Publications by authors named "Junghyung Park"

Article Synopsis
  • Researchers have developed a stealthy neural recorder designed to monitor brain signals in non-human primates, allowing for the study of their natural behaviors.
  • The device features a fully implantable, wireless, battery-free module that records brain activity and movement, along with a flexible 32-electrode neural probe.
  • Successfully tested on a freely moving monkey, the recorder gathered data for over a month, which was then used to train an AI model to classify the animal's eating behaviors.
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  • Researchers developed LAT1-targeting nanoparticles (Phe-NPs) to effectively deliver RNA-based drugs across the blood-brain barrier.
  • These nanoparticles utilize a 25% density of phenylalanine to enhance binding affinity to LAT1 in GL261-Luc cells.
  • Biodistribution studies showed Phe-NPs/ASOs reached brain tissue significantly better than standard ASOs, indicating their potential for treating central nervous system diseases, including neurodegenerative disorders.
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Oxidative stress plays an essential role in the progression of Alzheimer's disease (AD), the most common age-related neurodegenerative disorder. Streptozotocin (STZ)-induced abnormal brain insulin signaling and oxidative stress play crucial roles in the progression of Alzheimer's disease (AD)-like pathology. Peroxiredoxins (Prxs) are associated with protection from neuronal death induced by oxidative stress.

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  • Maladaptive feeding behaviors are identified as a leading cause of obesity in modern society, and while research on the lateral hypothalamic area (LHA) and its influence on eating exists for rodents, similar studies in primates were lacking.
  • A study involving three macaques utilized chemogenetics to activate LHA GABAergic neurons, revealing that this activation increased goal-directed eating behaviors and heightened motivation for palatable food.
  • The research confirmed the effects using imaging techniques, showing that LHA activation enhanced connectivity with frontal brain areas while reducing connectivity among those areas, suggesting potential implications for understanding obesity therapies in both primates and humans.
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Till date, researchers have been developing animal models of Alzheimer's disease (AD) in various species to understand the pathological characterization and molecular mechanistic pathways associated with this condition in humans to identify potential therapeutic treatments. A widely recognized AD model that mimics the pathology of human AD involves the intracerebroventricular (ICV) injection with streptozotocin (STZ). However, ICV injection as an invasive approach has several limitations related to complicated surgical procedures.

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  • * It investigates how the uneven distribution of MPTP due to varying cerebral blood flow affects damage in specific brain regions, particularly the striatum, in three monkeys.
  • * Findings indicate that differences in blood flow velocity and anatomical structure of the circle of Willis can lead to asymmetrical brain damage, suggesting these factors should be considered for better Parkinson's models.
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Symptoms of Parkinson's disease (PD) caused by loss of dopaminergic neurons are accompanied by movement disorders, including tremors, rigidity, bradykinesia, and akinesia. Non-human primate (NHP) models with PD play an essential role in the analysis of PD pathophysiology and behavior symptoms. As impairments of hand dexterity function can affect activities of daily living in patients with PD, research on hand dexterity function in NHP models with chronic PD is essential.

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Ischemic stroke results from arterial occlusion and can cause irreversible brain injury. A non-human primate (NHP) model of ischemic stroke was previously developed to investigate its pathophysiology and for efficacy testing of therapeutic candidates; however, fine motor impairment remains to be well-characterized. We evaluated hand motor function in a cynomolgus monkey model of ischemic stroke.

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Aberrant brain insulin signaling plays a critical role in the pathology of Alzheimer's disease (AD). Mitochondrial dysfunction plays a role in the progression of AD, with excessive mitochondrial fission in the hippocampus being one of the pathological mechanisms of AD. However, the molecular mechanisms underlying the progression of AD and mitochondrial fragmentation induced by aberrant brain insulin signaling in the hippocampal neurons are poorly understood.

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To date, researchers have developed various animal models of Alzheimer's disease (AD) to investigate its mechanisms and to identify potential therapeutic treatments. A widely recognized model that mimics the pathology of human sporadic AD involves intracerebroventricular (ICV) injection with streptozotocin (STZ). However, ICV injections are an invasive approach, which creates limitations in generalizing the results.

