Atnaujinkite slapukų nuostatas

Animal Models for Neurodegenerative Disease [Kietas viršelis]

Edited by (Universidad Autonoma de Madrid, Spain), Edited by (Universidad Autonoma de Madrid, Spain), Edited by (Universidad Autonoma de Madrid, Spain)
  • Formatas: Hardback, 306 pages, aukštis x plotis: 234x156 mm, weight: 601 g, No
  • Serija: Drug Discovery Series Volume 6
  • Išleidimo metai: 24-May-2011
  • Leidėjas: Royal Society of Chemistry
  • ISBN-10: 1849731845
  • ISBN-13: 9781849731843
Kitos knygos pagal šią temą:
Animal Models for Neurodegenerative DiseaseDidesnis paveikslėlis
  • Formatas: Hardback, 306 pages, aukštis x plotis: 234x156 mm, weight: 601 g, No
  • Serija: Drug Discovery Series Volume 6
  • Išleidimo metai: 24-May-2011
  • Leidėjas: Royal Society of Chemistry
  • ISBN-10: 1849731845
  • ISBN-13: 9781849731843
Kitos knygos pagal šią temą:
Pastovi nuoroda: https://www.kriso.lt/db/9781849731843.html
In recent years, medical developments have resulted in an increase in human life expectancy. Some developed countries now have a larger population of individuals aged over 64 than those under 14. One consequence of the ageing population is a higher incidence of certain neurodegenerative disorders. In order to prevent these, we need to learn more about them. This book provides up-to-date information on the use of transgenic mouse models in the study of neurodegenerative disorders such as Alzheimer's and Huntington's disease. By reproducing some of the pathological aspects of the diseases, these studies could reveal the mechanism for their onset or development. Some of the transgenic mice can also be used as targets for testing new compounds with the potential to prevent or combat these disorders. The editors have extensive knowledge and experience in this field and the book is aimed at undergraduates, postgraduates and academics. The chapters cover disorders including: Alzheimer's disease, Parkinson's disease, Huntington's and other CAG diseases, amyotrophic lateral sclerosis (ALS), recessive ataxias, disease caused by prions, and ischemia.

Daugiau informacijos

1. Provides up-to-date information on the use of transgenic mouse models in the study of neurodegenerative disorders 2. suitable for undergraduates, postgraduates and academics 3. Edited by experts with extensive knowledge in the field
Chapter 1 The Contribution of Transgenic Models to the Understanding of Alzheimer's Disease Progression and Therapeutic Development
1(14)
Meredith A. Chabrier
Kara M. Neely
Nicholas A. Castello
Frank M. LaFerla
1.1 Introduction
1(1)
1.2 Aβ and Tau Biology
2(1)
1.3 Modelling Plaques and Tangles
3(1)
1.4 Mechanisms of Disease Progression
4(3)
1.4.1 Aβ and Tau
4(1)
1.4.2 Inflammation
5(1)
1.4.3 Risk Factors
6(1)
1.5 Therapeutic Development in Transgenic Models
7(2)
1.5.1 Aβ Immunotherapy
7(1)
1.5.2 HDAC Inhibitors
8(1)
1.5.3 M1 Agonists
9(1)
1.6 Concluding Remarks
9(6)
References
9(6)
Chapter 2 Animal Models of Amyloid/PS-1 Pathology
15(24)
Akihiko Takashima
2.1 β-Amyloid Generation
15(1)
2.2 APP Transgenic Mouse Models
16(8)
2.2.1 PDAPP Transgenic Mouse Model
16(1)
2.2.2 Tg2576 Transgenic Mouse Model
17(2)
2.2.3 APP23 Transgenic Mouse Model
19(1)
2.2.4 APP Dutch Transgenic Mouse Model
20(1)
2.2.5 CRND8 Transgenic Mouse Model
21(1)
2.2.6 J20 Transgenic Mouse Model
21(1)
2.2.7 APPSwDI/NOS2-/- Transgenic Mouse Model
22(1)
2.2.8 Adeno-associated Virus (AAV)-mediated Gene Transfer of BRI-Aβ
