Article

Genetic screening and metabolomics identify glial adenosine metabolism as a therapeutic target in α-synucleinopathies

2024-05-15

Abstract excerpt

<h4>Background</h4> Parkinson’s disease (PD) and dementia with Lewy bodies (DLB) are common neurodegenerative “α-synucleinopathies” that lack disease-modifying therapies. Targeting non-neuronal mechanisms represents a major unmet opportunity, as glial contributions to α-synuclein toxicity remain poorly understood. <h4>Methods</h4> We developed a Drosophila α-synucleinopathy model for identifying novel glial-bas...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: ff0cef6d-48c0-5db2-8f35-ed5ca37df013
DOI: 10.1101/2024.05.15.594309

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Genetic screening and metabolomics identify glial adenosine metabolism as a therapeutic target in α-synucleinopathiesDOI 10.1101/2024.05.15.594309Read

Parkinson's disease risk genes act in glia to control neuronal α-synuclein toxicity.Semantic proximity Read

Longitudinal multi-omics in alpha-synuclein Drosophila model discriminates disease- from age-associated pathologies in Parkinson’s diseaseSemantic proximity Read

Glial α‐synuclein promotes neurodegeneration characterized by a distinct transcriptional program in vivoSemantic proximity Read

Comparative proteomic analysis highlights metabolic dysfunction in α-synucleinopathySemantic proximity Read

Metabolic and neurobehavioral disturbances induced by purine recycling deficiency in <i>Drosophila</i>Semantic proximity Read

Human α-synuclein overexpression in mouse serotonin neurons triggers a depressive-like phenotype. Rescue by oligonucleotide therapySemantic proximity Read

A Druggable Genome Screen Identifies Modifiers of α-Synuclein Levels via a Tiered Cross-Species Validation ApproachSemantic proximity Read

dAux orchestrates the phosphorylation-dependent assembly of the lysosomal V-ATPase in glia and contributes to α-synuclein degradationSemantic proximity Read

Modulating glial genes involved in synaptic function mitigates pathogenesis and behavioral deficits in a <i>Drosophila</i> model of Huntington’s DiseaseSemantic proximity Read

Spreading alpha-synuclein Oligomers Trigger Astrocyte Changes and Astrocyte-Glutamatergic Neuron system dysfunction in an Age-related MannerSemantic proximity Read

Human α-synuclein overexpression in mouse serotonin neurons triggers a depressive-like phenotype. Rescue by oligonucleotide therapy.Semantic proximity Read

Spatiotemporal transcriptomics reveals distinct responses of ALDH1A1-positive and ALDH1A1-negative midbrain dopaminergic neurons to alpha-synuclein overexpressionSemantic proximity Read