http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2010175140-A1
Outgoing Links
| Predicate | Object |
|---|---|
| assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_18d92c46f60af8af24e262b67381d7eb |
| classificationCPCAdditional | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2267-0318 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2227-706 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K2217-052 |
| classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K49-0008 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12N15-8509 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A01K67-0339 |
| classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K49-00 http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A01K67-00 |
| filingDate | 2009-12-21-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_ecb247e16ff733a30e0d664ae95cf979 |
| publicationDate | 2010-07-08-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber | US-2010175140-A1 |
| titleOfInvention | Leucine-rich repeat kinase (LRRK2) drosophila model for parkinson's disease: wildtype1 (WT1) and G2019S mutant flies |
| abstract | Mutations in the leucine-rich repeat kinase (LRRK2) gene cause late-onset autosomal dominant Parkinson's disease (PD) with pleiomorphic pathology. Previously, we and others found that expression of mutant LRRK2 causes neuronal degeneration in cell culture. Here we used the GAL4/UAS system to generate transgenic Drosophila expressing either wild-type (WT1) human LRRK2 or LRRK2-G2019S, the most common mutation associated with PD. Expression of either WT1 human LRRK2 or LRRK2-G2019S in the photoreceptor cells caused retinal degeneration. Expression of WT1 LRRK2 or LRRK2-G2019S in neurons produced adult-onset selective loss of dopaminergic neurons, locomotor dysfunction, and early mortality. Expression of mutant G2019S-LRRK2 caused a more severe parkinsonism-like phenotype than expression of equivalent levels of WT1 LRRK2. Treatment with L-DOPA improved mutant LRRK2-induced locomotor impairment but did not prevent the loss of tyrosine hydroxylase (TH)-positive neurons. To our knowledge, this is the first in vivo “gain-of-function” model which recapitulates several key features of LRRK2-linked human parkinsonism. These flies may provide a useful model for studying LRRK2-linked pathogenesis and for future therapeutic screens for PD intervention. |
| isCitedBy | http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-9695171-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-10039753-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/GB-2563551-A http://rdf.ncbi.nlm.nih.gov/pubchem/patent/JP-2014504362-A http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2017149307-A1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-9642855-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-9156845-B2 |
| priorityDate | 2008-12-19-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 113.