23(1)
2.2.9 Humanized Aβ Transgenic Mouse Models
23(1)
2.2.10 Amyloid Degradation
24(1)
2.3 Other Transgenic Mouse Models
24(3)
2.3.1 Physiological and Pathological Roles of PS-1
24(1)
2.3.2 PS-1 Transgenic Mouse Model
25(1)
2.3.3 3xTg Mouse Model
26(1)
2.4 hAPP Mouse Models and Treatment of AD
27(12)
References
28(11)
Chapter 3 The Ying and Yang of the Reelin Signalling Pathway in Alzheimer's Disease Pathology
39(13)
Eduardo Soriano
Daniela Rossi
Lluis Pujadas
3.1 The Extracellular Matrix Protein Reelin in the Developing and Adult Brain
39(1)
3.2 Generation of Conditional Transgenic Mice Overexpressing Reelin in the Adult Forebrain: A Tool to Dissect Reelin Functions in the Adult Brain
40(5)
3.3 Potential Role of Reelin in Alzheimer's Disease: A Unifying Hypothesis Linking Reelin to Amyloid Deposits, Tangles and Stress
45(3)
3.4 Conclusions
48(4)
Acknowledgements
48(1)
References
48(4)
Chapter 4 Transgenic Mice Overexpressing GSK-3β as Animal Models for Alzheimer's Disease
52(17)
Felix Hernandez
4.1 Introduction
52(1)
4.2 Glycogen Synthase Kinase-3
53(2)
4.3 Alzheimer's Disease and Glycogen Synthase Kinase-3
55(2)
4.4 Mouse Models Overexpressing Glycogen Synthase Kinase-3
57(3)
4.5 Animal Models with Reduced Glycogen Synthase Kinase-3 Activity
60(1)
4.6 GSK-3 Inhibition as a Therapy for Alzheimer's Disease
61(1)
4.7 Conclusions
62(7)
Acknowledgements
63(1)
References
63(6)
Chapter 5 Invertebrate and Vertebrate Models of Tauopathies
69(17)
Jurgen Gotz
Lars M. Ittner
Naeman N. Gotz
Hong Lam
Hannah R. Nicholas
5.1 Introduction
69(3)
5.2 Model Systems
72(14)
5.2.1 Wild-type Tau Transgenic Mice
72(1)
5.2.2 Mutant Tau Transgenic Mice
72(4)
5.2.3 Invertebrate and Non-rodent Models
76(2)
5.2.4 The Aβ---Tau Axis
78(1)
Acknowledgements
79(1)
References
79(7)
Chapter 6 Animal Models of Parkinson's Disease
86(27)
Hardy J. Rideout
Leonidas Stefanis
6.1 Introduction
86(1)
6.2 Genetic Models
87(10)
6.2.1 Animal Models Based on Manipulation of Alpha-synuclein
87(5)
6.2.2 LRRK2
92(4)
6.2.3 Models of Recessive Parkinson's Disease
96(1)
6.3 Toxin Models
97(5)
6.3.1 Mitochondrial Toxins
98(2)
6.3.2 6-Hydroxydopamine
100(1)
6.3.3 Proteasome Inhibition
101(1)
6.4 Other PD models
102(11)
References
103(10)
Chapter 7 Animal Models and the Pathogenesis of Parkinson's Disease
113(49)
Jose G. Castano
Teresa Iglesias
Justo G. de Yebenes
7.1 Introduction
113(3)
7.2 Genetics of Parkinson's Disease
116(8)
7.2.1 Alpha-Synuclein: PARK1/4
116(3)
7.2.2 DJ-1/PARK7
119(1)
7.2.3 PARKIN/PARK2 and PINK1/PARK6
120(2)
7.2.4 LRRK2/PARK8
122(1)
7.2.5 OMI/HTRA2/PARK13
123(1)
7.3 Environmental Factors in PD Pathology
124(4)
7.3.1 Toxins
124(3)
7.3.2 Inflammatory Response
127(1)
7.3.3 Viruses
128(1)
7.4 Protein Aggregation (Proteostasis) in PD
128(1)
7.5 Development and PD
129(4)
7.5.1 Human Model
130(1)
7.5.2 Animal Model
131(2)
7.6 Mitochondrial Dysfunction and PD
133(1)
7.6.1 Human Model
133(1)
7.6.2 Animal Model
134(1)
7.7 Learning from Models to Master a Complex Disease: Channels and Challenges
134(7)
7.8 Conclusions
141(21)
Acknowledgments
141(1)
References
142(20)
Chapter 8 Neuroprotection in Parkinson's Disease
162(15)
Alberto Pascual
Javier Villadiego
Maria Hidalgo-Figueroa
Simon Mendez-Ferrer
Raquel Gomez-Diaz
Juan Jose Toledo-Aral
Jose Lopez-Barneo
8.1 Neurotrophism and Neurotrophic Factors
162(1)
8.2 Neuroprotection of Mesencephalic Dopaminergic Neurons: Role of GDNF
163(5)
8.2.1 Biology of GDNF and Other Dopaminotrophic Factors
