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Neuroscience. Rudolph E. Tanzi 6, Amanda Venti 6, Sandra M. Payton 6, Tony Giordano 2, Seiichi Nagano 6, Catherine M. Cahill 4, Robert Moir 6, Debomoy K. Lahiri 5, Nigel Greig 3, Satinder Singh Sarang 1 & Steven R. Gullans 1 Journal of Molecular Neuroscience volume 19, pages 77 – 82 (2002)Cite this article. Google Scholar. Add co-authors Co-authors. The ones marked * may be different from the article in the profile. Thus far, in AD this has been achieved for four genes (APP, PSEN1, PSEN2, APOE), but only variation in the latter also plays a significant role in the most common late-onset form of the disorder (see below). PubMed; Google Scholar Patricia I. Bader. Google Scholar. Follow this author. This metalloprotease has been shown to degrade monomeric Aβ before it can aggregate into oligomeric forms and, ultimately, into β-amyloid plaques (49). et al. While in 2003 two studies reported significant evidence of association with the latter two genes (38,39), two other studies did not confirm these findings (40,41). While in some cases this could be due to factors that are disease-specific (e.g. Merged citations. and Contopoulos-Ioannidis, D.G. Rudolph Tanzi: Evolution of the Brain and Consciousness . Read this book using Google Play Books app on your PC, android, iOS devices. Google Scholar. Furthermore, in all of these studies the observed effect was most pronounced in carriers of the APOE ε4-allele, yielding significantly elevated odds ratios ranging from 2 to 7. While the former criterion is fulfilled for the vast majority of AD candidate genes investigated thus far, the latter condition has been more elusive. New articles related to this author's research . 2 and autism, Treatment with a copper-zinc chelator markedly and rapidly inhibits β-amyloid accumulation in Alzheimer's disease transgenic mice, Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease, Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo, The Wilson disease gene is a copper transporting ATPase with homology to the Menkes disease gene, The genetic defect causing familial Alzheimer's disease maps on chromosome 21, Mapping autism risk loci using genetic linkage and chromosomal rearrangements, Protease inhibitor domain encoded by an amyloid protein precursor mRNA associated with Alzheimer's disease, The Aβ peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction, Dramatic aggregation of Alzheimer Aβ by Cu (II) is induced by conditions representing physiological acidosis, Systematic meta-analyses and field synopsis of genetic association studies in schizophrenia: the SzGene database. For instance, a recent simulation study predicted the existence of four to seven additional AD genes when searching for age of onset modifiers simulating a variety of different disease and inheritance models (3). Dr. Rudolph E. Tanzi Rudolph Tanzi (also Rudy Tanzi) is the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University, and Vice-Chair of Neurology, Director of the Genetics and Aging Research Unit, and Co-Director of the Henry and Allison McCance Center for Brain Health at Massachusetts General Hospital (MGH). (, Oxford University Press is a department of the University of Oxford. Dr. Rudolph Tanzi is a Professor of Neurology and holder of the Joseph P. and Rose F. Kennedy Endowed Chair in Neurology at Harvard University. Based on these data, we suggest that it may be prudent for investigators to pay closer attention to issues such as power, replicability and haplotype structure prior to initial publication. Upload PDF. (, Farris, W., Mansourian, S., Chang, Y., Lindsley, L., Eckman, E.A., Frosch, M.P., Eckman, C.B., Tanzi, R.E., Selkoe, D.J. To date, no less than 12 full-genome screens using linkage- or association-based methodologies have been published for AD, some using overlapping or identical samples, but each employing different sets of genetic markers and/or analytic strategies (8–19) (Table 1). Unless this is done, similar to the situation encountered for the variants tested in IDE (see above), no firm conclusions can be reached as to whether or not the exon 5 polymorphism in BACE is a genetic risk factor for AD in these samples. Google Scholar; 119. larger than anticipated genetic heterogeneity and/or very small effect sizes of individual risk alleles), a good proportion of these controversies are probably caused by methodological issues. PERHAPS: Paired-End short Reads-based HAPlotyping from next-generation Sequencing data. Add co-authors Co-authors. Rudy Tanzi : Aug 1, 2017 7:23 AM: Posted in group: Sadhu-Sanga Under the holy association of Spd. The ones marked * may be different from the article in the profile. Thus, of the three known APP-cleaving enzymes and associated proteins [α- (ADAM9,10 and 17), β- (BACE, BACE2) and γ-secretase (PSEN1, APH1A, NCSTN, PEN2)], most of which have already been tested for genetic association with AD phenotypes, BACE currently shows the most promise of being a genuine and relevant risk factor for late-onset AD. Google Scholar provides a simple way to broadly search for scholarly literature. Done. A recent study estimated that the minimal number of cases and controls sufficient to achieve ∼80% power at α=0.05 is usually far greater than 200 when the actual disease allele is not tested directly, even under the most favorable of circumstances (26). and Selkoe, D.J. Carica PDF. the probability that an observed significant association is indeed genuine and not only observed by chance (24–26). (, Scott, W.K., Hauser, E.R., Schmechel, D.E., Welsh-Bohmer, K.A., Small, G.W., Roses, A.D., Saunders, A.M., Gilbert, J.R., Vance, J.M., Haines, J.L. The only locus found to be associated by more than one group of investigators is located between 90 and 94 Mb and encompasses the genes TNFRSF6 (90 Mb) and IDE/KIFF11/HHEX (46–48). Merged citations. Lars Bertram, Rudolph E. Tanzi, Alzheimer's disease: one disorder, too many genes?, Human Molecular Genetics, Volume 13, Issue suppl_1, 1 April 2004, Pages R135–R141, https://doi.org/10.1093/hmg/ddh077. New citations to this author. PDF Restore Delete Forever. In addition to increasing the power of the analyses, this approach also reduces the number of statistical tests that need to be performed, which should lead to a further decrease of false-positive findings. While most positive results were largely contradictory, we identified three loci—on chromosomes 6p21, 10q24, 11q23—that yielded positive results in three or more independent studies, in addition to the well-established AD association with the gene encoding apolipoprotein E (APOE). Abstract. Add co-authors Co-authors. PDF Restore Delete Forever. Re: Rudolph Tanzi, Physics and qualia. (, Shi, J., Zhang, S., Tang, M., Liu, X., Li, T., Wang, Y., Han, H., Guo, Y., Hao, Y., Zheng, K. et al. Heal Your Wounds and Find Your True Self Archives – Spirit Bear Coaching. Add co-authors Co-authors. Most interestingly—and in contrast to all other putative AD associations discussed above—there appears to be a high degree of consistency with respect to the site and allelic nature underlying these findings: all positive studies, including the initial report by Nowotny and colleagues published in 2001 (62), observe over-representations of the G-allele of a synonymous SNP located at codon 262 (in exon 5) in AD cases as compared with healthy controls. , J.M., Goddard, K.A these studies were not considered, total... And qualia their, this `` Cited by '' count includes citations to the following in... ; Home ; Toggle navigation on the other hand, the accuracy of a clinical AD diagnosis near! Case sensitive e.g the lipophilic metal chelator DP-109 reduces amyloid pathology in brains of human beta-amyloid precursor protein mice! U.S. hospitals alone Jarvik, G.P association findings between candidate genes and AD, 2015 Apr 10, 2018.! 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