• Biomedical Science Letters
• /
• v.26 no.1
• /
• pp.1-7
• /
• 2020

Alzheimer's disease (AD) is the most common neurodegenerative disorder and is expected to become more and more widespread as life expectancy increases. New therapeutic target, as well as the identification of mechanisms responsible for pathology, is urgently needed. Recently, microglial actin cytoskeleton has been proposed as a beneficial role in axon regeneration of brain injury. This review highlights in understanding of the characteristics of microglial actin cytoskeleton and discuss the role of specific actin-interacting proteins and receptors in AD. The precise mechanisms and functional aspects of motility by microglia require further study, and the regulation of microglial actin cytoskeleton might be a potential therapeutic strategy for neurological diseases.

• Korean Journal of Biological Psychiatry
• /
• v.17 no.4
• /
• pp.194-202
• /
• 2010

Alzheimer's disease(AD) is the most common neurodegenerative disorder and constitutes about two thirds of dementia. Despite a lot of effort to find drugs for AD worldwide, an efficient medicine that can cure AD has not come yet, which is due to the complicated pathogenic pathways and progressively degenerative properties of AD. In its early clinical phase, it is important to find the subtle alterations in synapses responsible for memory because symptoms of AD patients characteristically start with pure impairment of memory. Attempts to find the target synaptic proteins and their pathogenic pathways will be the most powerful alternative strategy for developing AD medicine. Here we review recent progress in deciphering the role of target synaptic proteins related to AD in hippocampal glutamatergic synapses.

• Nuclear Medicine and Molecular Imaging
• /
• v.41 no.2
• /
• pp.132-140
• /
• 2007

Parkinson's disease is a common neurodegenerative disorder that is mainly caused by dopaminergic neuron loss in the substantia nigra. Several radiopharmaceutics have been developed to evaluate the integrity of dopaminergic neuronal system. In vivo PET and SPECT imaging of presynaptic dopamine imaing are already applied to Parkinson's disease and other parkinsonism, and can demonstrate the dopaminergic dysfunction. This review summarized the use of the presynaptic dopaminergic imaging in PD as biomarkers in evaluation of disease progression as well as in diagnosis of PD.

• Journal of Yeungnam Medical Science
• /
• v.35 no.1
• /
• pp.1-6
• /
• 2018

Alzheimer's disease (AD) is a neurodegenerative disorder associated with extracellular plaques, composed of amyloid-beta ($A{\beta}$), in the brain. Although the precise mechanism underlying the neurotoxicity of $A{\beta}$ has not been established, $A{\beta}$ accumulation is the primary event in a cascade of events that lead to neurofibrillary degeneration and dementia. In particular, the $A{\beta}$ burden, as assessed by neuroimaging, has proved to be an excellent predictive biomarker. Positron emission tomography, using ligands such as $^{11}C$-labeled Pittsburgh Compound B or $^{18}F$-labeled tracers, such as $^{18}F$-florbetaben, $^{18}F$-florbetapir, and $^{18}F$-flutemetamol, which bind to $A{\beta}$ deposits in the brain, has been a valuable technique for visualizing and quantifying the deposition of $A{\beta}$ throughout the brain in living subjects. $A{\beta}$ imaging has very high sensitivity for detecting AD pathology. In addition, it can predict the progression from mild cognitive impairment to AD, and contribute to the development of disease-specific therapies.

• Proceedings of the PSK Conference
• /
• 2003.10a
• /
• pp.108-111
• /
• 2003

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra. While its precise etiology is unknown, such factors as oxidative stress, impairment of mitochondrial respiration, excitotoxicity and inflammation may play roles in its pathogenesis. Although the role of apoptosis in the process of dopaminergic neuronal death has been highlighted in studies using postmortem brains and experimental models of PD, other evidence implicates both apoptosis and non-apoptotic death in PD. (omitted)

• Biomolecules & Therapeutics
• /
• v.29 no.6
• /
• pp.596-604
• /
• 2021

Different lifestyles have an impact on useful metabolic functions, causing disorders. Different lipids are involved in the metabolic functions that play various vital roles in the body, such as structural components, storage of energy, in signaling, as biomarkers, in energy metabolism, and as hormones. Inter-related disorders are caused when these functions are affected, like diabetes, cancer, infections, and inflammatory and neurodegenerative conditions in humans. During the Covid-19 period, there has been a lot of focus on the effects of metabolic disorders all over the world. Hence, this review collectively reports on research concerning metabolic disorders, mainly cardiovascular and diabetes mellitus. In addition, drug research in lipid metabolism disorders have also been considered. This review explores lipids, metabolism, lipid metabolism disorders, and drugs used for these disorders.

