2002年7月3日 · These transgenic mice overexpress human α-synuclein with a PD-associated mutation (A53T). Hemizygous mice overexpress mutant α-synuclein in the brain at levels about sixfold higher than endogenous mouse α-synuclein. They develop severe progressive motor impairments around one year of age, but no overt neuronal loss (Lee et al., 2002). The ...

2025年2月26日 · The dbl-PAC-Tg(SNCA A53T) +/+;Snca-/-model, referred to here as double-transgenic mice, are mice lacking endogenous α-synuclein (Snca knockout mice) that were crossed with two homozygous transgenic lines overexpressing a full-length mutant (A53T) human α-synuclein. These mice, which are homozygous for both transgenes and the endogenous ...

2019年2月7日 · Quantitative proteomics in A30P*A53T α-synuclein transgenic mice reveals upregulation of Sel1l. PLoS One. 2017;12(8):e0182092. Epub 2017 Aug 3 PubMed. Chen L, Thiruchelvam MJ, Madura K, Richfield EK. Proteasome dysfunction in aged human alpha-synuclein transgenic mice. Neurobiol Dis. 2006 Jul;23(1):120-6. Epub 2006 May 19 PubMed.

2002年6月29日 · Giasson et al. demonstrate intriguing immunological, relevant biochemical, as well as histological and ultrastructural parallels between human α-synuclein-related PD and their A53T mice. The observed differences between these mice and A53T-linked familial Parkinsonism cases are that in the Giasson model,

2002年7月3日 · Lee observed that only mice expressing the A53T a-synuclein exhibit the loss of motor function; in this regard his mouse is similar to that of Giasson, and different from that of Kahle, which used an A30P-α-synuclein construct. Both Giasson and Lee used the PrP promoter, while Kahle et al. used the Thy1 promoter.

Parkinson's Disease Derived Exosomes Aggravate Neuropathology in SNCA*A53T Mice. Ann Neurol. 2022 Aug;92(2):230-245. Epub 2022 Jun 15 PubMed. Recommends. Please login to recommend the paper. Comments. No Available Comments. Make a Comment. To make a comment you must login or register.

2018年2月6日 · Transgenic mice overexpress full-length mutant human LRRK2 with the G2019S mutation. Transgene expression is driven by a hybrid CMVe-PDGFβ promoter, and the transgene is inserted in chromosome 3 (Kozina et al., 2018). Related Strains. LRRK2 G2019S Mouse (Tg) x α-synuclein (A53T) mice-(see Daher et al., 2012). Phenotype Characterization

Suppression of autophagy in the brain of transgenic mice with overexpression of А53Т-mutant α-synuclein as an early event at synucleinopathy progression. Neurosci Lett. 2018 Apr 13;672:140-144. Epub 2017 Dec 2 PubMed. Recommends. Please login to recommend the paper. Comments. No Available Comments. Make a Comment

2002年6月29日 · The A53T mice develop intracytoplasmic fibrillar inclusions, severe motor impairment, and neurodegeneration. The fibrillar inclusions are striking because they have a diameter of 10-16 nm, similar to that observed in human tissue. The wild-type mice, in contrast, do not develop disease. Yet the model is still not perfect.

2019年10月11日 · Survival of transgenic mice after this age can be improved by providing moistened mashed food and minimizing stress. Transgene expression Female Line 61 mice express lower levels of the human α-synuclein transgene because it is inserted in the X chromosome, which undergoes random chromosomal inactivation (Chesselet et …