Wild-type GBA1 increases the α-synuclein tetramer–monomer ratio, reduces lipid-rich aggregates, and...
Wild-type GBA1 increases the α-synuclein tetramer–monomer ratio, reduces lipid-rich aggregates, and attenuates motor and cognitive deficits in mice
About this item
Full title
Author / Creator
Publisher
United States: National Academy of Sciences
Journal title
Language
English
Formats
Publication information
Publisher
United States: National Academy of Sciences
Subjects
More information
Scope and Contents
Contents
Loss-of-function mutations in acid beta-glucosidase 1 (GBA1) are among the strongest genetic risk factors for Lewy body disorders such as Parkinson’s disease (PD) and Lewy body dementia (DLB). Altered lipid metabolism in PD patient–derived neurons, carrying either GBA1 or PD αS mutations, can shift the physiological α-synuclein (αS) tetramer–monome...
Alternative Titles
Full title
Wild-type GBA1 increases the α-synuclein tetramer–monomer ratio, reduces lipid-rich aggregates, and attenuates motor and cognitive deficits in mice
Authors, Artists and Contributors
Identifiers
Primary Identifiers
Record Identifier
TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8346893
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8346893
Other Identifiers
ISSN
0027-8424
E-ISSN
1091-6490
DOI
10.1073/pnas.2103425118