• Journal of Genetic Medicine
• /
• v.18 no.1
• /
• pp.16-23
• /
• 2021

GLB1-related disorders comprise two phenotypically unique disorders: GM1 gangliosidosis and Morquio B disease. These autosomal recessive disorders are caused by b-galactosidase deficiency. A hallmark of GM1 gangliosidosis is central nervous system degeneration where ganglioside synthesis is highest. The accumulation of keratan sulfate is the suspected cause of the bone findings in Morquio B disease. GM1 gangliosidosis is clinically characterized by a neurodegenerative disorder associated with dysostosis multiplex, while Morquio B disease is characterized by severe skeletal manifestations and the preservation of intelligence. Morquio B disease and GM1 gangliosidosis may be on a continuum of skeletal involvement. There is currently no effective treatment for GLB1-related disorders. Recently, multiple interventions have been developed and there are several ongoing clinical trials.

• International Journal of Advanced Culture Technology
• /
• v.11 no.3
• /
• pp.9-17
• /
• 2023

Parkinson's disease is a complex neurodegenerative disease characterized by the progressive loss of dopamine-producing neurons in the substantia nigra, resulting in a variety of motor and non-motor symptoms. This study aimed to provide a comprehensive overview of Parkinson's disease, including classification of Parkinson's disease, impairment due to impairment, how disability is assessed, and how it is treated. Major symptoms of Parkinson's disease include tremors, stiffness, bradykinesia, and postural instability, and treatment methods include rehabilitation through drugs, surgical procedures, physical therapy, and occupational therapy. Early diagnosis, individualized treatment interventions, and comprehensive treatment involving a multidisciplinary medical team will be essential to manage Parkinson's disease and improve patients' quality of life. In conclusion, this study will provide comprehensive information on the complex nature of Parkinson's disease and serve as a useful guide for healthcare providers designing treatment plans for Parkinson's patients.

• Journal of Microbiology and Biotechnology
• /
• v.17 no.12
• /
• pp.2027-2032
• /
• 2007

[ ${\alpha}$ ]-Synuclein is the major component of Lewy bodies and responsible for the amyloid deposits observed in Parkinson's disease. Ordered filamentous aggregate formation of the natively unfolded ${\alpha}$-synuclein was investigated in vitro with the periodic ultrasonication. The ultrasonication induced the fibrillation of ${\alpha}$-synuclein, as the random structure gradually converted into a ${\beta}$-sheet structure. The resulting fibrils obtained at the stationary phase appeared heterogeneous in their size distribution, with the average length and height of $0.28\;{\mu}m{\pm}0.21\;{\mu}m$ and $5.6\;nm{\pm}1.9\;nm$, respectively. After additional extensive ultrasonication in the absence of monomeric ${\alpha}$-synuclein, the equilibrium between the fibril formation and its breakdown shifted to the disintegration of the preexisting fibrils. The resulting fragments served as nucleation centers for the subsequent seed-dependent accelerated fibrillation under a quiescent incubation condition. This self-seeding amplification process depended on the seed formation and subsequent alterations in their properties by the ultrasonication to a state that accretes the monomeric soluble protein more effectively than their reassociation of the seeds back to the original fibrils. Since many neurodegenerative disorders have been considered to be propagated via the seed-dependent amyloidosis, this study would provide a novel aspect of the significance of the seed structure and its properties leading to the acce]erated amyloid formation.

• Korean Journal of Agricultural Science
• /
• v.45 no.3
• /
• pp.509-519
• /
• 2018

This study was investigated the anti-oxidant property and neuro-protective effect of Cirsium japonicum var. maackii (CJM) against oxidative stress in hydrogen peroxide ($H_2O_2$)-induced C6 glial cells. We measured the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, hydroxyl radical (${\cdot}OH$), and superoxide ($O_2{^-}$) radical scavenging activities of an ethanol extract and four fractions [n-Butanol, ethyl acetate (EtOAc), $CHCl_3$, and n-Hexane] from CJM. The results of this study show that the extract and all fractions from CJM had a dose-dependent DPPH radical scavenging activity. In particular, the EtOAc fraction exhibited the strongest scavenging effect with 88.23% at a concentration of $500{\mu}g/mL$. In addition, the EtOAc fraction from CJM also effectively scavenged ${\cdot}OH$ radicals and $O_2{^-}$ radicals, compared to other extract and fractions. In C6 glial cells, $H_2O_2$ markedly decreased the cell viability as well as increased lactate dehydrogenase (LDH) release and reactive oxygen species (ROS) production. However, the EtOAc fraction of CJM attenuated the cellular damage from the oxidative stress by elevating the cell viability and inhibiting the LDH release and ROS over-production compared with the $H_2O_2$-treated control group. Our findings indicate that the EtOAc fraction from CJM has antioxidant effect and neuro-protective effect against oxidative stress, suggesting that it can be used as a natural antioxidant and therapeutic agent for the prevention of neurodegenerative disorders.