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1. Assessment of the genetic variance of late-onset Alzheimer's disease

Author

Perry G. Ridge, Kaitlyn B. Hoyt, Kevin Boehme, Shubhabrata Mukherjee, Paul K. Crane, Jonathan L. Haines, Richard Mayeux, Lindsay A. Farrer, Margaret A. Pericak-Vance, Gerard D. Schellenberg, John S.K. Kauwe, Perrie M. Adams, Marilyn S. Albert, Roger L. Albin, Liana G. Apostolova, Steven E. Arnold, Sanjay Asthana, Craig S. Atwood, Clinton T. Baldwin, Robert C. Barber, Michael M. Barmada, Lisa L. Barnes, Sandra Barral, Thomas G. Beach, James T. Becker, Gary W. Beecham, Duane Beekly, David A. Bennett, Eileen H. Bigio, Thomas D. Bird, Deborah Blacker, Bradley F. Boeve, James D. Bowen, Adam Boxer, James R. Burke, Jeffrey M. Burns, Joseph D. Buxbaum, Nigel J. Cairns, Laura B. Cantwell, Chuanhai Cao, Chris S. Carlson, Cynthia M. Carlsson, Regina M. Carney, Minerva M. Carrasquillo, Steven L. Carroll, Helena C. Chui, David G. Clark, Jason Corneveaux, David H. Cribbs, Elizabeth A. Crocco, Carlos Cruchaga, Philip L. De Jager, Charles DeCarli, F. Yesim Demirci, Malcolm Dick, Dennis W. Dickson, Rachelle S. Doody, Ranjan Duara, Nilufer Ertekin-Taner, Denis A. Evans, Kelley M. Faber, Thomas J. Fairchild, Kenneth B. Fallon, David W. Fardo, Martin R. Farlow, Steven Ferris, Tatiana M. Foroud, Matthew P. Frosch, Douglas R. Galasko, Marla Gearing, Daniel H. Geschwind, Bernardino Ghetti, John R. Gilbert, Alison M. Goate, Neill R. Graff-Radford, Robert C. Green, John H. Growdon, Hakon Hakonarson, Ronald L. Hamilton, Kara L. Hamilton-Nelson, John Hardy, Lindy E. Harrell, Lawrence S. Honig, Ryan M. Huebinger, Matthew J. Huentelman, Christine M. Hulette, Bradley T. Hyman, Gail P. Jarvik, Gregory A. Jicha, Lee-Way Jin, Gyungah Jun, M. Ilyas Kamboh, Anna Karydas, Mindy J. Katz, Jeffrey A. Kaye, Ronald Kim, Neil W. Kowall, Joel H. Kramer, Walter A. Kukull, Brian W. Kunkle, Frank M. LaFerla, James J. Lah, Eric B. Larson, James B. Leverenz, Allan I. Levey, Ge Li, Andrew P. Lieberman, Chiao-Feng Lin, Richard B. Lipton, Oscar L. Lopez, Kathryn L. Lunetta, Constantine G. Lyketsos, Wendy J. Mack, Daniel C. Marson, Eden R. Martin, Frank Martiniuk, Deborah C. Mash, Eliezer Masliah, Wayne C. McCormick, Susan M. McCurry, Andrew N. McDavid, Ann C. McKee, Marsel Mesulam, Bruce L. Miller, Carol A. Miller, Joshua W. Miller, Thomas J. Montine, John C. Morris, Jill R. Murrell, Amanda J. Myers, Adam C. Naj, Sid O'Bryant, John M. Olichney, Vernon S. Pankratz, Joseph E. Parisi, Amanda Partch, Henry L. Paulson, William Perry, Elaine Peskind, Ronald C. Petersen, Aimee Pierce, Wayne W. Poon, Huntington Potter, Joseph F. Quinn, Ashok Raj, Murray Raskind, Eric M. Reiman, Barry Reisberg, Joan S. Reisch, Christiane Reitz, John M. Ringman, Erik D. Roberson, Ekaterina Rogaeva, Howard J. Rosen, Roger N. Rosenberg, Donald R. Royall, Mark A. Sager, Mary Sano, Andrew J. Saykin, Julie A. Schneider, Lon S. Schneider, William W. Seeley, Amanda G. Smith, Joshua A. Sonnen, Salvatore Spina, Peter St George-Hyslop, Robert A. Stern, Russell H. Swerdlow, Rudolph E. Tanzi, Tricia A. Thornton-Wells, John Q. Trojanowski, Juan C. Troncoso, Debby W. Tsuang, Otto Valladares, Vivianna M. Van Deerlin, Linda J. Van Eldik, Badri N. Vardarajan, Harry V. Vinters, Jean Paul Vonsattel, Li-San Wang, Sandra Weintraub, Kathleen A. Welsh-Bohmer, Jens R. Wendland, Kirk C. Wilhelmsen, Jennifer Williamson, Thomas S. Wingo, Ashley R. Winslow, Sarah Wishnek, Randall L. Woltjer, Clinton B. Wright, Chuang-Kuo Wu, Steven G. Younkin, Chang-En Yu, and Lei Yu

