• Journal of Oriental Neuropsychiatry
• /
• v.13 no.1
• /
• pp.53-77
• /
• 2002

Alzheimer's disease(AD) is a progressive neurodegenerative disease, which is pathologically characterized by neuritic plaques and neurofibrillary tangles associated with the acetylcholinesterase, apolipoprotein E and butylcholinesterase, and by mutations in the presenilin genes PS1 and PS2, and amyloid precursor proteins (APPs) overexpression. The present research is to examine the inhibitory effect of KGBH on PS1, PS2 and APPs overexpression detected by Western blotting. To verify the Effects of KGBH on cognitive deficits further, we tested it on the scopolamine(1mg/kg)-induced amnesia model of the mice using the Morris water maze tests, and there were ameliorative effects on memory impairment as a protection against scopolamine. KGBH only partially blocked the increase in blood serum level of acetylcholinesterase and Uric acid induced by scopolamine, where as blood glucose level was shown to attenuate the amnesia induced by scopolamine and inreased extracellular serum level. In conclusion, studies of KGBH that has been known as anti-choline and inhibitory ablilities of APPs overexpression, could also be used further as a important research data for a preventive and promising symptomatic treatment for Alzheimer's disease.

• Journal of Oriental Neuropsychiatry
• /
• v.14 no.1
• /
• pp.45-58
• /
• 2003

Alzheimer's disease(AD) is progressive neurodegenerative disease, which is pathologically characterized by neuritic plaques and neurofibrillary tangles associated with the acetylcholinesterase, apolipoprotein E and butylcholinesterase, and by mutations in the presenilin genes PS1 and PS2, and amyloid precursor proteins (APP) overexpression. The present research is to examine the inhibition effect of MDOF on PS-1, PS-2 and APP overexpression by detected to Western blotting. To verify the effects of MDOF on cognitive deficits further, we tested it on the scopolamine-induced amnesia model of the mice using the Morris water maze tests, and there was ameliorative effects of memory impairment as a protection to scopolamine. MDOF only partially blocked the increase in blood serum level of acetylcholinesterase and Uric acid induced by scopolamine, whereas blood glucose level was shown to attenuate the amnesia induced by scopolamine and inreased extracelluar serum level compared with only scopolamine injection. In conclusion, studies of MDOF that has been know as anti-choline and inhibition ablilities of APP overexpression, this could also be used further as a important research data for a preventive and promising symptomatic treatment for Alzheimer's disease.

• Journal of Oriental Neuropsychiatry
• /
• v.14 no.1
• /
• pp.59-74
• /
• 2003

Alzheimer's disease(AD) is a progressive neurodegenerative disease, which is pathologically characterized by neuritic plaques and neurofibrillary tangles associated with the acetylcholinesterase, apolipoprotein E and butylcholinesterase, and by mutations in the presenilin genes PS1 and PS2, and amyloid precursor proteins (APP) overexpression. The present research is to examine the inhibition effect of CPRT on PS-1, PS-2 and APP overexpression by detected to Western blotting. To verify the Effects of CPRT on cognitive deficits further, we tested it on the scopolamine-induced amnesia model of the mice using the Morris water maze tests, and there was ameliorative effects of memory impairment as a protection to scopolamine. CPRT only partially blocked the increase in blood serum level of acetylcholinesterase and Uric acid induced by scopolamine, whereas blood glucose level was shown to attenuate the amnesia induced by scopolamine and inreased extracellular serum level compared with only scopolamine injection. In conclusion, studies of CPRT that has been known as anti-choline and inhibition ablilities of APP overexpression, this could also be used further as a important research data for a preventive and promising symptomatic treatment for Alzheimer's disease.