164(1)
8.2.2 Dopaminotrophic Factor-Mediated Neuronal Protection
165(3)
8.3 Genetic Models of NTF Depletion: Conditional GDNF Knock-out Mice
168(3)
8.4 Clinical Effects of GDNF
171(1)
8.5 Conclusions and Perspectives
171(6)
Acknowledgements
172(1)
References
172(5)
Chapter 9 Animal Models for ALS
177(37)
Ritsuko Fujii
Toru Takumi
9.1 Introduction
177(2)
9.2 Genetics of ALS
179(1)
9.2.1 Genes Related to Familial ALS
179(1)
9.2.2 Genes Related to Sporadic ALS
179(1)
9.3 SOD1 Mouse Model of ALS
180(2)
9.3.1 SOD1 Mutations
180(1)
9.3.2 SOD1 Mutant Transgenic Mice
181(1)
9.4 Genetic Modifiers of ALS Mouse Model
182(11)
9.4.1 Glutamate Excitotoxicity
182(2)
9.4.2 Mitochondrial Dysfunction and Apoptosis
184(1)
9.4.3 Effects of Non-neuronal Cell Activation in ALS
185(2)
9.4.4 Axonal Transport Blockade
187(3)
9.4.5 Depletion of Neurotrophic Factors
190(1)
9.4.6 Protein Misfolding and Aggregation
190(1)
9.4.7 Neurofilament Defects
191(1)
9.4.8 Inflammatory Cytokines
192(1)
9.5 Protein Degradation in ALS Transgenic Mouse Model
193(1)
9.6 SOD1 Transgenic Rat Model of ALS
193(1)
9.7 VAPB Transgenic Mouse
194(1)
9.8 Alsin Transgenic Mouse
195(2)
9.8.1 Alsin
195(1)
9.8.2 Alsin Knock-out Mice
196(1)
9.8.3 Phenotypes of Alsin Knock-out Mice
196(1)
9.9 Transgenic Mutant TDP-43 Rodent
197(3)
9.9.1 TDP-43 in ALS
197(2)
9.9.2 Mutant TDP-43 Transgenic Mice
199(1)
9.9.3 TDP-43 and FUS/TLS
199(1)
9.9.4 Mutant TDP-43 Transgenic Rats
200(1)
9.10 Conclusions
200(14)
Acknowledgements
201(1)
References
202(12)
Chapter 10 Animal Models for Huntington's Disease
214(16)
Zaira Ortega
Jose J. Lucas
10.1 Huntington's Disease
214(1)
10.2 Invertebrate Models of Huntington's Disease
215(1)
10.2.1 Caenorhabditis elegans
215(1)
10.2.2 Drosophila melanogaster
216(1)
10.3 Vertebrate Models of Huntington's Disease
216(14)
10.3.1 Mouse Models
216(7)
10.3.2 Sheep Models
223(1)
10.3.3 Primate Models
224(1)
References
225(5)
Chapter 11 Mouse Models of Prion Protein Related Diseases
230(21)
Maria Gasset
Adriano Aguzzi
11.1 Introduction
230(1)
11.2 Notes on PrP Biology
231(4)
11.2.1 Molecular and Structural Diversity of PrPC
231(2)
11.2.2 PrPC Conversion: Prions, Amyloids and Other Toxic Forms
233(2)
11.3 Phenotyping PrPC Function: Ablation and Overexpression
235(2)
11.3.1 PrPC Ablation: Hints from Losing PrPC Function
235(1)
11.3.2 PrPC Overexpression also Leads to Pathology
236(1)
11.3.3 Sensitivity to Prion Infection: Dose and Site of PrPC Expression
236(1)
11.4 Models for PrPC Function---Structure Relationship: Spontaneous Generation of Disease or Increased Sensitivity to Acquisition
237(3)
11.4.1 Chain Length, Motifs and Covalent Modifications
237(1)
11.4.2 Sorting Signals: Hydrophobic Regions and their Messages
238(1)
11.4.3 Posttranslational Covalent Modifications: Glycosylations and Disulfide Bond
239(1)
11.5 Inherited Disease and Structurally-based Mutations: Susceptibility to Misfolding and Sensitization to Prion Infection
240(11)
11.5.1 Genetic CJD and its Mouse Models: Non-transmissible Spontaneous Degeneration
240(2)
11.5.2 Genetic GSS and its Mouse Models: Dose-dependent Spontaneous Diseases with no Transmissibility
242(1)
11.5.3 FFI and its Mouse Models: Transmissible Spontaneous Disease with Undetectable PrPres
242(1)
11.5.4 Structural-designed Mutations for Spontaneous Disorder: Spontaneous Disease with Full Transmissibility and PrPres
243(1)
11.5.5 A Molecular Switch Defining Cross-species Barriers for Prion Infections
