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The role of glucocerebrosidase in Parkinson disease pathogenesis

The FEBS journal, 2018-10, Vol.285 (19), p.3591-3603

2018

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Glucocerebrosidase-associated Parkinson disease: Pathogenic mechanisms and potential drug treatments

Neurobiology of disease, 2022-05, Vol.166, p.105663-105663, Article 105663

2022

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Mitochondria and Quality Control Defects in a Mouse Model of Gaucher Disease—Links to Parkinson’s Disease

Cell metabolism, 2013-06, Vol.17 (6), p.941-953

2013

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Autophagic lysosome reformation dysfunction in glucocerebrosidase deficient cells: relevance to Parkinson disease

Human molecular genetics, 2016-08, Vol.25 (16), p.3432-3445

2016

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Mitochondrial and lysosomal biogenesis are activated following PINK1/parkin‐mediated mitophagy

Journal of neurochemistry, 2016-01, Vol.136 (2), p.388-402

2016

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Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy

Human molecular genetics, 2010-12, Vol.19 (24), p.4861-4870

2010

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Glucocerebrosidase deficiency in substantia nigra of parkinson disease brains

Annals of neurology, 2012-09, Vol.72 (3), p.455-463

2012

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Mitochondrial dysfunction associated with glucocerebrosidase deficiency

Neurobiology of disease, 2016-06, Vol.90, p.43-50

2016

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Parkinson disease-linked GBA mutation effects reversed by molecular chaperones in human cell and fly models

Scientific reports, 2016-08, Vol.6 (1), p.31380-31380, Article 31380

2016

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Lysosomal-endolysomal dysfunction and neurodegenerative diseases

Neurobiology of disease, 2022-10, Vol.173, p.105843-105843, Article 105843

2022

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Silencing of PINK1 expression affects mitochondrial DNA and oxidative phosphorylation in dopaminergic cells

PloS one, 2009-03, Vol.4 (3), p.e4756-e4756

2009

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Glucocerebrosidase in the pathogenesis and treatment of Parkinson disease

Proceedings of the National Academy of Sciences - PNAS, 2013-02, Vol.110 (9), p.3214-3215

2013

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PINK1-parkin-dependent mitophagy involves ubiquitination of mitofusins 1 and 2: Implications for Parkinson disease pathogenesis

Autophagy, 2011-02, Vol.7 (2), p.243-245

2011

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Unexpected phenotypic and molecular changes of combined glucocerebrosidase and acid sphingomyelinase deficiency

Disease models & mechanisms, 2023-06, Vol.16 (6)

2023

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The role of DJ-1 complexes and catecholamine metabolism: relevance for familial and idiopathic Parkinson's disease

Neural regeneration research, 2018-05, Vol.13 (5), p.815-816

2018

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Mitochondrial impairment increases FL-PINK1 levels by calcium-dependent gene expression

Neurobiology of disease, 2014-02, Vol.62, p.426-440

2014

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Glucocerebrosidase deficiency promotes release of α-synuclein fibrils from cultured neurons

Human molecular genetics, 2020-06, Vol.29 (10), p.1716-1728

2020

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The importance of being connected: membrane contact sites and Parkinson's disease

Neural regeneration research, 2023-10, Vol.18 (10), p.2202-2203

Gegg, Matthew

2023

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No evidence for substrate accumulation in Parkinson brains with GBA mutations

Movement disorders, 2015-07, Vol.30 (8), p.1085-1089

2015

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The GBA variant E326K is associated with alpha-synuclein aggregation and lipid droplet accumulation in human cell lines

Human molecular genetics, 2023-02, Vol.32 (5), p.773-789

2023

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Endoplasmic reticulum and lysosomal Ca2+ stores are remodelled in GBA1 -linked Parkinson disease patient fibroblasts

Cell calcium (Edinburgh), 2016-01, Vol.59 (1), p.12-20

2016

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Mitochondria: Key Organelle in Parkinson's Disease

Parkinson's disease, 2016-01, Vol.2016, p.362-363

2016

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DJ-1 is a redox sensitive adapter protein for high molecular weight complexes involved in regulation of catecholamine homeostasis

Human molecular genetics, 2017-10, Vol.26 (20), p.4028-4041

2017

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α-Synuclein expression in response to bacterial ligands and metabolites in gut enteroendocrine cells: an in vitro proof of concept study

Brain communications, 2023-11, Vol.5 (6), p.fcad285-fcad285

2023

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The role of glucocerebrosidase in Parkinson disease pathogenesis

Glucocerebrosidase-associated Parkinson disease: Pathogenic mechanisms and potential drug treatments

Mitochondria and Quality Control Defects in a Mouse Model of Gaucher Disease—Links to Parkinson’s Disease

Autophagic lysosome reformation dysfunction in glucocerebrosidase deficient cells: relevance to Parkinson disease

Mitochondrial and lysosomal biogenesis are activated following PINK1/parkin‐mediated mitophagy

Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy

Glucocerebrosidase deficiency in substantia nigra of parkinson disease brains

Mitochondrial dysfunction associated with glucocerebrosidase deficiency

Parkinson disease-linked GBA mutation effects reversed by molecular chaperones in human cell and fly models

Lysosomal-endolysomal dysfunction and neurodegenerative diseases

Silencing of PINK1 expression affects mitochondrial DNA and oxidative phosphorylation in dopaminergic cells

Glucocerebrosidase in the pathogenesis and treatment of Parkinson disease

PINK1-parkin-dependent mitophagy involves ubiquitination of mitofusins 1 and 2: Implications for Parkinson disease pathogenesis

Unexpected phenotypic and molecular changes of combined glucocerebrosidase and acid sphingomyelinase deficiency

The role of DJ-1 complexes and catecholamine metabolism: relevance for familial and idiopathic Parkinson's disease

Mitochondrial impairment increases FL-PINK1 levels by calcium-dependent gene expression

Glucocerebrosidase deficiency promotes release of α-synuclein fibrils from cultured neurons

The importance of being connected: membrane contact sites and Parkinson's disease

No evidence for substrate accumulation in Parkinson brains with GBA mutations

The GBA variant E326K is associated with alpha-synuclein aggregation and lipid droplet accumulation in human cell lines

Elevated cholesterol in ATAD3 mutants is a compensatory mechanism that leads to membrane cholesterol aggregation

Endoplasmic reticulum and lysosomal Ca2+ stores are remodelled in GBA1 -linked Parkinson disease patient fibroblasts

Mitochondria: Key Organelle in Parkinson's Disease

DJ-1 is a redox sensitive adapter protein for high molecular weight complexes involved in regulation of catecholamine homeostasis

α-Synuclein expression in response to bacterial ligands and metabolites in gut enteroendocrine cells: an in vitro proof of concept study

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