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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.
Article
3D bioprinting of human neural tissues with functional connectivity
Probing how human neural networks operate is hindered by the lack of reliable human neural tissues amenable to the dynamic functional assessment of neural circuits. Team Scherzer developed a 3D bioprinting platform to assemble tissues with defined human neural cell types in a desired dimension using a commercial bioprinter.
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Chemically induced senescence in human stem cell‐derived neurons promotes phenotypic presentation of neurodegeneration
Published: Using embryonic stem-cell derived neurons to model age-related neurodegenerative diseases is inherently difficult. The authors thereby developed a chemical cocktail to induce cellular senescence (without causing DNA damage), thereby inducing embryonic cells to exhibit features characteristic of aged cells. The cocktail can help enhance disease-related phenotypes in iPSCs.
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Towards a phenome-wide view of Parkinson’s disease
Preprint: The authors examine that relationship between PD and the environment by holistically characterizing environmental, health, and pharmacological traits associated with PD patients. They found numerous traits that were positively and negatively associated with PD.
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Nicotine-mediated rescue of α-synuclein toxicity requires synaptic vesicle glycoprotein 2
Published: Parkinson’s disease likely reflects a complex interaction among genetic and environmental factors. Here, the role of nicotine, SV2 and the alpha-synuclein were examined. The study suggests that SV2 may be needed for the protection nicotine provides from Parkinson’s-related neurotoxicity. View original preprint.
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Targeting cellular senescence with senotherapeutics: senolytics and senomorphics
Review: This article reviews the current state of the development of senolytics and senomorphics for the treatment of age-related diseases and disorders and extension of healthy longevity. In addition, the challenges of documenting senolytic and senomorphic activity in pre-clinical models and the current state of the clinical application of the different senotherapeutics are discussed.
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Detecting Full-Length EccDNA with FLED and long-reads sequencing
The authors’ method takes advantage of nanopore long reads and enables unbiased reconstruction of full-length eccDNA sequences. FLED is implemented using Python3 which is freely available on GitHub (https://github.com/FuyuLi/FLED).
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The Parkinson’s disease protein alpha-synuclein is a modulator of processing bodies and mRNA stability
Genetic modulation of P-body components alters αS toxicity, and human genetic analysis lends support to the disease-relevance of these interactions. Beyond revealing an unexpected aspect of αS function and pathology, the authors’ data highlight the versatility of conformationally plastic proteins with high intrinsic disorder.
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α-synuclein promotes neuronal dysfunction and death by disrupting the binding of ankyrin to ß-spectrin
Published: The authors’ findings define a specific molecular mechanism by which elevated levels of α-synuclein in Parkinson’s disease and related α-synucleinopathies leads to neuronal dysfunction and death. View original preprint.
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Circular RNAs in the human brain are tailored to neuron identity and neuropsychiatric disease
Little is known about circular RNAs (circRNAs) in specific brain cells and human neuropsychiatric disease. This study shows that circular RNAs in the human brain are tailored to neuron identity and implicate circRNA-regulated synaptic specialization in neuropsychiatric diseases.
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Generation of locus coeruleus norepinephrine neurons from human pluripotent stem cells
Central norepinephrine (NE) neurons, located mainly in the locus coeruleus (LC), are implicated in diverse psychiatric and neurodegenerative diseases and are an emerging target for drug discovery. To facilitate their study, the authors developed a method to generate 40–60% human LC-NE neurons from human pluripotent stem cells.
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Transcriptional programs mediating neuronal toxicity and altered glial-neuronal signaling in a Drosophila knock-in tauopathy model
Mutations in the gene encoding tau cause autosomal dominant forms of frontotemporal dementia. Prior models of frontotemporal dementia replicate features of the disease but do not recreate the genetic context. This article presents a genetic model of tauopathy, which recapitulates the genetic context and phenotypic features of the disease.
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Pathways controlling neurotoxicity and proteostasis in mitochondrial complex I deficiency
Neuromuscular disorders caused by dysfunction of the mitochondrial respiratory chain are common, severe, and untreatable. The authors recovered a number of mitochondrial genes, including electron transport chain components, in a large forward genetic screen for mutations causing age-related neurodegeneration in the context of proteostasis dysfunction.
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Disease progression strikingly differs in research and real-world Parkinson’s populations
Characterization of Parkinson’s disease (PD) progression using real-world evidence could guide clinical trial design and identify subpopulations. This study characterizes Parkinson’s progression in diverse populations. It delineates systemic divergences in the patient populations enrolled in research settings vs. patients in the real world.
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Integrative analysis reveals a conserved role for the amyloid precursor protein in proteostasis during aging
Aβ peptides derived from the amyloid precursor protein (APP) have been implicated in the pathogenesis of Alzheimer’s disease. However, the normal function of APP is less clear. Results demonstrate a conserved role for APP in controlling age-dependent proteostasis with plausible relevance to Alzheimer’s disease.
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