, Longitudinal Studies, Male, Middle Aged, Alanine analogs & derivatives, Alzheimer Disease drug therapy, Alzheimer Disease enzymology, Amyloid Precursor Protein Secretases antagonists & inhibitors, Amyloid beta-Peptides antagonists & inhibitors, Azepines administration & dosage, Azepines adverse effects, Drug Delivery Systems methods, Protease Inhibitors pharmacology
- Abstract
Objective: To evaluate the safety, tolerability, and amyloid beta (Abeta) response to the gamma-secretase inhibitor LY450139 in Alzheimer disease., Design: Multicenter, randomized, double-blind, dose-escalation, placebo-controlled trial., Setting: Community-based clinical research centers. Patients Fifty-one individuals with mild to moderate Alzheimer disease were randomized to receive placebo (n=15) or LY450139 (100 mg [n=22] or 140 mg [n=14]), with 43 completing the treatment phase. Intervention The LY450139 groups received 60 mg/d for 2 weeks, then 100 mg/d for 6 weeks, and then either 100 or 140 mg/d for 6 additional weeks., Main Outcome Measures: Primary outcome measures were adverse events, plasma and cerebrospinal fluid Abeta levels, vital signs, electrocardiographic data, and laboratory safety test results. Secondary outcome measures included the Alzheimer's Disease Assessment Scale cognitive subscale and the Alzheimer's Disease Cooperative Study Activities of Daily Living Scale., Results: Group differences were seen in skin and subcutaneous tissue concerns (P=.05), including 3 possible drug rashes and 3 reports of hair color change in the treatment groups. There were 3 adverse event-related discontinuations, including 1 transient bowel obstruction. The plasma Abeta(40) concentration was reduced by 58.2% for the 100-mg group and 64.6% for the 140-mg group (P<.001). No significant reduction was seen in cerebrospinal fluid Abeta levels. No group differences were seen in cognitive or functional measures., Conclusions: LY450139 was generally well tolerated at doses of up to 140 mg/d for 14 weeks, with several findings indicating the need for close clinical monitoring in future studies. Decreases in plasma Abeta concentrations were consistent with inhibition of gamma-secretase. Trial Registration clinicaltrials.gov Identifier: NCT00244322.
- Published
- 2008
- Full Text
- View/download PDF
11. Age and apolipoprotein E*4 allele effects on cerebrospinal fluid beta-amyloid 42 in adults with normal cognition.
- Author
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Peskind ER, Li G, Shofer J, Quinn JF, Kaye JA, Clark CM, Farlow MR, DeCarli C, Raskind MA, Schellenberg GD, Lee VM, and Galasko DR
- Subjects
- Adult, Aged, Aged, 80 and over, Alleles, Apolipoprotein E4, Biomarkers cerebrospinal fluid, Brain physiology, Female, Genotype, Humans, Male, Middle Aged, Aging cerebrospinal fluid, Amyloid beta-Peptides cerebrospinal fluid, Apolipoproteins E genetics, Cognition physiology, Peptide Fragments cerebrospinal fluid
- Abstract
Background: Decreased cerebrospinal fluid (CSF) beta-amyloid 42 (A beta 42) concentration, but not A beta 40 concentration, is a biomarker for Alzheimer disease. This A beta 42 concentration decrease in CSF likely reflects precipitation of A beta 42 in amyloid plaques in brain parenchyma. This pathogenic plaque deposition begins years before the clinical expression of dementia in Alzheimer disease. Normal aging and the presence of the apolipoprotein E (APOE*4) allele are the most important known risk factors for Alzheimer disease., Objective: To estimate the interactive effects of normal aging and presence of the APOE*4 allele on CSF A beta 42 concentration in adults with normal cognition across the life span., Design: The CSF was collected in the morning after an overnight fast using Sprotte 24-g atraumatic spinal needles. The CSF A beta 42 and A beta 40 concentrations were measured in the 10th milliliter of CSF collected by sandwich enzyme-linked immunosorbent assay. The APOE genotype was determined by a restriction digest method. Subjects One hundred eighty-four community volunteers with normal cognition aged 21 to 88 years., Results: The CSF A beta 42, but not the A beta 40, concentration decreased significantly with age. There was a sharp decrease in CSF A beta 42 concentration beginning in the sixth decade in subjects with the APOE*4 allele. This age-associated decrease in CSF A beta 42 concentration was significantly and substantially greater in subjects with the APOE*4 allele compared with those without the APOE*4 allele., Conclusion: These CSF A beta 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic A beta 42 brain deposition starting in later middle age in persons with normal cognition.
- Published
- 2006
- Full Text
- View/download PDF
12. Cerebrospinal fluid tau and beta-amyloid: how well do these biomarkers reflect autopsy-confirmed dementia diagnoses?
- Author
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Clark CM, Xie S, Chittams J, Ewbank D, Peskind E, Galasko D, Morris JC, McKeel DW Jr, Farlow M, Weitlauf SL, Quinn J, Kaye J, Knopman D, Arai H, Doody RS, DeCarli C, Leight S, Lee VM, and Trojanowski JQ
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- Adult, Aged, Aged, 80 and over, Alzheimer Disease cerebrospinal fluid, Area Under Curve, Biomarkers cerebrospinal fluid, Case-Control Studies, Cohort Studies, Humans, Lewy Body Disease cerebrospinal fluid, Middle Aged, Prospective Studies, ROC Curve, Amyloid beta-Peptides cerebrospinal fluid, Dementia cerebrospinal fluid, Dementia diagnosis, tau Proteins cerebrospinal fluid
- Abstract
Background: Tau and beta-amyloid (Abeta) are proposed diagnostic biomarkers for Alzheimer disease (AD). Previous studies report their relationship to clinical diagnoses of AD and other dementias. To understand their value as predictors of disease-specific pathology, levels determined during life must be correlated with definitive diagnoses in mixed dementia groups and cognitively normal subjects., Objectives: To correlate antemortem cerebrospinal fluid (CSF) tau and Abeta levels with definitive dementia diagnosis in a diverse group of patients; to calculate statistics for CSF tau and Abeta., Design: Prospective study., Setting: Ten clinics experienced in the diagnosis of neurodegenerative dementias. Patients One hundred six patients with dementia and 4 cognitively normal subjects with a definitive diagnosis, and 69 clinically diagnosed cognitively normal subjects., Main Outcome Measures: Correlation of CSF tau and Abeta with final diagnosis., Results: Mean tau level was 612 pg/mL for the 74 patients with AD, 272 pg/mL for 10 patients with frontal dementia, 282 pg/mL for 3 patients with dementia with Lewy bodies, and 140 pg/mL for 73 cognitively normal control subjects. Tau was less than 334 pg/mL for 20 patients with AD. Abeta42 was reduced in patients with AD (61 fmol/mL) compared with patients with frontal dementia (133 fmol/mL) and control subjects (109 fmol/mL), but not compared with patients with dementia with Lewy bodies (14 fmol/mL) or prion disease (60 fmol/mL)., Conclusions: Elevated CSF tau levels are associated with AD pathology and can help discriminate AD from other dementing disorders. However, some patients with AD have a level less than the mean +/- 2 SDs of the cognitively normal cohort.
- Published
- 2003
- Full Text
- View/download PDF
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