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@INPROCEEDINGS{Endepols:1027717,
author = {Endepols, H. and Mandelkow, E. M. and Mandelkow, E. and
Schneider, Daniela and Neumaier, B. and Drzezga, A.},
title = {{SV}2{A}-{PET} in a tauopathy mouse model},
reportid = {FZJ-2024-04027},
year = {2023},
abstract = {Ziel/Aim Transgenic mouse models are frequently used to
study the mechanismsof neurodegenerative diseases and
possible therapeutic options. Weinvestigated the tauopathy
mouse model TauRDΔK, which expresses the repeatdomain of
human tau with deletion of the amino acid K280. TauRDΔK
mice showa slow disease progression which makes them a
suitable model for therapystudies. Unexpectedly, the PET
tracer [18F]MNI-1126, which binds to the synapticvesicle
protein SV2A, showed a significantly increased uptake in the
brainof 16–18 months old TauRDΔK mice in the summed image
analysis (n = 9; SUVRCer0.98 ± 0.03) compared to controls
(n = 7; SUVRCer: 0.94 ± 0.02; p < 0.005).This is in
contrast to studies with other tauopathy mouse models, which
alldemonstrated reduced SV2A binding.Methodik/Methods To
further investigate this surprising result, we
performedkinetic modeling using the simplified reference
tissue model in PMOD with thecerebellum as reference region
as well as Western blot.Ergebnisse/Results The whole brain
non-displaceable binding potential(BPnd) was significantly
higher in TauRDΔK mice (0.24 ± 0.03) compared to
controls(0.18 ± 0.06; p = 0.0276). This was confirmed by
globally increased SV2A/actin ratio in Western blot (0.98 ±
0.24 in TauRDΔK mice versus 0.84 ± 0.11 incontrols).
Voxel-wise comparison of BPnd revealed a wide-spead
significantincrease of BPnd mirroring the elevated SUVRCer.
Whole brain ratio of tracerdelivery R1 ( = K1/K1') was
comparable in TauRDΔK mice (0.98 ± 0.04) and controls(0.94
± 0.1; p = 0.2930). The efflux constant k2 was slightly
lower inTauRDΔK mice (0.07 ± 0.02 1/ml) compared to
controls (0.08 ± 0.03 1/ml), butnot statistically
significant (p = 0.5432).Schlussfolgerungen/Conclusions Our
results demonstrate that SV2A expressionwas globally
increased in TauRDΔK mice. It is unlikely that this
reflects synapticsprouting or a compensatory increase of
synaptic vesicles, since a previousstudy has demonstrated a
decline of synapsin expression as well as synapticdensity
from 9 months of age. One possible explanation could be the
increaseof mitochondrial SV2A expression, which will be
evaluated in further studies.},
month = {Apr},
date = {2023-04-19},
organization = {61. Jahrestagung der Deutschen
Gesellschaft für Nuklearmedizin,
Leipzig (Germany), 19 Apr 2023 - 22 Apr
2023},
subtyp = {After Call},
cin = {INM-5 / INM-2},
cid = {I:(DE-Juel1)INM-5-20090406 / I:(DE-Juel1)INM-2-20090406},
pnm = {5253 - Neuroimaging (POF4-525)},
pid = {G:(DE-HGF)POF4-5253},
typ = {PUB:(DE-HGF)6},
doi = {10.1055/s-0043-1766342},
url = {https://juser.fz-juelich.de/record/1027717},
}