What have we learned recently from transgenic mouse models about neurodegeneration? The most promising discoveries of this millennium

被引:5
作者
Kreiner, Grzegorz [1 ]
机构
[1] Polish Acad Sci, Inst Pharmacol, Dept Brain Biochem, Krakow, Poland
关键词
Neurodegeneration; Neurodegenerative diseases; Mice; Rats; Genetic models; Transgenic animals; AMYLOID-PRECURSOR-PROTEIN; ANTI-TAU ANTIBODIES; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; MUTANT HUNTINGTIN; ANIMAL-MODELS; DOPAMINERGIC-NEURONS; SUBSTANTIA-NIGRA; A-BETA; MEDIATED OVEREXPRESSION;
D O I
10.1016/j.pharep.2018.09.006
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Neurodegenerative diseases are currently a major challenge in elderly care due to demographic changes and dramatic increases in the aging population worldwide. This review is focused on the most promising research discovering ways to attenuate neural loss or enhance neuroprotection and unraveling the basis of neurodegeneration using transgenic mouse models. With the recent introduction of the powerful and relatively simple gene-editing tool CRISPR-Cas9, we have entered a new era in genetic engineering that will certainly lead to a variety of new transgenic models in the near future. The aim of this review is to note the most interesting avenues addressing unmet needs in neurodegenerative disease research that could provide promising targets for both the development of new models and the study of existing ones. (c) 2018 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1105 / 1115
页数:11
相关论文
共 166 条
[11]  
Barrera-Ocampo A, 2016, COLOMB MEDICA, V47, P203
[12]   Cancer risk in association with Parkinson disease: A population-based study [J].
Becker, Claudia ;
Brobert, Gunnar P. ;
Johansson, Saga ;
Jick, Susan S. ;
Meier, Christoph R. .
PARKINSONISM & RELATED DISORDERS, 2010, 16 (03) :186-190
[13]   Animal Models of Parkinson's Disease: Limits and Relevance to Neuroprotection Studies [J].
Bezard, Erwan ;
Yue, Zhenyu ;
Kirik, Deniz ;
Spillantini, Maria Grazia .
MOVEMENT DISORDERS, 2013, 28 (01) :61-70
[14]   MicroRNA pathways modulate polyglutamine-induced neurodegeneration [J].
Bilen, Julide ;
Liu, Nan ;
Burnett, Barrington G. ;
Pittman, Randall N. ;
Bonini, Nancy M. .
MOLECULAR CELL, 2006, 24 (01) :157-163
[15]   Recent findings on the physiological function of DJ-1: Beyond Parkinson's disease [J].
Biosa, Alice ;
Sandrelli, Federica ;
Beltramini, Mariano ;
Greggio, Elisa ;
Bubacco, Luigi ;
Bisaglia, Marco .
NEUROBIOLOGY OF DISEASE, 2017, 108 :65-72
[16]   Parkinson's disease: animal models and dopaminergic cell vulnerability [J].
Blesa, Javier ;
Przedborski, Serge .
FRONTIERS IN NEUROANATOMY, 2014, 8
[17]   The multifunctional nucleolus [J].
Boisvert, Francois-Michel ;
van Koningsbruggen, Silvana ;
Navascues, Joaquin ;
Lamond, Angus I. .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2007, 8 (07) :574-585
[18]   Calcium dysregulation in Alzheimer's disease [J].
Bojarski, Lukasz ;
Herms, Jochen ;
Kuznicki, Jacek .
NEUROCHEMISTRY INTERNATIONAL, 2008, 52 (4-5) :621-633
[19]   Induction of tau pathology by intracerebral infusion of amyloid-β-containing brain extract and by amyloid-β deposition in APP x tau transgenic mice [J].
Bolmont, Tristan ;
Clavaguera, Florence ;
Meyer-Luehmann, Melanie ;
Herzig, Martin C. ;
Radde, Rebecca ;
Staufenbiel, Matthias ;
Lewis, Jada ;
Hutton, Mike ;
Tolnay, Markus ;
Jucker, Mathias .
AMERICAN JOURNAL OF PATHOLOGY, 2007, 171 (06) :2012-2020
[20]   Familial Alzheimer's disease-linked presenilin 1 variants elevate A beta 1-42/1-40 ratio in vitro and in vivo [J].
Borchelt, DR ;
Thinakaran, G ;
Eckman, CB ;
Lee, MK ;
Davenport, F ;
Ratovitsky, T ;
Prada, CM ;
Kim, G ;
Seekins, S ;
Yager, D ;
Slunt, HH ;
Wang, R ;
Seeger, M ;
Levey, AI ;
Gandy, SE ;
Copeland, NG ;
Jenkins, NA ;
Price, DL ;
Younkin, SG .
NEURON, 1996, 17 (05) :1005-1013