Subjects
0301 basic medicine, Male, Risk, Aging, Neuroscience(all), Clinical Neurology, Datasets as Topic, Genome-wide association study, Single-nucleotide polymorphism, Receptors, Cell Surface, Biology, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, Amyloid beta-Protein Precursor, 0302 clinical medicine, Alzheimer Disease, Genetic variation, medicine, Genetics, Humans, Allele, Receptors, Immunologic, Genetic variance, Aged, Aged, 80 and over, Membrane Glycoproteins, TREM2, General Neuroscience, Genetic disorder, Genetic Variation, Alzheimer's disease, Explained variation, medicine.disease, Genetic architecture, 3. Good health, Ageing, 030104 developmental biology, Female, Neurology (clinical), Geriatrics and Gerontology, Netrin Receptors, 030217 neurology & neurosurgery, Genome-Wide Association Study, Developmental Biology
Abstract

Alzheimer's disease (AD) is a complex genetic disorder with no effective treatments. More than 20 common markers have been identified, which are associated with AD. Recently, several rare variants have been identified in Amyloid Precursor Protein (APP), Triggering Receptor Expressed On Myeloid Cells 2 (TREM2) and Unc-5 Netrin Receptor C (UNC5C) that affect risk for AD. Despite the many successes, the genetic architecture of AD remains unsolved. We used Genome-wide Complex Trait Analysis to (1) estimate phenotypic variance explained by genetics; (2) calculate genetic variance explained by known AD single nucleotide polymorphisms (SNPs); and (3) identify the genomic locations of variation that explain the remaining unexplained genetic variance. In total, 53.24% of phenotypic variance is explained by genetics, but known AD SNPs only explain 30.62% of the genetic variance. Of the unexplained genetic variance, approximately 41% is explained by unknown SNPs in regions adjacent to known AD SNPs, and the remaining unexplained genetic variance outside these regions.

Published
2016
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2. Antioxidants for Alzheimer Disease

Author

Douglas R. Galasko, Elaine Peskind, Christopher M. Clark, Joseph F. Quinn, John M. Ringman, Gregory A. Jicha, Carl Cotman, Barbara Cottrell, Thomas J. Montine, Ronald G. Thomas, Paul Aisen, and for the Alzheimer's Disease Cooperative Study

