• The Korean Journal of Nuclear Medicine
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• v.35 no.4
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• pp.231-240
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• 2001

Purpose: Normal aging results in detectable changes in the brain structure and function. We evaluated the changes of regional cerebral glucose metabolism in the normal aging process with FDG PET. Materials and Methods: Brain PET images were obtained in 44 healthy volunteers (age range 20-69 'y'; M:F = 29:15) who had no history of neuropsychiatric disorders. On 6 representative transaxial images, ROIs were drawn in the cortical and subcortical areas. Regional FDG uptake was normalized using whole brain uptake to adjust for the injection dose and correct for nonspecific declines of glucose metabolism affecting all brain areas equally. Results: In the prefrontal, temporoparietal and primary sensorimotor cortex, the normalized FDG uptake (NFU) reached a peak in subjects in their 30s. The NFU in the prefrontal and primary sensorimotor cortex declined with age after 30s at a rate of 3.15%/decade and 1.93%/decade, respectively. However, the NFU in the temporoparietal cortex did not change significantly with age after 30s. The anterior (prefrontal) posterior (temporoparietal) gradient peaked in subjects in their 30s and declined with age thereafter at a rate of 2.35%/decade. The NFU in the caudate nucleus was decreased with age after 20s at a rate of 2.39%/decade. On the primary visual cortex, putamen, and thalamus, the NFU values did not change significantly throughout the ages covered. These patterns were not significantly different between right and left cerebral hemispheres. Of interest was that the NFU in the left cerebellar cortex was increased with age after 20s at a rate of 2.86%/decade. Conclusion: These data demonstrate regional variation of the age-related changes in the cerebral glucose metabolism, with the most prominent age-related decline of metabolism in the prefrontal cortex. The increase in the cerebellar metabolism with age might reflect a process of neuronal plasticity associated with aging.

• Journal of Life Science
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• v.26 no.1
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• pp.129-139
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• 2016

Exercise increases the expression and interaction of major neurotrophic factors such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and vascular endothelial growth factor (VEGF) at both central and peripheral tissues, which contributes to improved brain and neural plasticity and cognitive function. Previous findings have been to understand the effect of light or moderate intensity aerobic exercise on neurotrophic factors and cognitive function, not that of high intensity aerobic exercise. However, recent findings suggest that high intensity interval training is a safe, less time-consuming, efficient way to improve cardiorespiratory fitness and weight control, thus American College of Sport Medicine (ACSM)’s guidelines for exercise prescription for various adult populations also recommend the application of high intensity interval training to promote their overall health. High intensity interval training also enhances the expression of BDNF, IGF-1, and VEGF at the brain and peripheral tissues, which improves cognitive function. Increased frequency of intermittent hypoxia and increased usage of lactate as a supplementary metabolic resource at the brain and neural components are considered a putative physiological mechanism by which high intensity interval training improves neurotrophic factors and cognitive function. Therefore, future studies are required to understand how increased hypoxia and lactate usage leads to the improvement of neurotrophic factors and what the related biological mechanisms are. In addition, by comparing with the iso-caloric moderate continuous exercise, the superiority of high intensity interval training on the expression of neurotrophic factors and cognitive function should be demonstrated by associated future studies.

• Physical Therapy Korea
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• v.12 no.2
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• pp.73-80
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• 2005

We investigated the activation of the cerebral cortex during active movement, passive movement, and functional electrical stimulation (FES), which was provided on wrist extensor muscles. A functional magnetic resonance imaging study was performed on 5 healthy volunteers. Tasks were the extension of right wrist by active movement, passive movement, and FES at the rate of .5 Hz. The regions of interest were measured in primary motor cortex (M1), primary somatosensory cortex (SI), secondary somatosensory cortex (SII), and supplementary motor area (SMA). We found that the contralateral SI and SII were significantly activated by all of three tasks. The additional activation was shown in the areas of ipsilateral S1 (n=2), and contralateral (n=1) or ipsilateral (n=2) SII, and bilateral SMA (n=3) by FES. Ipsilateral M1 (n=1), and contralateral (n=1) or ipsilateral SII (n=1), and contralateral SMA (n=1) were activated by active movement. Also, Contralateral SMA (n=3) was activated by passive movement. The number of activated pixels on SM1 by FES ($12{\pm}4$ pixels) was smaller than that by active movement ($18{\pm}4$ pixels) and nearly the same as that by passive movement ($13{\pm}4$ pixels). Findings reveal that active movement, passive movement, and FES had a direct effect on cerebral cortex. It suggests that above modalities may have the potential to facilitate brain plasticity, if applied with the refined-specific therapeutic intervention for brain-injured patients.

