Model organism development and evaluation for late-onset Alzheimer's disease: MODEL-AD.
Model organism development and evaluation for late-onset Alzheimer's disease: MODEL-AD.
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DOI：
10.1002/trc2.12110
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Consortium
中科院分区：
文献类型：
--
作者：
Oblak AL;Forner S;Territo PR;Sasner M;Carter GW;Howell GR;Sukoff-Rizzo SJ;Logsdon BA;Mangravite LM;Mortazavi A;Baglietto-Vargas D;Green KN;MacGregor GR;Wood MA;Tenner AJ;LaFerla FM;Lamb BT;and The MODEL‐AD;Consortium
Alzheimer's disease (AD) is a major cause of dementia, disability, and death in the elderly. Despite recent advances in our understanding of the basic biological mechanisms underlying AD, we do not know how to prevent it, nor do we have an approved disease‐modifying intervention. Both are essential to slow or stop the growth in dementia prevalence. While our current animal models of AD have provided novel insights into AD disease mechanisms, thus far, they have not been successfully used to predict the effectiveness of therapies that have moved into AD clinical trials. The Model Organism Development and Evaluation for Late‐onset Alzheimer's Disease (MODEL‐AD; www.model-ad.org) Consortium was established to maximize human datasets to identify putative variants, genes, and biomarkers for AD; to generate, characterize, and validate the next generation of mouse models of AD; and to develop a preclinical testing pipeline. MODEL‐AD is a collaboration among Indiana University (IU); The Jackson Laboratory (JAX); University of Pittsburgh School of Medicine (Pitt); Sage BioNetworks (Sage); and the University of California, Irvine (UCI) that will generate new AD modeling processes and pipelines, data resources, research results, standardized protocols, and models that will be shared through JAX's and Sage's proven dissemination pipelines with the National Institute on Aging–supported AD Centers, academic and medical research centers, research institutions, and the pharmaceutical industry worldwide.
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DOI：
10.1056/nejmoa1211851
发表时间：
2013-01-10
期刊：
The New England journal of medicine
影响因子：
--
作者：
Guerreiro R;Wojtas A;Bras J;Carrasquillo M;Rogaeva E;Majounie E;Cruchaga C;Sassi C;Kauwe JS;Younkin S;Hazrati L;Collinge J;Pocock J;Lashley T;Williams J;Lambert JC;Amouyel P;Goate A;Rademakers R;Morgan K;Powell J;St George-Hyslop P;Singleton A;Hardy J;Alzheimer Genetic Analysis Group
通讯作者：
Alzheimer Genetic Analysis Group
影响因子：
4.8
作者：
Moechars, D;Dewachter, I;Van Leuven, F
通讯作者：
Van Leuven, F
影响因子：
9.9
作者：
James, Bryan D.;Leurgans, Sue E.;Bennett, David A.
通讯作者：
Bennett, David A.
影响因子：
5.3
作者：
Born, Heather A.;Kim, Ji-Yoen;Jankowsky, Joanna L.
通讯作者：
Jankowsky, Joanna L.
影响因子：
--
作者：
Aizenstein, Howard Jay;Nebes, Robert D.;Saxton, Judith A.;Price, Julie C.;Mathis, Chester A.;Tsopelas, Nicholas D.;Ziolko, Scott K.;James, Jeffrey A.;Snitz, Beth E.;Houck, Patricia R.;Bi, Wenzhu;Cohen, Ann D.;Lopresti, Brian J.;DeKosky, Steven T.;Halligan, Edythe M.;Klunk, William E.
通讯作者：
Klunk, William E.