Subjects
Male, medicine.medical_specialty, Ubiquinone, medicine.medical_treatment, alpha-Tocopherol, tau Proteins, Ascorbic Acid, Placebo, Gastroenterology, Antioxidants, Article, law.invention, Double-Blind Method, Arts and Humanities (miscellaneous), Randomized controlled trial, Alzheimer Disease, Memantine, law, Internal medicine, Activities of Daily Living, medicine, Humans, Cognitive decline, Aged, Retrospective Studies, Aged, 80 and over, F2-Isoprostanes, Amyloid beta-Peptides, Thioctic Acid, business.industry, Vitamin E, Middle Aged, medicine.disease, Ascorbic acid, Peptide Fragments, Clinical trial, Endocrinology, Dietary Supplements, Biomarker (medicine), Female, Cholinesterase Inhibitors, Neurology (clinical), Alzheimer's disease, Mental Status Schedule, business, Biomarkers, Follow-Up Studies
Abstract

Objective To evaluate whether antioxidant supplements presumed to target specific cellular compartments affected cerebrospinal fluid (CSF) biomarkers. Design Double-blind, placebo-controlled clinical trial. Setting Academic medical centers. Participants Subjects with mild to moderate Alzheimer disease. Intervention Random assignment to treatment for 16 weeks with 800 IU/d of vitamin E (α-tocopherol) plus 500 mg/d of vitamin C plus 900 mg/d of α-lipoic acid (E/C/ALA); 400 mg of coenzyme Q 3 times/d; or placebo. Main Outcome Measures Changes from baseline to 16 weeks in CSF biomarkers related to Alzheimer disease and oxidative stress, cognition (Mini-Mental State Examination), and function (Alzheimer's Disease Cooperative Study Activities of Daily Living Scale). Results Seventy-eight subjects were randomized; 66 provided serial CSF specimens adequate for biochemical analyses. Study drugs were well tolerated, but accelerated decline in Mini-Mental State Examination scores occurred in the E/C/ALA group, a potential safety concern. Changes in CSF Aβ42, tau, and P-tau 181 levels did not differ between the 3 groups. Cerebrospinal fluid F2-isoprostane levels, an oxidative stress biomarker, decreased on average by 19% from baseline to week 16 in the E/C/ALA group but were unchanged in the other groups. Conclusions Antioxidants did not influence CSF biomarkers related to amyloid or tau pathology. Lowering of CSF F2-isoprostane levels in the E/C/ALA group suggests reduction of oxidative stress in the brain. However, this treatment raised the caution of faster cognitive decline, which would need careful assessment if longer-term clinical trials are conducted. Trial Registration clinicaltrials.gov Identifier: NCT00117403

