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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Spatial transcriptomics reveals molecular dysfunction associated with Lewy pathology
The results identify neurons vulnerable to Lewy pathology in the PD cortex and identify a conserved signature of molecular dysfunction in both mice and humans.
Synaptic Location Is a Determinant of the Detrimental Effects of α-Synuclein Pathology to Glutamatergic Transmission in the Basolateral Amygdala
Study explores α-synuclein's impact on amygdala in Parkinson's. Aggregation affects cortico-BLA transmission, linked to psychiatric deficits in PD.
Vibrational Stabilization of Cluster Synchronization in Oscillator Networks
Restoring normal cluster synchronization is crucial for system functioning. Vibrational control can stabilize synchronization without state measurements, offering a solution for challenging scenarios.
Vibrational Stabilization of Complex Network Systems
Many natural and man-made network systems need to maintain certain patterns, such as working at equilibria or limit cycles, to function properly. The authors provide some numerical results that demonstrate the validity of the theoretical findings.
A topographical atlas of α-synuclein dosage and cell type-specific expression in adult mouse brain and peripheral organs
This atlas provides much-needed insight into the cellular topography of αSyn, and provides a quantitative map to test assumptions about the role of αSyn in network vulnerability in PD and other αSynucleinopathies.
LRRK2 kinase inhibition reverses G2019S mutation-dependent effects on tau pathology spread
Mutations in LRRK2 are the most common cause of familial Parkinson’s disease. This work supports a protective role of LRRK2 kinase inhibition in G2019S carriers and provides a workflow for systematic evaluation of brain-wide phenotypes
Cortico-amygdala synaptic structural abnormalities produced by templated aggregation of α-synuclein
PD and DLB involve α-syn inclusions in the amygdala affecting cognition and emotions. Cortico-amygdala synapses with α-syn aggregates show increased volume of synapses, potentially contributing to behavioral impairments.
Vibrational Control of Complex Networks
Complex networks' stability is crucial, but real-time control can be challenging. This paper proposes using vibrational control on network edges instead of nodes to stabilize systems, providing graph-theoretic conditions and effective design methods.
Progressive vulnerability of cortical synapses in α-synucleinopathy
α-Synuclein aggregation is linked to progressive loss of intracortical VGLUT1+ excitatory synapses, spares VGLUT2+ long-range synapses, and impairs cortical excitatory transmission.
Network analysis of α-synuclein pathology progression reveals p21-activated kinases as regulators of vulnerability
Misfolded α-synuclein accumulation in PD leads to pathogenic processes. We mapped α-synuclein pathology in mice to identify vulnerable regions and potential therapeutic targets, highlighting group II PAK inhibitors as promising for treating PD.
Current safety recommendations for handling mouse and human αsynuclein pre-formed fibrils
The paper outlines best practices in conducting research with α-synuclein fibrils. We highlight steps in which extra precautions should be taken and how to minimize exposure and potential risk associated with use of PFFs in scientific research.
Network models of neurodegeneration: bridging neuronal dynamics and disease progression
We review computational models for Parkinson’s disease, covering neuronal dynamics and protein pathology spread and highlight how computational perspectives can improve understanding of disease progression in Parkinson’s disease.
