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@ARTICLE{VanDenBerge:904320,
author = {Van Den Berge, Nathalie and Ferreira, Nelson and Mikkelsen,
Trine Werenberg and Alstrup, Aage Kristian Olsen and
Tamgüney, Gültekin and Karlsson, Páll and Terkelsen,
Astrid Juhl and Nyengaard, Jens Randel and Jensen, Poul
Henning and Borghammer, Per},
title = {{A}geing promotes pathological alpha-synuclein propagation
and autonomic dysfunction in wild-type rats},
journal = {Brain},
volume = {144},
number = {6},
issn = {0006-8950},
address = {Oxford},
publisher = {Oxford Univ. Press},
reportid = {FZJ-2021-05890},
pages = {1853 - 1868},
year = {2021},
abstract = {Neuronal aggregates of misfolded alpha-synuclein protein
are found in the brain and periphery of patients with
Parkinson’s disease. Braak and colleagues have
hypothesized that the initial formation of misfolded
alpha-synuclein may start in the gut, and then spread to the
brain via peripheral autonomic nerves hereby affecting
several organs, including the heart and intestine. Age is
considered the greatest risk factor for Parkinson’s
disease, but the effect of age on the formation of pathology
and its propagation has not been studied in detail. We aimed
to investigate whether propagation of alpha-synuclein
pathology from the gut to the brain is more efficient in old
versus young wild-type rats, upon gastrointestinal injection
of aggregated alpha-synuclein. Our results demonstrate a
robust age-dependent gut-to-brain and brain-to-gut spread of
alpha-synuclein pathology along the sympathetic and
parasympathetic nerves, resulting in age-dependent
dysfunction of the heart and stomach, as observed in
patients with Parkinson’s disease. Moreover,
alpha-synuclein pathology is more densely packed and
resistant to enzymatic digestion in old rats, indicating an
age-dependent maturation of alpha-synuclein aggregates. Our
study is the first to provide a detailed investigation of
alpha-synuclein pathology in several organs within one
animal model, including the brain, skin, heart, intestine,
spinal cord and autonomic ganglia. Taken together, our
findings suggest that age is a crucial factor for
alpha-synuclein aggregation and complete propagation to
heart, stomach and skin, similar to patients. Given that age
is the greatest risk factor for human Parkinson’s disease,
it seems likely that older experimental animals will yield
the most relevant and reliable findings. These results have
important implications for future research to optimize
diagnostics and therapeutics in Parkinson’s disease and
other age-associated synucleinopathies. Increased emphasis
should be placed on using aged animals in preclinical
studies and to elucidate the nature of age-dependent
interactions.},
cin = {IBI-7},
ddc = {610},
cid = {I:(DE-Juel1)IBI-7-20200312},
pnm = {5244 - Information Processing in Neuronal Networks
(POF4-524)},
pid = {G:(DE-HGF)POF4-5244},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:33880502},
UT = {WOS:000710929200029},
doi = {10.1093/brain/awab061},
url = {https://juser.fz-juelich.de/record/904320},
}