Published
2012

3. Novel late-onset Alzheimer disease loci variants associate with brain gene expression

Author

Mariet, Allen, Fanggeng, Zou, High Seng, Chai, Curtis S, Younkin, Julia, Crook, V Shane, Pankratz, Minerva M, Carrasquillo, Christopher N, Rowley, Asha A, Nair, Sumit, Middha, Sooraj, Maharjan, Thuy, Nguyen, Li, Ma, Kimberly G, Malphrus, Ryan, Palusak, Sarah, Lincoln, Gina, Bisceglio, Constantin, Georgescu, Debra, Schultz, Fariborz, Rakhshan, Christopher P, Kolbert, Jin, Jen, Jonathan L, Haines, Richard, Mayeux, Margaret A, Pericak-Vance, Lindsay A, Farrer, Gerard D, Schellenberg, Ronald C, Petersen, Neill R, Graff-Radford, Dennis W, Dickson, Steven G, Younkin, Nilüfer, Ertekin-Taner, Liana G, Apostolova, Steven E, Arnold, Clinton T, Baldwin, Robert, Barber, Michael M, Barmada, Thomas, Beach, Gary W, Beecham, Duane, Beekly, David A, Bennett, Eileen H, Bigio, Thomas D, Bird, Deborah, Blacker, Bradley F, Boeve, James D, Bowen, Adam, Boxer, James R, Burke, Jacqueline, Buros, Joseph D, Buxbaum, Nigel J, Cairns, Laura B, Cantwell, Chuanhai, Cao, Chris S, Carlson, Regina M, Carney, Steven L, Carroll, Helena C, Chui, David G, Clark, Jason, Corneveaux, Carl W, Cotman, Paul K, Crane, Carlos, Cruchaga, Jeffrey L, Cummings, Philip L, De Jager, Charles, DeCarli, Steven T, DeKosky, F Yesim, Demirci, Ramon, Diaz-Arrastia, Malcolm, Dick, Beth A, Dombroski, Ranjan, Duara, William D, Ellis, Denis, Evans, Kelley M, Faber, Kenneth B, Fallon, Martin R, Farlow, Steven, Ferris, Tatiana M, Foroud, Matthew, Frosch, Douglas R, Galasko, Paul J, Gallins, Mary, Ganguli, Marla, Gearing, Daniel H, Geschwind, Bernardino, Ghetti, John R, Gilbert, Sid, Gilman, Bruno, Giordani, Jonathan D, Glass, Alison M, Goate, Robert C, Green, John H, Growdon, Hakon, Hakonarson, Ronald L, Hamilton, John, Hardy, Lindy E, Harrell, Elizabeth, Head, Lawrence S, Honig, Matthew J, Huentelman, Christine M, Hulette, Bradley T, Hyman, Gail P, Jarvik, Gregory A, Jicha, Lee-Way, Jin, Gyungah, Jun, M Ilyas, Kamboh, Jason, Karlawish, Anna, Karydas, John S K, Kauwe, Jeffrey A, Kaye, Nancy, Kennedy, Ronald, Kim, Edward H, Koo, Neil W, Kowall, Patricia, Kramer, Walter A, Kukull, James J, Lah, Eric B, Larson, Allan I, Levey, Andrew P, Lieberman, Oscar L, Lopez, Kathryn L, Lunetta, Wendy J, Mack, Daniel C, Marson, Eden R, Martin, Frank, Martiniuk, Deborah C, Mash, Eliezer, Masliah, Wayne C, McCormick, Susan M, McCurry, Andrew N, McDavid, Ann C, McKee, Marsel, Mesulam, Bruce L, Miller, Carol A, Miller, Joshua W, Miller, Thomas J, Montine, John C, Morris, Amanda J, Myers, Adam C, Naj, Petra, Nowotny, Joseph E, Parisi, Daniel P, Perl, Elaine, Peskind, Wayne W, Poon, Huntington, Potter, Joseph F, Quinn, Ashok, Raj, Ruchita A, Rajbhandary, Murray, Raskind, Eric M, Reiman, Barry, Reisberg, Christiane, Reitz, John M, Ringman, Erik D, Roberson, Ekaterina, Rogaeva, Roger N, Rosenberg, Mary, Sano, Andrew J, Saykin, Julie A, Schneider, Lon S, Schneider, William, Seeley, Michael L, Shelanski, Michael A, Slifer, Charles D, Smith, Joshua A, Sonnen, Salvatore, Spina, Peter, St George-Hyslop, Robert A, Stern, Rudolph E, Tanzi, John Q, Trojanowski, Juan C, Troncoso, Debby W, Tsuang, Vivianna M, Van Deerlin, Badri Narayan, Vardarajan, Harry V, Vinters, Jean Paul, Vonsattel, Li-San, Wang, Sandra, Weintraub, Kathleen A, Welsh-Bohmer, Jennifer, Williamson, and Randall L, Woltjer

Subjects
Male, Candidate gene, Genotype, Apolipoprotein E4, Gene Dosage, Gene Expression, Single-nucleotide polymorphism, Genome-wide association study, Locus (genetics), Biology, Gene dosage, Polymorphism, Single Nucleotide, PICALM, Alzheimer Disease, Risk Factors, Humans, Genetic Predisposition to Disease, Alleles, Genetic association, Aged, Temporal cortex, Genetics, Brain Chemistry, Temporal Lobe, Linear Models, RNA, Female, Neurology (clinical), Autopsy
Abstract

