• BMB Reports
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• v.41 no.8
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• pp.560-567
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• 2008

The importance of lipids in cell signaling and tissue physiology is demonstrated by the many CNS pathologies involving deregulated lipid metabolism. One such critical metabolic event is the activation of phospholipase $A_2$ ($PLA_2$), which results in the hydrolysis of membrane phospholipids and the release of free fatty acids, including arachidonic acid, a precursor for essential cell-signaling eicosanoids. Reactive oxygen species (ROS, a product of arachidonic acid metabolism) react with cellular lipids to generate lipid peroxides, which are degraded to reactive aldehydes (oxidized phospholipid, 4-hydroxynonenal, and acrolein) that bind covalently to proteins, thereby altering their function and inducing cellular damage. Dissecting the contribution of $PLA_2$ to lipid peroxidation in CNS injury and disorders is a challenging proposition due to the multiple forms of $PLA_2$, the diverse sources of ROS, and the lack of specific $PLA_2$ inhibitors. In this review, we summarize the role of $PLA_2$ in CNS pathologies, including stroke, spinal cord injury, Alzheimer's, Parkinson's, Multiple sclerosis-Experimental autoimmune encephalomyelitis and Wallerian degeneration.

• Clinical and Experimental Pediatrics
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• v.64 no.3
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• pp.103-110
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• 2021

Inflammatory or immune-mediated demyelinating central nervous system (CNS) syndromes include a broad spectrum of clinical phenotype and different overlapping diseases. Antibodies against myelin oligodendrocyte glycoprotein (MOG-Ab) have been found in some cases of these demyelinating diseases, particularly in children. MOG-Ab is associated with a wider clinical phenotype not limited to neuromyelitis optica spectrum disorder, with most patients presenting with optic neuritis, acute disseminated encephalomyelitis (ADEM) or ADEM-like encephalitis with brain demyelinating lesions, and/or myelitis. Using specific cell-based assays, MOG-Ab is becoming a potential biomarker of inflammatory demyelinating disorders of the CNS. A humoral immune reaction against MOG was recently found in monophasic diseases and recurrent/multiphasic clinical progression, particularly in pediatric patients. This review summarizes the data regarding MOG-Ab as an impending biological marker for discriminating between these diverse demyelinating CNS diseases and discusses recent developments, clinical applications, and findings regarding the immunopathogenesis of MOG-Ab-associated disorders.

• Journal of Ginseng Research
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• v.37 no.1
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• pp.8-29
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• 2013

Ginseng is one of the most widely used herbal medicines in human. Central nervous system (CNS) diseases are most widely investigated diseases among all others in respect to the ginseng's therapeutic effects. These include Alzheimer's disease, Parkinson's disease, cerebral ischemia, depression, and many other neurological disorders including neurodevelopmental disorders. Not only the various types of diseases but also the diverse array of target pathways or molecules ginseng exerts its effect on. These range, for example, from neuroprotection to the regulation of synaptic plasticity and from regulation of neuroinflammatory processes to the regulation of neurotransmitter release, too many to mention. In general, ginseng and even a single compound of ginsenoside produce its effects on multiple sites of action, which make it an ideal candidate to develop multi-target drugs. This is most important in CNS diseases where multiple of etiological and pathological targets working together to regulate the final pathophysiology of diseases. In this review, we tried to provide comprehensive information on the pharmacological and therapeutic effects of ginseng and ginsenosides on neurodegenerative and other neurological diseases. Side by side comparison of the therapeutic effects in various neurological disorders may widen our understanding of the therapeutic potential of ginseng in CNS diseases and the possibility to develop not only symptomatic drugs but also disease modifying reagents based on ginseng.

