Hong‐Yuan Chu

ORCID: 0000-0003-0923-683X
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About
Contact & Profiles
Research Areas
  • Neurological disorders and treatments
  • Neuroscience and Neuropharmacology Research
  • Parkinson's Disease Mechanisms and Treatments
  • Neuroscience and Neural Engineering
  • Neurotransmitter Receptor Influence on Behavior
  • Genetic Neurodegenerative Diseases
  • Receptor Mechanisms and Signaling
  • Neural dynamics and brain function
  • Attention Deficit Hyperactivity Disorder
  • EEG and Brain-Computer Interfaces
  • Ion channel regulation and function
  • Functional Brain Connectivity Studies
  • Nerve injury and regeneration
  • Epilepsy research and treatment
  • Photoreceptor and optogenetics research
  • Zebrafish Biomedical Research Applications
  • Pharmacological Effects and Toxicity Studies
  • Motor Control and Adaptation
  • Transcranial Magnetic Stimulation Studies
  • Hemoglobinopathies and Related Disorders
  • Ginseng Biological Effects and Applications
  • Cardiovascular Health and Risk Factors
  • Infectious Encephalopathies and Encephalitis
  • Neurology and Historical Studies
  • Global Public Health Policies and Epidemiology

Van Andel Institute
2020-2025

Georgetown University
2024-2025

Research Network (United States)
2022-2025

Georgetown University Medical Center
2024-2025

Peking University First Hospital
2023-2025

Peking University
2023-2025

Georgetown College
2024

Aligning Science Across Parkinson's
2024

Northwestern University
2015-2019

Northwestern University
2018

Abstract Background Cardiovascular diseases (CVD) represent a major global health challenge, necessitating up-to-date data on its burden for effective care planning and resource allocation. This study comprehensively analyzes the global, regional, national CVD associated risks from 1990 to 2021. Methods Results We performed secondary analysis of risk factors using Global Burden Disease (GBD) 2021 study. In 2021, there were 612 million cases globally, accounting 26.8% all deaths. From...

10.1093/qjmed/hcaf022 article EN QJM 2025-01-23

Dopamine (DA) in the basolateral amygdala (BLA) promotes fear learning by disinhibiting principal neurons (PNs) and enabling synaptic plasticity their sensory inputs. While BLA interneurons (INs) are heterogeneous, it is unclear which interneuron subtypes decrease GABAergic input to PNs presence of DA. Here, using cell type-selective photostimulation channelrhodopsin 2 slices from mouse brain, we examined role parvalbumin-positive INs (PV-INs), major interneuronal subpopulation BLA,...

10.1523/jneurosci.2997-12.2012 article EN cc-by-nc-sa Journal of Neuroscience 2012-10-17

The hypokinetic motor symptoms of Parkinson's disease (PD) are closely linked with a decreased cortical output as consequence elevated basal ganglia inhibition. However, whether and how the loss dopamine (DA) alters cellular properties neurons in PD remains undefined. We induced parkinsonism adult C57BL/6 mice both sexes by injecting neurotoxin, 6-hydroxydopamine (6-OHDA), into medial forebrain bundle. By using

10.1523/jneurosci.2694-20.2021 article EN cc-by-nc-sa Journal of Neuroscience 2021-05-18

The presynaptic protein α-synuclein (αSyn) has been suggested to be involved in the pathogenesis of Parkinson’s disease (PD). In PD, amygdala is prone develop insoluble αSyn aggregates, and it that circuit dysfunction involving contributes psychiatric symptoms. Yet, how aggregates affect function unknown. this study, we examined glutamatergic axon terminals impact its aggregation on transmission basolateral (BLA). We found primarily present vesicular glutamate transporter 1-expressing...

10.7554/elife.78055 article EN cc-by eLife 2022-07-01

Abnormal subthalamic nucleus (STN) activity is linked to impaired movement in Parkinson’s disease (PD). The autonomous firing of STN neurons, which contributes their tonic excitation the extrastriatal basal ganglia and shapes integration synaptic input, downregulated PD models. Using electrophysiological, chemogenetic, genetic, optical approaches, we find that chemogenetic activation indirect pathway striatopallidal neurons downregulates intrinsic normal mice but this effect occluded...

10.1016/j.celrep.2019.06.076 article EN cc-by-nc-nd Cell Reports 2019-07-01

Degeneration of midbrain dopaminergic (DA) neurons alters the connectivity and functionality basal ganglia-thalamocortical circuits in Parkinson’s disease (PD). Particularly, aberrant outputs primary motor cortex (M1) contribute to parkinsonian deficits. However, cortical adaptations at cellular synaptic levels parkinsonism remain poorly understood. Using multidisciplinary approaches, we found that DA degeneration induces cell subtype– input-specific reduction thalamic excitation M1...