Objective: Recent genome-wide association studies (GWAS) of late-onset Alzheimer disease (LOAD) identified 9 novel risk loci. Discovery of functional variants within genes at these loci is required to confirm their role in Alzheimer disease (AD). Single nucleotide polymorphisms that influence gene expression (eSNPs) constitute an important class of functional variants. We therefore investigated the influence of the novel LOAD risk loci on human brain gene expression. Methods: We measured gene expression levels in the cerebellum and temporal cortex of autopsied AD subjects and those with other brain pathologies (∼400 total subjects). To determine whether any of the novel LOAD risk variants are eSNPs, we tested their cis -association with expression of 6 nearby LOAD candidate genes detectable in human brain ( ABCA7, BIN1, CLU, MS4A4A, MS4A6A, PICALM ) and an additional 13 genes ±100 kb of these SNPs. To identify additional eSNPs that influence brain gene expression levels of the novel candidate LOAD genes, we identified SNPs ±100 kb of their location and tested for cis -associations. Results: CLU rs11136000 ( p = 7.81 × 10 −4 ) and MS4A4A rs2304933/rs2304935 ( p = 1.48 × 10 −4 –1.86 × 10 −4 ) significantly influence temporal cortex expression levels of these genes. The LOAD-protective CLU and risky MS4A4A locus alleles associate with higher brain levels of these genes. There are other cis -variants that significantly influence brain expression of CLU and ABCA7 ( p = 4.01 × 10 −5 –9.09 × 10 −9 ), some of which also associate with AD risk ( p = 2.64 × 10 −2 –6.25 × 10 −5 ). Conclusions: CLU and MS4A4A eSNPs may at least partly explain the LOAD risk association at these loci. CLU and ABCA7 may harbor additional strong eSNPs. These results have implications in the search for functional variants at the novel LOAD risk loci.

Published
2012

4. Age-varying association between blood pressure and risk of dementia in those aged 65 and older: a community-based prospective cohort study

Author

Ge, Li, Isaac C, Rhew, Jane B, Shofer, Walter A, Kukull, John C S, Breitner, Elaine, Peskind, James D, Bowen, Wayne, McCormick, Linda, Teri, Paul K, Crane, and Eric B, Larson

Subjects
Aged, 80 and over, Male, Risk Factors, Hypertension, Age Factors, Humans, Blood Pressure, Dementia, Female, Prospective Studies, Aged
Abstract

To assess variation in the association between blood pressure (BP) and risk for dementia across a spectrum of older ages and to examine BP changes before dementia onset.Prospective cohort study.A large health maintenance organization in Seattle, Washington.A cohort of 2,356 members of a large health maintenance organization aged 65 and older who were initially without dementia.Dementia diagnosis was assessed biennially, and systolic (SBP) and diastolic BP (DBP) were measured at baseline and at four follow-up assessments. Cox proportional hazards models were used to estimate hazard ratios (HRs) for dementia and Alzheimer's disease (AD) associated with baseline BP in different age groups.Within the youngest age group (65-74 at enrollment) a greater risk for dementia was found in participants with high SBP (or = 160 mmHg) (hazard ratio (HR) = 1.60, 95% confidence interval (CI) = 1.01-2.55) or borderline-high DBP (80-89 mmHg) (HR = 1.59, 95% CI = 1.07-2.35) than for those with normal BP (SBP140 mmHg and DBP80 mmHg). The dementia risk associated with SBP declined with increasing age (SBP-by-age interaction, P=.01). SBP declined similarly with aging in subjects who developed dementia and those who did not. Thus, in this sample, the association between SBP and dementia risk was not dependent on when BP was measured in relation to onset of dementia.High SBP was associated with greater risk of dementia in the young elderly (75) but not in older subjects. Adequate control of hypertension in early old age may reduce the risk for dementia.

Published
2007

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