Download Animal Models for Neurodegenerative Disease by Jesús Avila PDF

By Jesús Avila

Content material: Preface; Animal versions on Alzheimer disorder; Animal types for Amyloid/PS-1 Pathology; Transgenic mice overexpressing GSK-3beta as animal versions of Alzheimer ailment; Reelin and Alzheimer ailment; Tauopathy types; Animal types for Parkinson ailment I; Animal types for Parkinson sickness II; Neuroprotection in Parkinson ailment; Animal versions for ALS; Mouse versions of Huntington's sickness; Recesive Ataxias; Mouse types in PrP-related illnesses; Mouse versions of ischemia

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Schenk, D. Games and B. T. Hyman, J. , 1997, 17(18), 7053–7059. 41. E. Masliah, A. Sisk, M. Mallory and D. Games, J. Neuropathol. Exp. , 2001, 60(4), 357–368. 42. G. Chen, K. S. Chen, J. Knox, J. Inglis, A. Bernard, S. J. Martin, A. Justice, L. McConlogue, D. Games, S. B. Freedman and R. G. Morris, Nature, 2000, 408(6815), 975–979. 43. D. Schenk, R. Barbour, W. Dunn, G. Gordon, H. Grajeda, T. Guido, K. Hu, J. Huang, K. Johnson-Wood, K. Khan, D. Kholodenko, M. Lee, Z. Liao, I. Lieberburg, R. Motter, L.

This is because extracellular Ab deposition is similar to that observed in AD patients. 1 PDAPP Transgenic Mouse Model This transgenic mouse was the first recognized AD model with AD-type pathological accumulation of Ab peptide in the brain. This line was generated using a platelet-derived growth factor b-promoter (PDGF),37 which drives a human APP minigene encoding alternative spliced hAPP. 39 In addition, these mice produce increased amounts of Ab42, which is the predominant form of Ab in brain plaques of AD cases observed at neuropathological evaluation.

The Thy1 promoter causes expression of mutant hAPP and generates Ab in neurons. Neuron-derived Ab is deposited extracellularly and then accumulates in the vessel wall, leading to disruption of vessel walls. This, in turn leads to parenchymal haemorrhage,61 which is observed as CAA-associated haemorrhagic stroke in AD. 65 However in APP23 mice, the number of synaptophysin-positive presynaptic terminals is maintained in the face of robust parenchymal Ab deposition. Thus, Ab deposition alone may not be sufficient to account for age-dependent behavioural changes in APP23.

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