Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Loss of GBA in zebrafish leads to dopaminergic neurodegeneration, but overexpression of α-synuclein does not further worsen degeneration.

Neuroreport - 4 May 2022

Kodera Kazuki, Matsui Noriko, Saitoh Akihiko, Matsui Hideaki

Abstract excerpt

OBJECTIVES: Parkinson's disease is a neurodegenerative disorder that causes motor and nonmotor symptoms due to the loss of dopaminergic nerves and is characterized by the presence of Lewy bodies, which are mainly composed of α-synuclein. Glucosylceramidase beta (GBA), which is a causative gene of autosomal recessive Gaucher disease, is also known to be a risk gene for Parkinson's disease. In this study, we tried...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to alpha-Synuclein
Share to Disease Models, Animal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Dopamine

Share to Mutation

Share to Neurodegenerative Diseases

Share to Parkinson Disease

Share to Zebrafish

Source

Identifiers

PMID: 35594444
DOI: 10.1097/WNR.0000000000001788

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of GBA in zebrafish leads to dopaminergic neurodegeneration, but overexpression of α-synuclein does not further worsen degeneration.PMID 35594444Read ↗

Hypokinesia and Reduced Dopamine Levels in Zebrafish Lacking β- and γ1-SynucleinsSemantic proximity Read ↗

Viable Neuronopathic Gaucher Disease Model in Medaka (Oryzias latipes) Displays Axonal Accumulation of Alpha-SynucleinSemantic proximity Read ↗

Glucocerebrosidase haploinsufficiency in A53T α-synuclein mice impacts disease onset and course.Semantic proximity Read ↗

Fishing for synucleinopathy modelsSemantic proximity Read ↗

D409H GBA1 mutation accelerates the progression of pathology in A53T α-synuclein transgenic mouse model.Semantic proximity Read ↗

GBA haploinsufficiency accelerates alpha-synuclein pathology with altered lipid metabolism in a prodromal model of Parkinson’s diseaseSemantic proximity Read ↗

An In Vivo Model of α-Synuclein Spread from Gut to BrainSemantic proximity Read ↗

Impact of GBA2 on Neuronopathic Gaucher’s Disease and α-Synuclein Accumulation in Medaka (Oryzias Latipes)Semantic proximity Read ↗

Impact of Gba2 on neuronopathic Gaucher's disease and α-synuclein accumulation in medaka (Oryzias latipes).Semantic proximity Read ↗

The L444P Gba1 mutation enhances alpha-synuclein induced loss of nigral dopaminergic neurons in mice.Semantic proximity Read ↗

Glucocerebrosidase Deficiency in Drosophila Results in α-Synuclein-Independent Protein Aggregation and Neurodegeneration.Semantic proximity Read ↗

Glucocerebrosidase deficiency in dopaminergic neurons induces microglial activation without neurodegenerationSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.