• Korean Journal of Biological Psychiatry
• /
• v.23 no.2
• /
• pp.48-56
• /
• 2016

Alzheimer's disease (AD) is a neurodegenerative disorder in which neuronal loss causes cognitive decline and other neuropsychiatric problems. It can be diagnosed based on history, examination, and appropriate objective assessments, using standard criteria such as the Diagnostic and Statistical Manual of Mental Disorders or the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA). Brain imaging and biomarkers are making progress in the differential diagnoses among the different disorders. The cholinesterase inhibitors, donepezil, rivastigmine and galantamine and N-methyl-D-aspartate receptors antagonist memantine are approved by the US Food and Drug Administration for AD. Recently some acetylcholinesterase inhibitors gained approval for the treatment of severe AD and became available in a higher dose formulation or a patch formulation. Optimal care in AD is multifactorial and it should include early diagnosis and multidisciplinary care with pharmacological and nonpharmacological interventions including exercise interventions, cognitive interventions and maintenance of social networks.

• Journal of Acupuncture Research
• /
• v.20 no.2
• /
• pp.184-194
• /
• 2003

Objective : This study was designed fo find out whether Astragali Radix Herbal-Acupuncture Solution(ARHA) can scavenge NO, DPPH and IL-4 or not. Astragali Radix has been clinically used to reforce the depression of immune reponse etc. in Oriental Medicine. Methods : Free radical metabolism seems to occupy a remarkably common position in the mechanisms of ageing and ageing related disease. Oxidative damage to DNA, lipids, proteins and other molecules may contribute to the development of cancer, cardiovascular disease and possibly neurodegenerative disease. The effects of ARHA on NO, DPPH and IL-4 were measured. Results : The followings are the summary of the result; (1) There is a significant scavenging effect of ARHA on NO in 1, $10mg/m{\ell}$ group in after 24hrs. (2) There is no significant scavenging effect of ARHA on DPPH. (3) There is a significant scavenging effect of ARHA on IL-4 in 1, $10,100{\mu}g/m{\ell}$ group. Conclusions : These results suggest that ARHA has significant scavenging effect on NO, IL-4 and not on DPPH. This study shows that ARHA can be used for ageing related disease and further studies are required to investigate the antioxidative effects of it.

• The Korean Journal of Nuclear Medicine
• /
• v.38 no.3
• /
• pp.209-217
• /
• 2004

Evaluation of dementia in patients with early symptoms of cognitive decline is clinically challenging, but the need for early, accurate diagnosis has become more crucial, since several medication for the treatment of mild to moderate Alzheimer' disease are available. Many neurodegenerative diseases produce significant brain function alteration even when structural imaging (CT or MRI) reveal no specific abnormalities. The role of PET and SPECT brain imaging in the initial assessment and differential diagnosis of dementia is beginning to evolve vapidly and growing evidence indicates that appropriate incorporation of PET into the clinical work up can improve diagnostic and prognostic accuracy with respect to Alzheimer's disease, the most common cause of dementia in the geriatric population. in the fast few years, studios comparing neuropathologic examination with PET have established reliable and consistent accuracy for diagnostic evaluations using PET - accuracies substantially exceeding those of comparable studies of diagnostic value of SPECT or of both modalities assessed side by side, or of clinical evaluations done without nuclear imaging. This review deals the role of functional brain imaging techniques in the evaluation of dementias and the role of nuclear neuroimaging in the early detection and diagnosis of Alzheimer's disease.

• Journal of Oriental Neuropsychiatry
• /
• v.13 no.2
• /
• pp.149-171
• /
• 2002

Alzheimer's disease(AD) is a progressive neurodegenerative disease, which is pathologically characterized by neuritic plaques and neurofibrillary tangles associated with the acetylcholinesterase, apolipoprotein E and butylcholinesterase, and by mutations in the presenilin genes PS1 and PS2, and amyloid precursor proteins (APPs)'s overexpression. The present research is to examine the inhibitory effect of CWBD on PS1, PS2 and APPs's overexpression detected by Western blotting. To verify further the effects of CWBD on cognitive deficits, we tested it on the scopolamine(1mg/kg)-induced amnesia model of the mice using the Morris water maze tests, and there were ameliorative effects on memory impairment as a protection from scopolamine. CWBD only partially blocked the increase in blood serum level of acetylcholinesterase and Uric acid induced by scopolamine, whereas blood glucose level was shown to attenuate the amnesia induced by scopolamine and increased extracellular serum level. In conclusion, studies of CWBD that has been known as anti-choline and inhibitory ablilities of APPs's overexpression could also be used further as a important research data for a preventive and promising symptomatic treatment for Alzheimer's disease.