• Sleep Medicine and Psychophysiology
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• v.24 no.1
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• pp.5-11
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• 2017

The use of alcohol is associated with the development and worsening of sleep disorder. Alcohol is generally known to have a sedative effect, but it has an arousal or sedative effect depending on the timing and drinking dose and directly affects REM sleep physiology. Alcohol acts on the central nervous system (CNS) to interfere with the sleep-wake cycle and to affect sleep-related hormone secretion. In addition, the ingestion of alcohol pre-sleep is associated with deterioration and development of sleep related breathing disorders (SBD). The increase in resistance of the upper respiratory tract and the decrease in sensitivity of the CNS respiratory center and the respiratory muscles are major mechanisms of alcohol-induced SBD, and result in snoring or apnea in healthy men or aggravating apnea in patients with OSA. Sleep-related restless leg syndrome and circadian rhythm disorders are common in alcohol use disorder patients. This review provides an assessment of scientific studies that investigated on the impact of alcohol ingestion on nocturnal sleep physiology and sleep disorders.

• Interdisciplinary Bio Central
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• v.2 no.4
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• pp.9.1-9.5
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• 2010

Many neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, are devastating disorders that affect millions of people worldwide. However, the number of therapeutic options remains severely limited with only symptomatic management therapies available. With the better understanding of the pathogenesis of neurodegenerative diseases, discovery efforts for disease-modifying drugs have increased dramatically in recent years. However, the process of translating basic science discovery into novel therapies is still lagging behind for various reasons. The task of finding new effective drugs targeting central nervous system (CNS) has unique challenges due to blood-brain barrier (BBB). Furthermore, the relatively slow progress of neurodegenerative disorders create another level of difficulty, as clinical trials must be carried out for an extended period of time. This review is intended to provide molecular and cell biologists with working knowledge and resources on CNS drug discovery and development.

• Sleep Medicine and Psychophysiology
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• v.12 no.1
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• pp.58-63
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• 2005

Objectives: REM sleep behavior disorder (RBD), characterized by excessive motor activity during REM sleep, is associated with loss of muscle atonia. In recent years, it has been reported that RBD has high co-morbidity with CNS disorders (especially, Parkinson's disease, dementia, multiple system atrophy, etc.). We aimed to assess differences in clinical and polysomnographic findings among RBD patients, depending on the presence or absence of central nervous system (CNS) disorders. Methods: The medical records and polysomnographic data of 81 patients who had been diagnosed as having RBD were reviewed. The patients were classified into two groups: associated RBD (aRBD, i.e., with a clinical history and/or brain MRI evidence of CNS disorder) and idiopathic RBD (iRBD, i.e., without a clinical history and/or brain MRI evidence of CNS disorder) groups. Twenty-one patients (25.9%) belonged to the aRBD group and 60 patients (74.1%) belonged to the iRBD group. The clinical characteristics and polysomnographic findings of the two groups were compared. Results: Periodic limb movement disorder (PLMD), i.e., PLMI (periodic limb movement index)>5, was observed more frequently in the aRBD group than in the iRBD group (p<0.001, Fisher's exact test). Also, obstructive sleep apnea syndrome (OSAS), i.e., RDI (respiratory disturbance index)>5, was found more frequently in the aRBD group (p=0.0042, Fisher's exact test). The percentages for slow wave sleep and sleep efficiency were significantly lower in the aRBD group than in the iRBD group. Conclusion: We found that 1 out of 4 RBD patients had associated CNS disorders, warranting more careful neurological evaluation and follow-up in this category of RBD. In this category of RBD patients, we also found more frequent PLMD and OSAS. These patients were also found to have lower slow wave sleep and sleep efficiency. In summary, RBD patients with associated CNS disorders suffer from more disturbed sleep than those without them.

• Molecules and Cells
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• v.25 no.2
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• pp.149-157
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• 2008

Dopamine is a major neurotransmitter in the mammalian central nervous system (CNS) that regulates neuroendocrine functions, locomotor activity, cognition and emotion. The dopamine system has been extensively studied because dysfunction of this system is linked to various pathological conditions including Parkinson's disease, schizophrenia, Tourette's syndrome, and drug addiction. Accordingly, intense efforts to delineate the full complement of signaling pathways mediated by individual receptor subtypes have been pursued. Dopamine D1-like receptors are of particular interest because they are the most abundant dopamine receptors in CNS. Recent work suggests that dopamine signaling could be regulated via dopamine receptor interacting proteins (DRIPs). Unraveling these DRIPs involved in the dopamine system may provide a better understanding of the mechanisms underlying CNS disorders related to dopamine system dysfunction and may help identify novel therapeutic targets.

