{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["11(1)"],"submitter":["Pang SY"],"funding":["The Henry G. Leong Endowed Professorship in Neurology","Tai Hung Fai Charitable Foundation - Edwin S H Leong Research Programme for Parkinson’s Disease","The Donation Fund for Neurology Research"],"pubmed_abstract":["Mutations in leucine-rich repeat kinase 2 (LRRK2) and glucocerebrosidase (GBA) represent two most common genetic causes of Parkinson's disease (PD). Both genes are important in the autophagic-lysosomal pathway (ALP), defects of which are associated with α-synuclein (α-syn) accumulation. LRRK2 regulates macroautophagy via activation of the mitogen activated protein kinase/extracellular signal regulated protein kinase (MAPK/ERK) kinase (MEK) and the calcium-dependent adenosine monophosphate (AMP)-activated protein kinase (AMPK) pathways. Phosphorylation of Rab GTPases by LRRK2 regulates lysosomal homeostasis and endosomal trafficking. Mutant LRRK2 impairs chaperone-mediated autophagy, resulting in α-syn binding and oligomerization on lysosomal membranes. Mutations in GBA reduce glucocerebros"],"journal":["Translational neurodegeneration"],"pagination":["5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8805403"],"repository":["biostudies-literature"],"pubmed_title":["LRRK2, GBA and their interaction in the regulation of autophagy: implications on therapeutics in Parkinson's disease."],"pmcid":["PMC8805403"],"pubmed_authors":["Ramsden DB","Wong WY","Malki Y","Choi ZY","Chang EES","Ho PW","Pang SY","Liu HF","Ho SL","Lo RCN","Leung CT","Kung MH"],"additional_accession":[]},"is_claimable":false,"name":"LRRK2, GBA and their interaction in the regulation of autophagy: implications on therapeutics in Parkinson's disease.","description":"Mutations in leucine-rich repeat kinase 2 (LRRK2) and glucocerebrosidase (GBA) represent two most common genetic causes of Parkinson's disease (PD). Both genes are important in the autophagic-lysosomal pathway (ALP), defects of which are associated with α-synuclein (α-syn) accumulation. LRRK2 regulates macroautophagy via activation of the mitogen activated protein kinase/extracellular signal regulated protein kinase (MAPK/ERK) kinase (MEK) and the calcium-dependent adenosine monophosphate (AMP)-activated protein kinase (AMPK) pathways. Phosphorylation of Rab GTPases by LRRK2 regulates lysosomal homeostasis and endosomal trafficking. Mutant LRRK2 impairs chaperone-mediated autophagy, resulting in α-syn binding and oligomerization on lysosomal membranes. Mutations in GBA reduce glucocerebros","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2025-04-19T10:50:05.266Z","creation":"2025-04-19T10:50:05.266Z"},"accession":"S-EPMC8805403","cross_references":{"pubmed":["35101134"],"doi":["10.1186/s40035-022-00281-6"]}}