% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Kedariti:164913,
author = {Kedariti, Maria and Frattini, Emanuele and Baden, Pascale
and Cogo, Susanna and Civiero, Laura and Ziviani, Elena and
Zilio, Gianluca and Bertoli, Federico and Aureli, Massimo
and Kaganovich, Alice and Cookson, Mark R and Stefanis,
Leonidas and Surface, Matthew and Deleidi, Michela and Di
Fonzo, Alessio and Alcalay, Roy N and Rideout, Hardy and
Greggio, Elisa and Plotegher, Nicoletta},
title = {{LRRK}2 kinase activity regulates {GC}ase level and
enzymatic activity differently depending on cell type in
{P}arkinson's disease.},
journal = {npj Parkinson's Disease},
volume = {8},
issn = {2373-8057},
address = {London [u.a.]},
publisher = {Nature Publ. Group},
reportid = {DZNE-2022-01324},
pages = {92},
year = {2022},
note = {CC BY},
abstract = {Leucine-rich repeat kinase 2 (LRRK2) is a kinase involved
in different cellular functions, including autophagy,
endolysosomal pathways, and immune function. Mutations in
LRRK2 cause autosomal-dominant forms of Parkinson's disease
(PD). Heterozygous mutations in GBA1, the gene encoding the
lysosomal enzyme glucocerebrosidase (GCase), are the most
common genetic risk factors for PD. Moreover, GCase function
is altered in idiopathic PD and in other genetic forms of
the disease. Recent work suggests that LRRK2 kinase activity
can regulate GCase function. However, both a positive and a
negative correlation have been described. To gain insights
into the impact of LRRK2 on GCase, we performed a
comprehensive analysis of GCase levels and activity in
complementary LRRK2 models, including (i) LRRK2 G2019S knock
in (GSKI) mice, (ii) peripheral blood mononuclear cell
(PBMCs), plasma, and fibroblasts from PD patients carrying
LRRK2 G2019S mutation, (iii) patient iPSCs-derived neurons;
(iv) endogenous and overexpressed cell models. In some of
these models we found a positive correlation between the
activities of LRRK2 and GCase, which was further confirmed
in cell lines with genetic and pharmacological manipulation
of LRRK2 kinase activity. GCase protein level is reduced in
GSKI brain tissues and in G2019S iPSCs-derived neurons, but
increased in fibroblasts and PBMCs from patients, suggesting
cell-type-specific effects. Overall, our study indicates
that LRRK2 kinase activity affects both the levels and the
catalytic activity of GCase in a cell-type-specific manner,
with important implications in the context of therapeutic
application of LRRK2 inhibitors in GBA1-linked and
idiopathic PD.},
cin = {AG Deleidi},
ddc = {610},
cid = {I:(DE-2719)1210011},
pnm = {352 - Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35853899},
pmc = {pmc:PMC9296523},
doi = {10.1038/s41531-022-00354-3},
url = {https://pub.dzne.de/record/164913},
}