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.
Analysis codes related to “Disruption of lysosomal proteolysis in astrocytes facilitates midbrain organoid proteostasis failure in an early-onset Parkinson’s disease model”
Analysis codes related to “Disruption of lysosomal proteolysis in astrocytes facilitates midbrain organoid proteostasis failure in an early-onset Parkinson’s disease model.”
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ATP13A2 Regulates Cellular α-Synuclein Multimerization, Membrane Association, and Externalization
Published: ATP13A2 loss-of-function mutations cause lysosomal deficiency and are linked to Parkinson’s disease and alpha-synuclein pathology. The authors found that loss of ATP13A2 disrupts lysosomal membrane integrity and causes alpha-synuclein multimerization. Further, they showed that increased levels of ATP13A2 had a protective effect on alpha-synuclein aggregation.
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The lysosome as a master regulator of iron metabolism
Review: This review focuses on the role that the lysosome plays in maintaining iron homeostasis and how lysosomal iron dysregulation contributes to disease.
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Lysosomal dysfunction in neurodegeneration: emerging concepts and methods
Review: This review summarizes key technological advances that have led to a better understanding of the contribution of the lysosome to neurodegeneration and highlights key questions to be addressed moving forward.
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Rodent models based on endolysosomal genes involved in Parkinson’s disease
Review: This review summarizes parkinsonian phenotypes in rodent models targeting genes that have a role in endolysosomal pathways and future steps to better understand the contribution of endolysosomal dysfunction to PD.
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Inter-organellar communication in Parkinson’s and Alzheimer’s disease: looking beyond endoplasmic reticulum-mitochondria contact sites
Review: Here, authors summarize the contributions of membrane contact sites in dysregulation of inter-organellar communication, taking findings from Parkinson’s and Alzheimer’s as major examples.
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Neuropathological Features of Gaucher Disease and Gaucher Disease with Parkinsonism
Review: To better understand the disease pathogenesis of Gaucher Disease, the authors reviewed the neuropathological features associated with glucocerebrosidase deficiency, examining autopsy studies of rare patients with GD.
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Lyso-IP: Uncovering Pathogenic Mechanisms of Lysosomal Dysfunction
Review: The development of the Lyso-IP approach and similar methods now allow for lysosomal purification within ten minutes. This review discusses the impact of this new methodology in uncovering the role of lysosomes in neurodegenerative conditions.
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Disruption of lysosomal proteolysis in astrocytes facilitates midbrain proteostasis failure in an early-onset PD model
Published: Accumulation of advanced glycation end products (AGEs) on biopolymers accompany cellular aging and drives poorly understood disease processes. Here, authors studied how AGEs contribute to development of early on-set Parkinson’s disease (PD) caused by loss-of-function of DJ1, a protein deglycase. View original preprint.
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pLenti HsATP10B_WT-T2A-His-flag-TMEM30A
Transfer plasmid for lentiviral vector production expressing Hs ATP10B WT and His/Flag tagged Hs TMEM30A.
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pLenti HsATP10B_D433N-T2A-His-flag-TMEM30A
Transfer plasmid for lentiviral vector production expressing Hs ATP10B D433N mutant and His/flag tagged Hs TMEM30A.
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Lysosome proteolysis analysis with DQ-BSA
Protocol to analyze lysosomal proteolysis in astrocytes generated from iPSCs.
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Astrocyte extraction from brain organoids V.2
Protocol for astrocyte extraction from brain organoids.
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P5B-ATPases in the mammalian polyamine transport system and their role in disease
Review: This review brings together the current knowledge of the cellular function of the mammalian polyamine transport system, focusing on the role of P5B-ATPases ATP13A2-5.
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