• The Korean Journal of Cytopathology
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• v.11 no.2
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• pp.65-73
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• 2000

Cytologlc evaluation of cerebrospinal fluid(CSF) is an effective mean for diagnosing many disorders involving the central nervous systems(CNS). One of the most important reasons for cytologic examination of CSF is to detect metastatic or primary neoplasms of the CNS. We did a retrospective study of 1,438 CSF specimens obtained between 1992 and 1996. A total of 1,205 adult and 233 pediatric CSF specimens from 947 patients were accessed at the Department of Pathology of Seoul National University Hospital and Children's Hospital, respectively. Among 1,438 CSF cytology specimens, 169 cases(11.8%, 77 patients) including 135 adult cases(59 patients) and 34 pediatric cases(18 patients) were positive for malignant cells. Diagnoses included 50 metastatic carcinomas(adult, 60; pediatric, 0); 46 malignant lymphomas(adult, 44; pediatric, 2); 21 leukemias(adult, 20; pediatric, 1); 4 retinoblastomas(adult, 0; pediatric 4); 2 rhabdomyosarcomas(adult, 0; pediatric, 2); 1 multiple myeloma(adult, 1; pediatric, 0), and 35 primary CNS neoplasms(adult, 10; pediatric, 25). The most commonly identified metastatic carcinomas in adults were adenocarcinoma. Their primary sites were the lung, gastrointestinal tract, and breast in order of frequency. The most common primary CNS neoplasm in children was medulloblastoma.

• Science of Emotion and Sensibility
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• v.7 no.2
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• pp.179-186
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• 2004

Acute spinal cord injury can produce neurologic injury with many physical, psychological and social ramifications. It has been shown that two separate components combine to produce neurologic damage in acute spinal cord injury : the primary and secondary injuries. The primary mediators of spinal cord injury include the actual mechanical tissue disruption which is a passive process that occurs immediately following the trauma. A secondary injury cascade follows which appears mediated by cellular and molecular processes working through complex mechanisms. Both the primary and secondary injury cascades produce cell death both in neuronal and supporting cell tissues. Recovery from central nervous system(CNS) disorders is hindered by the limited ability of the vertebrate CNS to regenerate injured cells, replace damaged myelin sheath, and re-establish functional neuronal connections. Of many CNS disorders including multiple sclerosis, stroke, and other trauma, spinal cord injury is one of the important diseases because of the direct association with the functional loss of the body. Previous studies suggest that substantial recovery of function might be achieved through regeneration of lost neuronal cells and remyelination of intact axon in spinal cord injury which is occurred frequently. As a therapeutic approach in spinal cord injury, recently, cell transplantation provides a potential solution for the treatment of spinal cord injury. This review describes the characteristics of spinal cord injury and presents some evidence supporting functional recovery after cell transplantation following spinal cord injury.

• Journal of Yeungnam Medical Science
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• v.15 no.2
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• pp.371-380
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• 1998

Systemic lupus erythematosus(SLE) is an autoimmune disease which may affect many different organs and disclose various clinical manifestations. Recently central nervous system(CNS) involvement has been recognized as an increasingly significant contributor to morbidity and mortality of SLE. The clinical manifestations of CNS-lupus are highly variable and range from mild cognitive dysfunction, movement disorder, headache, psychosis to life-threatening stroke and coma. Among the neuropsychiatric disorders encountered in patients with SLE, cerebrovascular disease has been a relatively rare complication. The diagnosis and management of CNS-lupus is difficult because of the lack of useful diagnostic methods. If cerebrovascular involvement is suspected, aggressive treatment such as high dose steroid, immunosuppressive therapy, plasma exchange may be required to reduce high mortality rate. We experienced 2 cases cerebrovascular dis eases occurring in SLE patients which presented with various neuropsychiatric manifestations. They were diagnosed as CNS-lupus by neuropsychiatric symptoms, brain MRI, and BEG, and showed good response to high dose steroid pulse therapy.