• Title/Summary/Keyword: Alzheimer's Disease

Search Result 1,144, Processing Time 0.037 seconds

Mean Phase Coherence as a Supplementary Measure to Diagnose Alzheimer's Disease with Quantitative Electroencephalogram (qEEG)

  • Che, Hui-Je;Jung, Young-Jin;Lee, Seung-Hwan;Im, Chang-Hwan
    • Journal of Biomedical Engineering Research
    • /
    • v.31 no.1
    • /
    • pp.27-32
    • /
    • 2010
  • Noninvasive detection of patients with probable Alzheimer's disease (AD) is of great importance for assisting a medical doctor's decision for early treatment of AD patients. In the present study, we have extracted quantitative electroencephalogram (qEEG) variables, which can be potentially used to diagnose AD, from resting eyes-closed continuous EEGs of 22 AD patients and 27 age-matched normal control (NC) subjects. We have extracted qEEG variables from mean phase coherence (MPC) and EEG coherence, evaluated for all possible combinations of electrode pairs. Preliminary trials to discriminate the two groups with the extracted qEEG variables demonstrated that the use of MPC as a supplementary or alternative measure for the EEG coherence may enhance the accuracy of noninvasive diagnosis of AD.

Effects of Added Chongmyung-tang on Behavior and Molecular Factors in the Alzheimer's Disease Model (ACM의 알츠하이머 생쥐 모델의 행동과 생체인자에 미치는 영향)

  • Kim, Kook Ki;Choi, Woo Chang;Kim, Seung Hyung;Namgung, Uk;Park, Yang Chun;Kang, Wee Chang;Lee, Sang Ryong;Jung, In Chul
    • Journal of Physiology & Pathology in Korean Medicine
    • /
    • v.29 no.1
    • /
    • pp.39-45
    • /
    • 2015
  • This experiment was designed to investigate the effect of Added Chongmyung-tang (ACM) on Alzheimer's disease mouse model. Effects of ACM on learning behavior were investigated using the Morris water maze method. Expression levels of molecular factors related to Alzheimer's disease such as glial fibrillary acidic protein (GFAP), cluster of differentiation antigen 68 (CD68), and tau protein in the hippocampus of APP-SWE Tg2576 mice were analyzed by immunofluorescence staining method. ACM reduced escape latency in the Morris water maze test. ACM decreased the expression level of GFAP and tau protein in the hippocampus. These results suggest that ACM may be involved in regulating molecules that are known to play an important role in the pathogenesis of Alzheimer's disease.

Synthesis and cyclooxygenase-2 inhibitory activity of tetrahydroaminoacridine and their analogues

  • Shin, H.S.;Kang, J.Y.;Park, M.S.;Kwon, S.K.
    • Proceedings of the PSK Conference
    • /
    • 2003.04a
    • /
    • pp.248.3-249
    • /
    • 2003
  • A series of tetrahydroaminoacridine and their analogues were synthesized. Tetrahydroaminoacridine(tacrine) is an anticholinesterase agent used in the treatment of Alzheimer's disease. Introduction of piperidine group at the para position enhanced anti-inflamatory activity for Alzheimer's disease. We investigated their ability to inhibit cyclooxygenase-1 and 2 isoforms. (omitted)

  • PDF

PET studies in Alzheimer Disease and Other Degenerative Dementias (알쯔하이머병과 다른 퇴행성 치매에서의 양전자방출단층촬영)

  • Jeong, Yong;Na, Duk-L.
    • The Korean Journal of Nuclear Medicine
    • /
    • v.37 no.1
    • /
    • pp.13-23
    • /
    • 2003
  • Neurodegenerative disorders cause a variety of dementia including Alzheimer disease, frontotemporal dementia, dementia with Lewy bodies, corticobasal degeneration, progressive supranuclear palsy, and Huntington's disease. PET scan is useful for early detection and differential diagnosis of these dementing disorders. Also, it provides valuable information about clinico-anatomical correlation, allowing better understanding of function of brain. Here we discuss recent achievements PET studies regarding these dementing disorders. Future progress in PET technology, new tracers, and image analysis will play an important role in further clarifying the disease pathophysiology and brain functions.

Molecular and Cellular Basis of Neurodegeneration in Alzheimer's Disease

  • Jeong, Sangyun
    • Molecules and Cells
    • /
    • v.40 no.9
    • /
    • pp.613-620
    • /
    • 2017
  • The most common form of senile dementia is Alzheimer's disease (AD), which is characterized by the extracellular deposition of amyloid ${\beta}-peptide$ ($A{\beta}$) plaques and the intracellular formation of neurofibrillary tangles (NFTs) in the cerebral cortex. Tau abnormalities are commonly observed in many neurodegenerative diseases including AD, Parkinson's disease, and Pick's disease. Interestingly, tau-mediated formation of NFTs in AD brains shows better correlation with cognitive impairment than $A{\beta}$ plaque accumulation; pathological tau alone is sufficient to elicit frontotemporal dementia, but it does not cause AD. A growing amount of evidence suggests that soluble $A{\beta}$ oligomers in concert with hyperphosphorylated tau (pTau) serve as the major pathogenic drivers of neurodegeneration in AD. Increased $A{\beta}$ oligomers trigger neuronal dysfunction and network alternations in learning and memory circuitry prior to clinical onset of AD, leading to cognitive decline. Furthermore, accumulated damage to mitochondria in the course of aging, which is the best-known nongenetic risk factor for AD, may collaborate with soluble $A{\beta}$ and pTau to induce synapse loss and cognitive impairment in AD. In this review, I summarize and discuss the current knowledge of the molecular and cellular biology of AD and also the mechanisms that underlie $A{\beta}-mediated$ neurodegeneration.