• Annals of Clinical Neurophysiology
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• v.16 no.2
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• pp.62-69
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• 2014

Background: Neuromodulation therapy has been used to an adjunctive treatment promoting motor recovery in stroke patients. The objective of the study was to determine the effect of repetitive transcranial magnetic stimulation (rTMS) on neurobehavioral recovery and evoked potentials in rats with middle cerebral artery occlusion. Methods: Seventy Sprague-Daley rats were induced permanent middle cerebral artery occlusion (MCAO) stroke model and successful stroke rats (n=56) assigned to the rTMS (n=28) and sham (n=28) group. The 10 Hz, high frequency rTMS gave on ipsilesional forepaw motor cortex during 2 weeks in rTMS group. The somatosensory evoked potential (SSEP) and motor evoked potential (MEP) were used to evaluate the electrophysiological changes. Behavioral function of the stroke rat was evaluated by the Rota rod and Garcia test. Results: Forty rats ($N_{rTMS}=20;\;N_{sham}=20$) completed all experimental course. The rTMS group showed better performance than sham group in Rota rod test and Garcia test at day 11 (p<0.05) but not day 18 (p>0.05). The amplitude of MEP and SSEP in rTMS group was larger than sham group at day 18 (p<0.05). Conclusions: These data confirm that the high frequency rTMS on ipsilesional cerebral motor cortex can help the early recovery of motor performance in permanent middle cerebral artery stroke model and it may simultaneously associate with changes in neurophysiological activity in brain.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.6
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• pp.517-527
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• 2020

Layer 2/3 pyramidal neurons (L2/3 PyNs) of the cortex extend their basal dendrites near the soma and as apical dendritic tufts in layer 1, which mainly receive feedforward and feedback inputs, respectively. It is suggested that neuromodulators such as serotonin and acetylcholine may regulate the information flow between brain structures depending on the brain state. However, little is known about the dendritic compartment-specific induction of synaptic transmission in single PyNs. Here, we studied layer-specific serotonergic and cholinergic induction of long-term synaptic plasticity in L2/3 PyNs of the agranular insular cortex, a lateral component of the orbitofrontal cortex. Using FM1-43 dye unloading, we verified that local electrical stimulation to layers 1 (L1) and 3 (L3) activated axon terminals mostly located in L1 and perisomatic area (L2/3). Independent and AMPA receptor-mediated excitatory postsynaptic potential was evoked by local electrical stimulation of either L1 or L3. Application of serotonin (5-HT, 10 μM) induced activity-dependent longterm depression (LTD) in L2/3 but not in L1 inputs. LTD induced by 5-HT was blocked by the 5-HT₂ receptor antagonist ketanserin, an NMDA receptor antagonist and by intracellular Ca²⁺ chelation. The 5-HT₂ receptor agonist α-me-5-HT mimicked the LTD induced by 5-HT. However, the application of carbachol induced muscarinic receptor-dependent LTD in both inputs. The differential layer-specific induction of LTD by neuromodulators might play an important role in information processing mechanism of the prefrontal cortex.

• Korean Journal of Acupuncture
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• v.35 no.4
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• pp.187-202
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• 2018

Objectives : Non-invasive transcranial electrical stimulation is one of therapeutic interventions to change in neural excitability of the cortex. Transcranial electro-acupuncture (TEA) can modulate brain functions through changes in cortical excitability as a model of non-invasive transcranial electrical stimulation. Some composites of fermented Scutellaria baicalenis (FSB) can activate intercellular signaling pathways for activation of brain-derived neurotrophic factor that is critical for formation of neural plasticity in stroke patients. This study was aimed at evaluation of combinatory treatment of TEA and FSB on behavior recovery and cortical neural excitability in rodent focal stroke model. Methods : Focal ischemic stroke was induced by photothrombotic injury to the motor cortex of adult rats. Application of TEA with 20 Hz and $200{\mu}A$ in combination with daily oral treatment of FBS was given to stroke animals for 3 weeks. Motor recovery was evaluated by rotating bean test and ladder working test. Electrical activity of cortical pyramidal neurons of stroke model was evaluated by using multi-channel extracellular recording technique and thallium autometallography. Results : Compared with control stroke group who did not receive any treatment, Combination of TEA and FSB treatment resulted in more rapid recovery of forelimb movement following focal stroke. This combination treatment also elicited increase in spontaneous firing rate of putative pyramidal neurons. Furthermore expression of metabolic marker for neural excitability was upregulated in peri-infract area under thallium autometallography. Conclusions : These results suggest that combination treatment of TEA and FSB can be a possible remedy for motor recovery in focal stroke.

