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Output Catalog

ASAP is committed to accelerating the pace of discovery and informing a path to a cure for Parkinson’s disease through collaboration, research-enabling resources, and data sharing. We’ve created this catalog to showcase the research outputs and tools developed by ASAP-funded programs.

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Iron mishandling in the brain and periphery in Parkinson’s disease

The prodromal phase of Parkinson’s disease is complex. Gastrointestinal dysfunction and iron dysregulation may drive neurodegenerative risk. Identifying catalysts in the gut is crucial for developing disease-modifying therapies.

Program: Collaborative Research Network
Team:
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Metagenomics of Parkinson’s disease implicates the gut microbiome in multiple disease mechanisms

A study on Parkinson's disease links gut microbiome to brain health. Analysis of 490 PD patients and 234 controls reveals dysbiosis, microbial clusters, and disease-promoting factors in PD microbiome, offering insights for future research.

Program: Collaborative Research Network
Team:
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Population fraction of Parkinson’s disease attributable to preventable risk factors

Parkinson's disease is a fast-growing neurologic disease with no known prevention. Environmental factors like head trauma in sports/combat and pesticide exposure contribute significantly to the disease, suggesting preventable causes for some cases.

Program: Collaborative Research Network
Team:
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Gut mucosal cells transfer α-synuclein to the vagus nerve

Published: These findings highlight a potential non-neuronal source of fibrillar α-synuclein protein that might arise in gut mucosal cells. View original preprint.

Program: Collaborative Research Network
Team:
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Microbial amyloids in neurodegenerative amyloid diseases

Published: Inhibiting microbial amyloids or their interactions with the host, may therefore represent a tangible target to limit various amyloid pathologies.

Program: Collaborative Research Network
Team:
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Anionic nanoplastic contaminants promote Parkinson’s disease–associated α-synuclein aggregation

Studies show nanoplastic pollution can trigger α-synuclein protein fibrils formation and spread in the brain, potentially linking nanoplastics to Parkinson's disease and related dementias.

Program: Collaborative Research Network
Team:
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A leaky gut dysregulates gene networks in the brain associated with immune activation, oxidative stress, and myelination in a mouse model of colitis

The gut and brain are interconnected in human disease. Colitis models show reproducible genetic programs affecting both colon and brain, highlighting immune activation and potential therapeutic targets in the gut-brain axis.

Program: Collaborative Research Network
Team:
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The R1441C-LRRK2 mutation induces myeloid immune cell exhaustion in an age- and sex-dependent manner

Aging is a neglected factor in neurodegeneration research. LRRK2 gene variations impact PD risk.R1441C mutation boosts immune response in young, but leads to immune exhaustion with age.Understanding LRRK2's immune effects is crucial for PD treatment.

Program: Collaborative Research Network
Team:
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Central and peripheral innate and adaptive immunity in Parkinson’s disease

Parkinson’s disease is a chronic inflammatory disorder affecting multiple systems. Innovative immunomodulatory interventions are needed to address central and peripheral immune responses during disease onset and progression.

Program: Collaborative Research Network
Team:
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Calcium influx into astrocytes plays a pivotal role in inflammation-driven behaviors

Systemic inflammation can lead to astrogliosis, affecting neuronal activity linked to depressive behaviors. Orai1 calcium channel is crucial in this.Deleting Orai1 in astrocytes prevents astrogliosis, preserving normal neuronal activity and behavior.

Program: Collaborative Research Network
Team:
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Alpha-synuclein overexpression can drive microbiome dysbiosis in mice

Persons with PD have a unique gut microbe composition. Studies on human and rodent microbiomes before and during the disease are lacking. α-syn overexpression in mice alters gut microbiome with age, potentially impacting disease progression.

Program: Collaborative Research Network
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Mouse α-synuclein fibrils are structurally and functionally distinct from human fibrils associated with Lewy body diseases

Mouse α-synuclein fibrils have been studied to understand Parkinson's disease and multiple system atrophy. They differ from human fibrils in structure and behavior, impacting research on related diseases and potential treatments.

Program: Collaborative Research Network
Team:
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Biochemical Fractionation of Human α-Synuclein in a Drosophila Model of Synucleinopathies

Synucleinopathies involve α-synuclein accumulation in Lewy Bodies. A-synuclein in Drosophila helps understand its effects. A method using detergents and sonication separates soluble/insoluble forms of human α-synuclein from fly brains aiding…

Program: Collaborative Research Network
Team:
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Locus coeruleus injury modulates ventral midbrain neuroinflammation during DSS-induced colitis

PD is preceded by non-motor symptoms like gastrointestinal issues and mood changes. A two-hit mouse model shows gut inflammation and LC lesioning affect neuroimmune responses, highlighting the role of NEergic interventions in PD progression.

Program: Collaborative Research Network
Team:
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A comparative analysis of Parkinson’s disease and inflammatory bowel disease gut microbiomes highlights shared depletions in key butyrate-producing bacteria

Epidemiological studies show a link between IBD and PD. Gut microbiome alterations, specifically depletions in SCFA-producing bacteria, may contribute to this connection. Comparing PD and IBD microbiomes can help identify shared features.

Program: Collaborative Research Network
Team:
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Aligning Science Across Parkinson's
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