Epigenetic modification is linked to Alzheimer's disease: is it a maker or a marker?

  • Lee, Jung-Hee;Ryu, Hoon
    • BMB Reports
    • /
    • v.43 no.10
    • /
    • pp.649-655
    • /
    • 2010
  • Alzheimer's disease (AD) is the most common age-dependent neurodegenerative disorder and shows progressive memory loss and cognitive decline. Intraneuronal filaments composed of aggregated hyperphosphorylated tau protein, called neurofibrillary tangles, along with extracellular accumulations of amyloid $\beta$ protein (A$\beta$), called senile plaques, are known to be the neuropathological hallmarks of AD. In light of recent studies, epigenetic modification has emerged as one of the pathogenic mechanisms of AD. Epigenetic changes encompass an array of molecular modifications to both DNA and chromatin, including transcription factors and cofactors. In this review, we summarize how DNA methylation and changes to DNA chromatin packaging by post-translational histone modification are involved in AD. In addition, we describe the role of SIRTs, histone deacetylases, and the effect of SIRT-modulating drugs on AD. Lastly, we discuss how amyloid precursor protein (APP) intracellular domain (AICD) regulates neuronal transcription. Our understanding of the epigenomes and transcriptomes of AD may warrant future identification of novel biological markers and beneficial therapeutic targets for AD.

Inhibitory potency of Acetylcholinesterase and Amyloid beta(1-42) peptide aggregation to the Extracts of Enthusiasm Reducing herbals (청열약 추출물들의 아세틸콜린에스테라제 저해와 베타아밀로이드 펩티드 응집 억제 효능)

  • Kwon, Young-Ee
    • Korean Journal of Pharmacognosy
    • /
    • v.38 no.4
    • /
    • pp.308-311
    • /
    • 2007
  • Inhibition of acetylcholinesterase and amyloid beta(1-42) peptide is good drug targets for Alzheimer's disease therapeutics. Among the twenty enthusiasm reducing herbals, the 70% methanol extracts (1 mg/ml) of Moutan Radicis Cortex and Forsythiae Fructus showed 91.5% and 85.3% about acethylcholinesterase inhibition, respectively. The extracts (1 mg/ml) of Coptidis Rhizoma and Paeoniae Radix Rubra showed more than 85% inhibition rate against amyloid beta (1-42) peptide aggregation. The neuroprotective effect of the extracts (1 mg/ml) of Moutan Radicis Cortex, Forsythiae Fructus and Paeoniae Radix Rubra showed 90.0%, 87.4% and 85.1% to compare with amyloid beta (1-42) peptide treated cells (IMR-32), respectively. Three herbs, Moutan Radicis Cortex, Forsythiae Fructus and Paeoniae Radix Rubra are promising candidates from natural products for development of Alzheimer's disease therapeutics.

Alternation of Sleep Structure and Circadian Rhythm in Alzheimer's Disease (알츠하이머 치매에서 수면구조 및 일주기리듬의 변화)

  • Sohn, Chang-Ho
    • Sleep Medicine and Psychophysiology
    • /
    • v.9 no.1
    • /
    • pp.9-13
    • /
    • 2002
  • Alzheimer's disease (AD) is one of the most common and devastating dementing disorders of old age. Most AD patients showed significant alternation of sleep structure as well as cognitive deficit. Typical findings of sleep architecture in AD patients include lower sleep efficiency, higher stage 1 percentage, and greater frequency of arousals. The slowing of EEG activity is also noted. Abnormalities in REM sleep are of particular interest in AD because the cholinergic system is related to both REM sleep and AD. Several parameters representing REM sleep structure such as REM latency, the amount of REM sleep, and REM density are change in patients with AD. Especially, measurements of EEG slowing during tonic REM sleep can be used as an EEG marker for early detection of possible AD. In addition, a structural defect in the suprachiasmatic nucleus is suggested to cause various chronobiological alternations in AD. Most of alternations related to sleep make sleep disturbances common and disruptive symptoms of AD. In this article, the author reviewed the alternation of sleep structure and circadian rhythm in AD patients.

  • PDF

Development of functional substances on Alzheimer's disease

  • Heo, Ho-Jin
    • Proceedings of the Korean Society of Postharvest Science and Technology of Agricultural Products Conference
    • /
    • 2007.11a
    • /
    • pp.65-72
    • /
    • 2007
  • Phytochemicals have long been known to hold a number of physiological benefits, including antioxidant, anticardiovascular activities and anticancer. The profitable effects of phytochemicals from food sources such as vegetables and fruits, with respect to neurodegeneration, are only beginning to receive increased attention. Alzheimer's disease (AD) is one of the major neurodegenerative diseases for which no treatment is available, and characterized by loss of cognition and memory. Many recent studies show that the brain of AD patient is subjected to increased oxidative stress resulting from free radical damage, and the resulting cellular malfunctions are widely believed to be responsible for neuronal degeneration in AD. In this study, the relative relation between AD and phytochemicals were surveyed.

  • PDF