• Journal of Oriental Neuropsychiatry
• /
• v.12 no.1
• /
• pp.151-167
• /
• 2001

Alzheimer's disease(AD) is a progressive neurodegenerative disease, which is pathologically characterized by neuritic plaques and neurofibrillary tangles associated with the acetylchohnesterase, apolipoprotein E and butylcholinesterase, and by mutations in the presenilin genes PS1 and PS2, and amyloid precursor proteins (APPs)'s overexpression. The present research is to examine the inhibition effect of BYCNT on PS-1, PS-2 and APPs's overexpression by detected to Western blotting. To verify the effects of BYCNT on cognitive deficits further, we tested it on the scopolamine(1mg/kg)-induced amnesia model of the mice using the Morris water maze tests, and there was ameliorative effects of memory impairment as a protection from scopolamine. BYCNT only partially blocked the increase in blood serum level of acetylcholinesterase and Uric acid induced by scopolamine, whereas blood glucose level was shown to attenuate the amnesia induced by scopolamine and inreased extracellular serum level compared with only scopolamine injection. In conclusion, studies of BYCNT that has been known as anti-choline and inhibition ablilities of APPs overexpression, this could also be used further as a important research data for a preventive and promising symptomatic treatment for Alzheimer's disease.

• Biomolecules & Therapeutics
• /
• v.30 no.5
• /
• pp.409-417
• /
• 2022

Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide, and accumulating evidence indicates that mitochondrial dysfunction is associated with progressive deterioration in PD patients. Previous studies have shown that sinapic acid has a neuroprotective effect, but its mechanisms of action remain unclear. The neuroprotective effect of sinapic acid was assayed in a PD mouse model generated by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) as well as in SH-SY5Y cells. Target protein expression was detected by western blotting. Sinapic acid treatment attenuated the behavioral defects and loss of dopaminergic neurons in the PD models. Sinapic acid also improved mitochondrial function in the PD models. MPTP treatment increased the abundance of mitochondrial fission proteins such as dynamin-related protein 1 (Drp1) and phospho-Drp1 Ser616. In addition, MPTP decreased the expression of the REV-ERB α protein. These changes were attenuated by sinapic acid treatment. We used the pharmacological REV-ERB α inhibitor SR8278 to confirmation of protective effect of sinapic acid. Treatment of SR8278 with sinapic acid reversed the protein expression of phospho-Drp1 Ser616 and REV-ERB α on MPTP-treated mice. Our findings demonstrated that sinapic acid protects against MPTP-induced PD and these effects might be related to the inhibiting abnormal mitochondrial fission through REV-ERB α.

• Molecules and Cells
• /
• v.27 no.6
• /
• pp.621-627
• /
• 2009

Spinocerebellar ataxia type 1 (SCA1) is an autosomal-dominant neurodegenerative disorder characterized by ataxia and progressive motor deterioration. SCA1 is associated with an elongated polyglutamine tract in ataxin-1, the SCA1 gene product. As summarized in this review, recent studies have clarified the molecular mechanisms of SCA1 pathogenesis and provided direction for future therapeutic approaches. The nucleus is the subcellular site where misfolded mutant ataxin-1 acts to cause SCA1 disease in the cerebellum. The role of these nuclear aggregates is the subject of intensive study. Additional proteins have been identified, whose conformational alterations occurring through interactions with the polyglutamine tract itself or non-polyglutamine regions in ataxin-1 are the cause of SCA-1 cytotoxicity. Therapeutic hope comes from the observations concerning the reduction of nuclear aggregation and alleviation of the pathogenic phenotype by the application of potent inhibitors and RNA interference.