• Proceedings of the PSK Conference
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• 2002.04a
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• pp.148.1-148.1
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• 2002

• Biomedical Science Letters
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• v.21 no.1
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• pp.1-8
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• 2015

Alzheimer's disease is a common form of dementia occurring among the elderly population and can be identified by symptoms such as cognition impairments, memory loss and neuronal dysfunction. Alzheimer's disease was found to be caused by the deposition of $\beta$-amyloid plaques and neurofibrillary tangles. In addition, mutation in the APP (Amyloid precursor protein), Presenilin 1 (PSEN1) and Presenilin 2 (PSEN2) genes were also found to contribute to Alzheimer's disease. Since the potential conformational diagnosis of Alzheimer's disease requires histopathological tests on brain through autopsy, potential early diagnosis still remains challenging. In recent years, several researches have proposed the use of biomarkers for early diagnosis. In cerebrospinal fluid (CSF), $\beta$-amyloid(1-42), phosphorylated-tau and total tau were suggested to be effective biomarkers for Alzheimer's disease diagnosis. However, a single biomarker might not be sufficient for potential diagnosis of Alzheimer's disease. Thus, the use of RNA interference (RNAi) through microRNAs (miRNAs) has been proposed by several researchers for simultaneous analysis of several biomarkers using microarray technology. These miRNA based biomarkers can be analysed from both blood and CSF, but miRNAs from blood are advantageous over CSF as they are non-invasive and simple for collection. Moreover, the RNAi based therapeutics by siRNA (short interference RNA) or shRNA (short hairpin RNA) have also been proposed to be effective in the treatment of Alzheimer's disease. This review describes the promising application of RNAi technology in therapeutics and as a biomarker for both Alzheimer's disease diagnosis and treatment.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.111-111
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• 2002

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.150-151
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• 2003

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the progressive deterioration of cognition and memory in association with widespread neuronal loss. AD is supposed to be very often associated with missense mutation located on homologous protein Presenilin (PS1) and (PS2). Up to now, the molecular mechanisms underlying the role of the gene mutation in AD still remain unclear. (omitted)

• Korean Journal of Biological Psychiatry
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• v.6 no.2
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• pp.149-152
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• 1999

Transgenic mice models of Alzheimer's disease were produced by overexpressing APP(amyloid precursor protein) mutant and presenilin mutant genes using the promotors that induced neuronal expression. The neuropathologies, electrophysiological changes and behavioral changes that were demonstrated in these transgenic mice models were amyloid changes, gliotic changes, A-beta increases, deficit in LTP(long-term potentiation) and behavioral changes. Some or all of the above changes were found in each transgenic mice model. These models generally showed amyloid neuropathology but they usually lacked the neurofibrillary tangles. So, they can be regarded as partial models of Alzheimer's disease. The development of them is undoubtedly the great progress toward future research.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.108-108
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• 2002

Mutations in the presenilin genes (PS-1 and PS-2) are linked to early onset familial Alzheimer's disease(AD), but its underlying cellular mechanisms have not been clear. 15-Deoxy-Δ12, 14-prostaglandin J2 (15-deoxy-PGJ2) is know as a naturally occurring ligand of the peroxisome proliferator-activated receptor-${\gamma}$ (PPAR-${\gamma}$).(omitted)

• Journal of Oriental Neuropsychiatry
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• v.13 no.2
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• pp.149-171
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• 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
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• v.11 no.2
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• pp.23-42
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• 2000

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 PSI and PS2, and amyloid precursor proteins (APP) overexpression. The present research is to examine the inhibition effect of YJJHT on PS-1, PS-2 and APP overexpression by detected to Western blotting. To verify the EFFects of YJJHT 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 s a protection to scopolamine. YJJHT 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 YJJHT 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
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• v.13 no.1
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• pp.53-77
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• 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
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• v.14 no.1
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• pp.45-58
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• 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.