The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Transgenic animal models of neurodegenerative diseases and their application to treatment development
Abstract
Neurodegenerative disorders of the aging population affect over 5 million people in the US and Europe alone. The common feature is the progressive accumulation of misfolded proteins with the formation of toxic oligomers. Previous studies show that while in Alzheimer's disease (AD) misfolded amyloid-beta protein accumulates both in the intracellular and extracellular space, in Lewy body disease (LBD), Parkinson's disease (PD), Multiple System Atrophy (MSA), Fronto-Temporal dementia (FTD), prion diseases, amyotrophic lateral sclerosis (ALS) and trinucleotide repeat disorders (TNRD), the aggregated proteins accumulate in the plasma membrane and intracellularly. Protein misfolding and accumulation is the result of an altered balance between protein synthesis, aggregation rate and clearance. Based on these studies, considerable advances have been made in the past years in developing novel experimental models of neurodegenerative disorders. This has been in part driven by the identification of genetic mutations associated with familial forms of these conditions and gene polymorphisms associated with the more common sporadic variants of these diseases. Transgenic and knock out rodents and Drosophila as well as viral vector driven models of Alzheimer's disease (AD), PD, Huntington's disease (HD) and others have been developed, however the focus for this review will be on rodent models of AD, FTD, PD/LBD, and MSA. Promising therapeutic results have been obtained utilizing amyloid prec…
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Defective spatial learning and memory are also observed in 8-month or older Tg2576 mice that express APPswe.
“They are also observed in 8-mo or older Tg2576 mice that express APPswe (Hsiao et al., 1996; Chapman et al., 1999; Rockenstein et al., 2007).”
From VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology (2011) · cites this paper as Rockenstein et al., 2007
Tg2576 mice express the Swedish mutant form of human APP (APPswe) under the control of prion promoter.
“we crossed Tg2576 mice, a well-established AD mouse model that expresses the Swedish mutant form of human APP (APPswe) under the control of prion promoter (Chapman et al., 1999; Rockenstein et al., 2007)”
From VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology (2011) · cites this paper as Rockenstein et al., 2007
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-Synuclein in Parkinson's Disease
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C9orf72 BAC Transgenic Mice Display Typical Pathologic Features of ALS/FTD
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VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology
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“Human Ab (1-42) (from AnaSpec, Fremont, CA, USA) was used.”
BackgroundMethodInfluentialUbhi, K., Rockenstein, E., Vazquez‐Roque, R., Mante, M., Inglis, C., Patrick, C., Adame, A., Fahnestock, M., Doppler, E., Novak, P., et al. (2013) · Journal of Neuroscience Research · doi:10.1002/jnr.23142 · Cited by 65
Self-citationKim, C., Ojo-Amaize, E., Spencer, B., Rockenstein, E., Mante, M., Desplats, P., Wrasidlo, W., Adame, A., Nchekwube, E., Oyemade, O., et al. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0455-9 · Cited by 45
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Metadata
- Authors
- ROCKENSTEIN, E., CREWS, L., & MASLIAH, E.
- Venue
- Advanced Drug Delivery Reviews
- Publisher
- Elsevier BV
- Published
- 2007-09-30
- Volume
- 59
- Issue
- 11
- Pages
- 1093-1102
- ISSN
- 0169-409X
- Cited by
- 65
- References
- 13
- Language
- en
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