Publications by authors named "Kyung-Rok Nam"

Purpose: Many patients with Alzheimer's disease (AD) also have psychosis, and it has been reported that these patients have more severely impaired cognitive functions than patients without psychosis. The glutamatergic system in the brain is known to play an important role in memory and learning in the neural circuits. However, there has been limited research on how antipsychotic drugs affect the glutamatergic system of AD.

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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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Objectives: Alzheimer's disease (AD) is characterised by amyloid-beta accumulation (A), tau aggregation (T) and neurodegeneration (N). Vascular (V) burden has been found concomitantly with AD pathology and has synergistic effects on cognitive decline with AD biomarkers. We determined whether cognitive trajectories of AT(N) categories differed according to vascular (V) burden.

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  • The study evaluated escitalopram's effectiveness on adolescent depression using animal models and brain imaging techniques.
  • Restraint stress was applied to create depression-like conditions, and escitalopram treatment showed no significant changes in behavior or body weight compared to the control group.
  • Results indicated no notable improvements in neural activity or cell survival in the brain, leading to the conclusion that escitalopram may not be beneficial for treating adolescent depression.
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Introduction: Traumatic events in early life have a deleterious effect on the development of normal brain developments, which may be a cause of various psychiatric disorders in adulthood. Most prior studies focused on molecular biological aspects, and research on functional changes in neural circuits is still limited. We aimed to elucidate the effect of early life stress on excitation-inhibition and serotonergic neurotransmission in the adulthood using non-invasive functional molecular imaging (positron emission tomography, PET).

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  • The article in question has been amended to address some inaccuracies or issues that were identified.
  • The DOI provided (10.3389/fnins.2022.930613) leads to the original article, which now has a corrected version available.
  • Readers are encouraged to refer to the updated version for accurate information and findings.
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This study aimed to investigate how amyloid pathology affects the functional aspects of neurotransmitter systems in Alzheimer's disease. APPswe/PS2 mice (21 months of age) and wild-type (WT) mice underwent positron emission tomography (PET) and magnetic resonance spectroscopy (MRS). First, we obtained F-FDG and F-florbetaben PET scans to evaluate neuronal integrity and amyloid pathology.

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Developmental complex trauma is strongly associated with various psychiatric disorders in adulthood. Multiple lines of evidence have demonstrated that the amygdala-mPFC circuit regulates emotion and plays an important role in stress reactions. However, most studies on developmental trauma have mainly focused on neurological aspects in biological, behavioral, and structural changes with regard to a single stressor.

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: Micro-positron emission tomography (micro-PET), a small-animal dedicated PET system, is used in biomedical studies and has the quantitative imaging capabilities of radiotracers. A single-bed system, commonly used in micro-PET, is laborious to use in large-scale studies. Here, we evaluated the image qualities of a multi-bed system.

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Early life stress (ELS) is strongly associated with psychiatric disorders such as anxiety, depression, and schizophrenia in adulthood. To date, biological, behavioral, and structural aspects of ELS have been studied extensively, but their functional effects remain unclear. Here, we examined NeuroPET studies of dopaminergic, glutamatergic, and serotonergic systems in ELS animal models.

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Alzheimer's disease (AD) is a chronic neurodegenerative disorder and the leading cause of dementia, but therapeutic treatment options are limited. Taurine has been reported to have neuroprotective properties against dementia, including AD. The present study aimed to investigate the treatment effect of taurine in AD mice by functional molecular imaging.

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  • Alzheimer's disease (AD) is a progressive brain disorder characterized by the accumulation of amyloid-beta (Aβ), and this study focused on how eliminating microglia affects its progression in 5xFAD mice.
  • The administration of PLX3397, a drug that inhibits specific receptors, led to a significant reduction in Aβ deposits and improved levels of key proteins related to synaptic function in the brain.
  • Results showed that PLX3397 not only reversed changes in synaptic markers but also enhanced dopaminergic signaling, indicating that targeting microglial cells may offer a promising treatment strategy for neurodegenerative diseases like AD.
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Purpose: Neuroinflammation in Parkinson's disease (PD) is known to play a pivotal role in progression to neuronal degeneration. It has been reported that colony-stimulation factor 1 receptor (CSF-1R) inhibition can effectively deplete microglia. However, its therapeutic efficacy in PD is unclear still now.

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The major pathologies of Alzheimer's disease (AD) are amyloid plaques and hyperphosphorylated tau. The deposition of amyloid plaques leads to synaptic dysfunction, neuronal cell death, and cognitive impairment. Among the neurotransmitters, glutamate is the most abundant in the mammalian brain and plays an important role in synaptic plasticity.

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The purpose of this study was to determine whether the brain uptake of [ F]FPEB is influenced by P-glycoprotein (P-gp) and breast cancer resistance protein (Bcrp) as efflux transporters in rodents. To assess this possible modulation, positron emission tomography studies were performed in animal models of pharmacological or genetic ablation of these transporters. Compared with the control conditions, when P-gp was blocked with tariquidar, there was an 8%-12% increase in the brain uptake of [ F]FPEB.

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