10.1126/sciadv.adg3038 article EN cc-by-nc Science Advances 2023-08-23

10.4103/1673-5374.392884 article EN cc-by-nc-sa Neural Regeneration Research 2024-01-08

Abstract The small molecule protein α-synuclein forms insoluble aggregates in a group of neurological disorders, including Parkinson’s disease and dementia with Lewy bodies (DLB), which are collectively called synucleinopathies. In PD DLB, the amygdala has been identified as particularly susceptible region brain for deposition Lewy-like aggregates. Though aggregation is closely associated neurodegeneration, there poor correlation between neurodegeneration clinical features PD/DLB. We...

10.1101/2024.05.20.594995 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2024-05-20

Abstract Decreased excitability of pyramidal tract neurons in layer 5B (PT5B) primary motor cortex (M1) has recently been shown a dopamine-depleted mouse model parkinsonism. We hypothesized that decreased PT5B neuron would substantially disrupt oscillatory and non-oscillatory firing patterns 5 (L5) (M1). To test this hypothesis, we performed computer simulations using previously validated M1. Inclusion the experimentally identified parkinsonism-associated decrease into our computational...

10.1101/2024.05.23.595566 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2024-05-23

ΑBSTRACT: In Parkinson's disease (PD), Lewy pathology deposits in the cerebral cortex, but how disrupts cortical circuit integrity and function remains poorly understood. To begin to address this question, we injected α-synuclein (αSyn) preformed fibrils (PFFs) into dorsolateral striatum of mice seed αSyn cortex induce degeneration midbrain dopaminergic neurons. We reported that aggregates accumulate motor a layer- cell-subtype-specific pattern. Specifically, aggregates-bearing...

10.1038/s41531-024-00867-z article EN cc-by npj Parkinson s Disease 2025-01-15

<title>Abstract</title> Recent evidence suggests that the primary motor cortex (M1) layer 5B pyramidal tract (PT5B) neurons show a decreased intrinsic excitability in mouse models of parkinsonism, which perhaps plays an important role pathophysiology parkinsonian symptoms. PT5B project to outputs brainstem and spinal cord, leading direct expression Parkinson’s disease (PD) pathology. We set out explore how neuron influences activity patterns M1 network. Using NEURON/NetPyNE simulators, we...

10.21203/rs.3.rs-6254909/v1 preprint EN Research Square (Research Square) 2025-04-11

Dopamine (DA) profoundly modulates excitatory synaptic transmission and plasticity in the brain. In present study effects of SKF83959, selective agonist phosphatidylinositol (PI)-linked D(1) -like receptor, on were investigated rat hippocampus. SKF83959 (10-100 μM) reversibly suppressed field postsynaptic potential (fEPSP) elicited by stimulating Schaffer's collateral-commissural fibers CA1 area hippocampal slices. However, inhibition was not blocked receptor antagonist SCH23390, D(2)...

10.1002/jnr.22653 article EN Journal of Neuroscience Research 2011-05-02

The primary motor cortex (M1) integrates sensory and cognitive inputs to generate voluntary movement. Its functional impairments have been implicated in the pathophysiology of symptoms Parkinson's disease (PD). Specifically, dopaminergic degeneration basal ganglia dysfunction entrain M1 neurons into abnormally synchronized bursting pattern activity throughout cortico-basal ganglia-thalamocortical network. However, how midbrain affects anatomy, microcircuit connectivity, function network...

10.1523/eneuro.0010-24.2024 article EN cc-by-nc-sa eNeuro 2024-04-24

Abnormal accumulation of insoluble α-synuclein (α-Syn) inclusions in neurons, neurites, and glial cells is the defining neuropathology synucleinopathies, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), multiple system atrophy. Accumulation α-Syn amygdala has been well-documented post-mortem studies PD DLB brains, as well preclinical animal models these conditions. Though pathology closely associated neurodegeneration, there a poor correlation between neuronal loss...

10.1016/j.nbd.2024.106702 article EN cc-by Neurobiology of Disease 2024-10-13

Although the potent anti-parkinsonian action of atypical D₁-like receptor agonist SKF83959 has been attributed to selective activation phosphoinositol(PI)-linked D₁ receptor, whereas mechanism underlying its neuroprotective effect is not fully understood. In present study, actions on neuronal membrane potential and excitability were investigated in CA1 pyramidal neurons rat hippocampal slices. (10-100 µM) caused a concentration-dependent depolarization, associated with reduction input...

10.1371/journal.pone.0013118 article EN cc-by PLoS ONE 2010-10-01

l-Stepholidine (l-SPD), a tetrahydroprotoberberine alkaloid, possesses pharmacological profile of D₁/5-HT(1A) agonist and D₂ antagonist. This unique makes it promising novel antipsychotic candidate. Preliminary clinical trials animal experiments suggest that l-SPD improves both positive negative symptoms schizophrenia without producing significant extrapyramidal side effects. To further explore the mechanisms drug, we studied effects on activity dopamine (DA) neurons in ventral tegmental...

10.1002/syn.20855 article EN Synapse 2010-08-31
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