243(1)
Acknowledgements
244(1)
References
244(7)
Chapter 12 Mouse Models of Ischemia
251(23)
David C. Henshall
Roger P. Simon
12.1 Introduction
251(1)
12.2 Stroke: Incidence, Causes and Definitions
252(2)
12.2.1 Stroke: Terms and Conditions
252(2)
12.2.2 Transient vs. Permanent Ischemia
254(1)
12.3 Pathophysiology of Ischemic Brain Injury: Penumbra, Cell Death and Neuroprotection
254(2)
12.3.1 Cause of Tissue Injury in Ischemia
254(1)
12.3.2 Post-stroke Repair
255(1)
12.3.3 Neuroprotection and Translation
255(1)
12.4 Mouse Models of Ischemia
256(8)
12.4.1 General
256(1)
12.4.2 Tools of the Trade
257(1)
12.4.3 Surgical Occlusion of the Middle Cerebral Artery
258(1)
12.4.4 Intraluminal Filament Occlusion
258(1)
12.4.5 Thromboembolic Occlusion
259(1)
12.4.6 Photothrombotic
260(2)
12.4.7 Endothelin/vasoconstrictors
262(1)
12.4.8 Global Ischemia Models
262(2)
12.5 Problems and Pitfalls Specific to Mouse Models of Ischemia
264(1)
12.5.1 General Challenges for Modelling Stroke in Mice
264(1)
12.5.2 Inter-strain Differences in Intrinsic Vulnerability to Excitotoxicity
265(1)
12.6 Other Problems and Pitfalls of Mouse Models
265(1)
12.6.1 Stroke Size
265(1)
12.6.2 Lacunar Strokes
265(1)
12.6.3 Narrow Temporal Relationship Between Occlusion Duration and Infarction
266(1)
12.6.4 Animal Age, Co-morbidities and Other Variables
266(1)
12.7 Ischemic Tolerance in Mice
266(2)
12.8 Conclusions
268(6)
References
268(6)
Chapter 13 A Non-transgenic Rat Model of Sporadic Alzheimer's Disease
274(10)
Khalid Iqbal
Xiaochuan Wang
Julie Blanchard
Inge Grundke-Iqbal
13.1 Introduction
274(2)
13.2 A Mechanism of AD Involving Cleavage of SETα
276(1)
13.3 Generation of an AAV1-I2CTF Rat Model of AD
276(5)
13.4 Conclusions
281(3)
Acknowledgements
281(1)
References
281(3)
Subject Index 284
Jesus Avila is a Professor and former Director of the Centre of Molecular Biology in Madrid. Over the last thirty years, his work has focused on the cytoskeleton of the neuron. He is now investigating on the role of tau proteins in neurodegenerative disorders (tauopathies) such as Alzheimer's disease. Professor Avila is a member of several professional organizations including EMBO, the European Academy, and the Spanish Royal Academy of Sciences. He is also on the Editorial Board of a number of scholarly journals and has more than 300 publications to his name. Jose J. Lucas is Research Professor of the Spanish National Research Council (CSIC) at the Centre for Molecular Biology (CBMSO) in Madrid. He obtained his PhD from the Cajal Institute in 1993 and then moved to Columbia University in New York for his postdoctoral training. He subsequently returned to Spain to join CBMSO and, in recent years, his research has focused on the generation of mouse models to study neurodegeneration and other CNS diseases. Professor Lucas is a member of several professional organizations including the European Huntington's Disease Network (EHDN) and the Spanish Royal Academy of Pharmacy. He has authored more than 70 papers including contributions on the potential for reversibility of neurodegenerative disorders. FŚlix Hernßndez lectures on Biochemistry and Molecular Biology at Autonoma University in Madrid. His main research focus is on neurodegenerative diseases, such as Alzheimer's and related tauopathies, using genetically modified mouse models - especially those over-expressing mutated tau protein and its main kinase, GSK-3?.