TY  - THES
AU  - Lohmann, Stephanie
TI  - Neuroinvasion and cerebral ischemia as possible sources for alpha-synuclein prions in Parkinson's disease
PB  - Rheinische Friedrich-Wilhelms-Universität Bonn
VL  - Dissertation
M1  - DZNE-2021-00617
SP  - 88 pages, 24 figures, 7 tables
PY  - 2021
N1  - Dissertation, Rheinische Friedrich-Wilhelms-Universität Bonn, 2021
AB  - In synucleinopathies such as Parkinson's disease misfolding of a-synuclein, normally a cellular and soluble protein, leads to the accumulation of insoluble protein aggregates and to central nervous system disease (CNS). Misfolded a-synuclein acts as a seed, by recruiting native a-synuclein and inducing its misfolding into insoluble a-synuclein aggregates. Aggregated a-synuclein shows prion-like characteristics and spreads via cell-to-cell transmission throughout the central nervous system but also within the periphery, ultimately causing neurological disease.Because the spatiotemporal spreading of pathological a-synuclein from the periphery to the CNS is not fully elucidated this work investigated and compared the spreading of pathological a-synuclein after intravenous or oral inoculation with that after intracerebral or intraperitoneal inoculation of TgM83+1- mice overexpressing the A53T mutant of human a-synuclein with a-synuclein fibrils. In accordance with previous studies, an infection rate of 100
LB  - PUB:(DE-HGF)11
UR  - https://pub.dzne.de/record/155350
ER  -