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  • The study explores how interactions between the nervous system and immune system contribute to the development of Parkinson's disease (PD) and potential treatment options.
  • Research with non-human primates revealed chronic infiltration of T lymphocytes in the brain and changes in microglial activation after exposure to a specific neurotoxin (MPTP), which mimics PD.
  • Findings highlight the role of CD4+ and CD8+ T lymphocytes in neuron loss and suggest that understanding these immune responses could lead to better prevention and therapy for PD.
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  • Scientists studied brain cells (microglia/macrophages) after strokes in monkeys to learn more about their role.
  • They used special scans (MRI) to see how the brain injuries changed over time and how the monkeys' movements improved.
  • The study found that certain brain cells were important for healing and could help with treatments for strokes in the future.
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Pigs are often selected for large animal models including for neuroscience and behavioral research, because their anatomy and biochemistry are similar to those of humans. However, behavioral assessments, in combination with objective long-term monitoring, is difficult. In this study, we introduced an automated video tracking system which was previously used in rodent studies, for use with pig models.

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Mitochondria continuously fuse and divide to maintain homeostasis. An impairment in the balance between the fusion and fission processes can trigger mitochondrial dysfunction. Accumulating evidence suggests that mitochondrial dysfunction is related to neurodegenerative diseases such as Parkinson's disease (PD), with excessive mitochondrial fission in dopaminergic neurons being one of the pathological mechanisms of PD.

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Background: The guidelines for applying individual adjustments to macaques according to the severity of behavioral symptoms during 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment were provided to reproduce stable chronic Parkinsonism in a recent study (Potts et al., 2014). But, since there are insufficient guidelines regarding objective severity criteria of individual symptoms for adjustments of MPTP treatment, it is difficult to develop MPTP-induced chronic non-human primate (NHP) models with stable symptoms.

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Dysregulation of the production of pro-inflammatory mediators in microglia exacerbates the pathologic process of neurodegenerative disease. ROS actively affect microglia activation by regulating transcription factors that control the expression of pro-inflammatory genes. However, accurate information regarding the function of ROS in different subcellular organelles has not yet been established.

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This study was conducted to compare 3D-printed polycaprolactone (PCL) and polycaprolactone/β-tricalcium phosphate (PCL/β-TCP) membranes with a conventional commercial collagen membrane in terms of their abilities to facilitate guided bone regeneration (GBR). Fabricated membranes were tested for dry and wet mechanical properties. Fibroblasts and preosteoblasts were seeded into the membranes and rates and patterns of proliferation were analyzed using a kit-8 assay and by scanning electron microscopy.

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Oleuropein is a primary phenolic compound found in olive leaf and Fraxinus rhynchophylla. Here, we investigated the impact of oleuropein on LPS-induced BV-2 microglial cells. Oleuropein suppressed the LPS-induced increase in pro-inflammatory mediators, such as nitric oxide, and pro-inflammatory cytokines, via inhibition of ERK/p38/NF-κB activation and reactive oxygen species (ROS) generation.

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Aims: Aberrant Cdk5 (cyclin-dependent kinase 5) and oxidative stress are crucial components of diverse neurodegenerative disorders, including Alzheimer's disease (AD). We previously reported that a change in peroxiredoxin (Prx) expression is associated with protection from neuronal death. The aim of the current study was to analyze the role of Prx in regulating Cdk5 activation in AD.

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Microglial activation is a hallmark of neurodegenerative diseases. ROS activates microglia by regulating transcription factors to express pro-inflammatory genes and is associated with disruption of Ca homeostasis through thiol redox modulation. Recently, we reported that Prx5 can regulate activation of microglia cells by governing ROS.

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Iron is necessary for neuronal functions; however, excessive iron accumulation caused by impairment of iron balance could damage neurons. Neuronal iron accumulation has been observed in several neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. Nevertheless, the precise mechanisms underlying iron toxicity in neuron cells are not fully understood.

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Somatic cell nuclear transfer (SCNT) has been widely used as an efficient tool in biomedical research for the generation of transgenic animals from somatic cells with genetic modifications. Although remarkable advances in SCNT techniques have been reported in a variety of mammals, the cloning efficiency in domestic animals is still low due to the developmental defects of SCNT embryos. In particular, recent evidence has revealed that mitochondrial dysfunction is detected during the early development of SCNT embryos.

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Alzheimer's disease (AD), a neurodegenerative disorder, is caused by amyloid-beta oligomers (AβOs). AβOs induce cell death by triggering oxidative stress and mitochondrial dysfunction. A recent study showed that AβO-induced oxidative stress is associated with extracellular signal-regulated kinase (ERK)-dynamin related protein 1 (Drp1)-mediated mitochondrial fission.

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The accumulation of iron in neurons has been proposed to contribute to the pathology of numerous neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. However, insufficient research has been conducted on the precise mechanism underlying iron toxicity in neurons. In this study, we investigated mitochondrial dynamics in hippocampal HT-22 neurons exposed to ferric ammonium citrate (FAC) as a model of iron overload and neurodegeneration.

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