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@ARTICLE{Catterson:292292,
author = {J. H. Catterson and E. N. Mouofo and I. López De Toledo
Soler and G. Lean and S. Dlamini and P. Liddell and G. Voong
and T. Katsinelos$^*$ and Y.-C. Wang and N. Schoovaerts and
P. Verstreken and T. L. Spires-Jones and C. S. Durrant},
title = {{D}rosophila appear resistant to trans-synaptic tau
propagation.},
journal = {Brain communications},
volume = {6},
number = {4},
issn = {2632-1297},
address = {[Großbritannien]},
publisher = {Guarantors of Brain},
reportid = {DKFZ-2024-01653},
pages = {fcae256},
year = {2024},
abstract = {Alzheimer's disease is the most common cause of dementia in
the elderly, prompting extensive efforts to pinpoint novel
therapeutic targets for effective intervention. Among the
hallmark features of Alzheimer's disease is the development
of neurofibrillary tangles comprised of hyperphosphorylated
tau protein, whose progressive spread throughout the brain
is associated with neuronal death. Trans-synaptic
propagation of tau has been observed in mouse models, and
indirect evidence for tau spread via synapses has been
observed in human Alzheimer's disease. Halting tau
propagation is a promising therapeutic target for
Alzheimer's disease; thus, a scalable model system to screen
for modifiers of tau spread would be very useful for the
field. To this end, we sought to emulate the trans-synaptic
spread of human tau in Drosophila melanogaster. Employing
the trans-Tango circuit mapping technique, we investigated
whether tau spreads between synaptically connected neurons.
Immunohistochemistry and confocal imaging were used to look
for tau propagation. Examination of hundreds of flies
expressing four different human tau constructs in two
distinct neuronal populations reveals a robust resistance in
Drosophila to the trans-synaptic spread of human tau. This
resistance persisted in lines with concurrent expression of
amyloid-β, in lines with global human tau knock-in to
provide a template for human tau in downstream neurons, and
with manipulations of temperature. These negative data are
important for the field as we establish that Drosophila
expressing human tau in subsets of neurons are unlikely to
be useful to perform screens to find mechanisms to reduce
the trans-synaptic spread of tau. The inherent resistance
observed in Drosophila may serve as a valuable clue,
offering insights into strategies for impeding tau spread in
future studies.},
keywords = {Alzheimer’s disease (Other) / Drosophila melanogaster
(Other) / neurodegeneration (Other) / tau (Other) /
trans-synaptic (Other)},
cin = {B180},
ddc = {610},
cid = {I:(DE-He78)B180-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39130515},
pmc = {pmc:PMC11316205},
doi = {10.1093/braincomms/fcae256},
url = {https://inrepo02.dkfz.de/record/292292},
}