This title appears in the Scientific Report :
2022
Please use the identifier:
http://dx.doi.org/10.1016/j.nbd.2022.105626 in citations.
Please use the identifier: http://hdl.handle.net/2128/31815 in citations.
Clinical and imaging evidence of brain-first and body-first Parkinson's disease
Clinical and imaging evidence of brain-first and body-first Parkinson's disease
Braak's hypothesis has been extremely influential over the last two decades. However, neuropathological and clinical evidence suggest that the model does not conform to all patients with Parkinson's disease (PD). To resolve this controversy, a new model was recently proposed; in brain-firs...
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Personal Name(s): | Horsager, Jacob (Corresponding author) |
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Knudsen, Karoline / Sommerauer, Michael | |
Contributing Institute: |
Kognitive Neurowissenschaften; INM-3 |
Published in: | Neurobiology of disease, 164 (2022) S. 105626 - |
Imprint: |
Orlando, Fla.
Academic Press
2022
|
DOI: |
10.1016/j.nbd.2022.105626 |
Document Type: |
Journal Article |
Research Program: |
Brain Dysfunction and Plasticity |
Link: |
OpenAccess |
Publikationsportal JuSER |
Please use the identifier: http://hdl.handle.net/2128/31815 in citations.
Braak's hypothesis has been extremely influential over the last two decades. However, neuropathological and clinical evidence suggest that the model does not conform to all patients with Parkinson's disease (PD). To resolve this controversy, a new model was recently proposed; in brain-first PD, the initial α-synuclein pathology arise inside the central nervous system, likely rostral to the substantia nigra pars compacta, and spread via interconnected structures – eventually affecting the autonomic nervous system; in body-first PD, the initial pathological α-synuclein originates in the enteric nervous system with subsequent caudo-rostral propagation to the autonomic and central nervous system. |