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.
-
Output Type
-
Program
-
CRN Team Name
-
Theme
Therapeutic deep brain stimulation disrupts movement-related subthalamic nucleus activity in Parkinsonian mice
Subthalamic nucleus deep brain stimulation (STN DBS) relieves many motor symptoms of Parkinson's Disease (PD), but its underlying therapeutic mechanisms remain unclear. Since its advent, three major theories have been proposed: (1) DBS inhibits…
Adaptor protein-3 produces synaptic vesicles that release phasic dopamine
The burst firing of midbrain dopamine neurons releases a phasic dopamine signal that mediates reinforcement learning. At many synapses, however, high firing rates deplete synaptic vesicles (SVs), resulting in synaptic depression that limits release.…
Reduced striatal M4-cholinergic signaling following dopamine loss contributes to parkinsonian and l-DOPA–induced dyskinetic behaviors
Imbalances in dopamine and acetylcholine affect motor function in Parkinson's disease. Contrary to conventional theories, reduced cholinergic transmission at M4 receptors in dopamine-depleted mice alleviated motor deficits and dyskinetic behavior.
Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production
Respiratory chain dysfunction affects ATP and ROS levels. Knockdown of genes in specific respiratory complexes increases ROS, while metabolic conditions have little impact on ROS. Ether lipids play a role in regulating ROS independently of ATP.
Dopamine across timescales and cell types: Relevance for phenotypes in Parkinson’s disease progression
Dopamine neurons in the SNc are crucial for movement and learning. In Parkinson's Disease, their degeneration leads to various symptoms. Recent research highlights heterogeneity in these neurons, impacting PD progression and treatment development.
Alterations in neurotransmitter co-release in Parkinson’s disease
Parkinson's disease involves degeneration of dopamine neurons, leading to basal ganglia circuit changes. These neurons also release glutamate and GABA. Understanding co-release dynamics could help identify circuit dysfunction in Parkinson's disease.
The role of α-synuclein in exocytosis
Review focuses on α-synuclein's role in exocytosis, a key process in Parkinson's disease. Despite unclear pathogenesis, evidence points to αsyn's involvement in regulating cellular processes.
Role of dopamine neuron activity in Parkinson’s disease pathophysiology
Neural activity disruptions in neurodegenerative diseases like Parkinson's may occur early. Abnormal dopamine neuron activity in PD could worsen neurotoxic effects, offering insight for future treatments to protect these neurons.
Chronic hyperactivation of midbrain dopamine neurons causes preferential dopamine neuron degeneration
Parkinson’s disease is linked to substantia nigra dopamine neuron death. To determine if chronic changes in activity of these neurons plays a role, the authors created a mouse model. This resulted in altered motor activity and selective neuron…
Aberrant striatal firing mediates impulsive decision-making in a mouse model of Parkinson’s disease
Neurodegeneration in Parkinson's disease causes motor and non-motor symptoms. Dopamine therapy helps motor symptoms but can lead to impulse disorders. A mouse model showed how dopamine agonists affect striatal neurons to drive impulsive decisions.
Excessive firing of dyskinesia-associated striatal direct pathway neurons is gated by dopamine and excitatory synaptic input
-FosTRAP captures striatal neurons activated in levodopa-induced dyskinesia -Levodopa evokes high firing rates in TRAPed direct pathway striatal neurons (dMSNs) -TRAPed dMSNs show enhanced dopamine sensitivity and excitatory synaptic input
CHCHD2 mutant mice link mitochondrial deficits to PD pathophysiology
Mutations in mitochondrial protein CHCHD2 lead to a form of Parkinson's disease. CHCHD2 T61I mutant mice show molecular changes in the brain, altered metabolism favoring glycolysis, and disrupted mitochondrial function in dopamine neurons.
⍺-Synuclein levels in Parkinson’s disease – Cell types and forms that contribute to pathogenesis
Parkinson's disease is characterized by dopamine neuron loss and ⍺-synuclein aggregations in neurons. Research focuses on understanding the levels, modifications, and impact of ⍺-synuclein in brain cells, including non-neuronal cells.
Postsynaptic adaptations in direct pathway muscarinic M4-receptor signaling follow the temporal and regional pattern of dopaminergic degeneration
Imbalances in dorsal striatum output in Parkinson's disease are driven by dopamine loss and disrupted acetylcholine signaling. These changes occur in response to dopamine loss, affecting M4 receptors in striatal neurons, crucial for PD progression.
Leveraging animal models to understand non-motor symptoms of Parkinson’s disease
Parkinson's disease diagnosis focuses on motor symptoms, but non-motor symptoms like cognitive issues and sleep disorders significantly affect patients. Research on non-motor signs in animals aims to improve understanding of the disease.