• BMB Reports
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• v.56 no.9
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• pp.520-525
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• 2023

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline. Several recent studies demonstrated that impaired adult neurogenesis could contribute to AD-related cognitive impairment. Adult subventricular zone (SVZ) neurogenesis, which occurs in the lateral ventricles, plays a crucial role in structural plasticity and neural circuit maintenance. Alterations in adult SVZ neurogenesis are early events in AD, and impaired adult neurogenesis is influenced by the accumulation of intracellular Aβ. Although Aβ-overexpressing transgenic 5XFAD mice are an AD animal model well representative of Aβ-related pathologies in the brain, the characterization of altered adult SVZ neurogenesis following AD progression in 5XFAD mice has not been thoroughly examined. Therefore, we validated the characterization of adult SVZ neurogenesis changes with AD progression in 2-, 4-, 8-, and 11-monthold male 5XFAD mice. We first investigated the Aβ accumulation in the SVZ using the 4G8 antibody. We observed intracellular Aβ accumulation in the SVZ of 2-month-old 5XFAD mice. In addition, 5XFAD mice exhibited significantly increased Aβ deposition in the SVZ with age. Next, we performed a histological analysis to investigate changes in various phases of adult neurogenesis, such as quiescence, proliferation, and differentiation, in SVZ. Compared to age-matched wild-type (WT) mice, quiescent neural stem cells were reduced in 5XFAD mice from 2-11 months of age. Moreover, proliferative neural stem cells were decreased in 5XFAD mice from 2 to 8 months of age. Furthermore, differentiations of neuroblasts were diminished in 5XFAD mice from 2-11 months of age. Intriguingly, we found that adult SVZ neurogenesis was reduced with aging in healthy mice. Taken together, our results revealed that impairment of adult SVZ neurogenesis appears with aging or AD progression.

• The Journal of Korean Physical Therapy
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• v.22 no.3
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• pp.31-35
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• 2010

Purpose: The aim of this study was to use fMRI and clinical prognosis criteria to evaluate therapeutic interventions in stroke patients with corona radiata infarct and acquire fundamental information about recovery mechanisms. Methods: Four subjects (2 men, 2 women) who had strokes with corona radiata infarct were recruited. For all subjects, motor functions such as motricity index (MI), modified brunnstrom classification (MBC), functional ambulatory category (FAC), and bathel index (BI) were evaluated. Evaluations were done at least 4 times over a period of approximately 6~7 months from stroke onset. We compared the final evaluation with the first. Results: All patients with corona radiata infarct showed improvement in motor outcomes with the passing of time. The strength of all patients improved from zero or trace levels to normal or good levels in the MI (Motricity Index) test. Other motor outcomes including the modified brunnstrom classification (MBC), the functional ambulatory category (FAC), and the bathel index (BI) also improved with the passing of time. Conclusion: Stroke patients with corona radiata infarcts change for the better over time. Therefore, one can introduce clinical interventions by the aspect of progress in functional motor recovery.

• Journal of International Academy of Physical Therapy Research
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• v.3 no.2
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• pp.429-434
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• 2012

Ischemia, the leading cause of strokes, is known to be deeply related to synaptic plasticity and apoptosis in tissue damage due to ischemic conditions or trauma. The purpose of this study was to research the effects of NEES(needle electrode electrical stimulation) in brain cells of ischemia-induced rat, more specifically the effects of Poly[ADP-ribose] polymerase(PARP) on the corpus striatum. Ischemia was induced in SD mice by occluding the common carotid artery for 5 minutes, after which blood was re-perfused. NEES was applied to acupuncture points, at 12, 24, and 48 hours post-ischemia on the joksamri, and at 24 hours post-ischemia on the hapgok. Protein expression was investigated through PARP antibody immuno-reactive cells in the cerebral nerve cells and western blotting. The number of PARP reactive cells in the corpus striatum 24 hours post-ischemia was significantly(p<.05) smaller in the NEES group compared to the global ischemia(GI) group. PARP expression 24 hours post-ischemia was very significantly smaller in the NEES group compared to the GI group. Results show that ischemia increases PARP expression and stimulates necrosis, making it a leading cause of death of nerve cells. NEES can decrease protein expression related to cell death, protecting neurons and preventing neuronal apoptosis.

• Journal of International Academy of Physical Therapy Research
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• v.7 no.2
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• pp.1031-1036
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• 2016

c-Fos is known to related to synaptic plasticity and apoptosis in damage from ischemia or external injury. The purpose of this study was to investigate whether needle electrode electrical stimulation(NEES) is effective in increasing the number of c-Fos response cells and c-Fos expression in striatum after global ischemia in rats. There were no treatment and occlusion in the control group, global ischemia(GI) group were no treatment after carotid artery occlusion, and needle electrode electrical stimulation(NEES) group were treated with NEES after GI induced. The number of striatum c-Fos response cells and c-Fos protein expression significantly decreased in the NEES group compared to the GI group after 12, 24, 48 hours. The results of the present study suggest that NEES is ineffective in improving global ischemia in rats and may also be ineffective in the globally ischemic human brain.