アルツハイマー型老人性認知症 SDAT
WordNet
- write by means of a keyboard with types; "type the acceptance letter, please" (同)typewrite
- a small metal block bearing a raised character on one end; produces a printed character when inked and pressed on paper; "he dropped a case of type, so they made him pick them up"
- (biology) the taxonomic group whose characteristics are used to define the next higher taxon
- a subdivision of a particular kind of thing; "what type of sculpture do you prefer?"
- all of the tokens of the same symbol; "the word `element contains five different types of character"
- printed characters; "small type is hard to read"
- identify as belonging to a certain type; "Such people can practically be typed" (同)typecast
- mental deterioration of organic or functional origin (同)dementedness
PrepTutorEJDIC
- 〈C〉(…の)『型』,タイプ,類型,種類(kind)《+of+名》 / 〈C〉(その種類の特質を最もよく表している)『典型』,手本,模範《+of+名》 / 〈U〉《集合的に》活字;〈C〉(1個の)活字 / 〈U〉(印刷された)字体,活字 / 〈C〉(貨幣・メダルなどの)模様,図柄 / 〈C〉血液型(blood group) / …‘を'タイプに打つ / (…として)…‘を'分類する《+名+as+名(doing)》 / …‘の'型を決める / タイプライターを打つ
- 《所有・所属》…『の』,…のものである,…に属する・《材料・要素》…『でできた』,から成る・《部分》…『の』[『中の』] ・《数量・単位・種類を表す名詞に付いて》…の・《原因・動機》…『で』,のために(because of) ・《主格関係》…『の』,による,によって・《目的格関係》…『を』,の・《同格関係》…『という』・《関係・関連》…『についての』[『の』],の点で・《抽象名詞などと共に》…の[性質をもつ] ・《『It is』+『形』+『of』+『名』+『to』 doの形で,ofの後の名詞を意味上の主語として》・《分離》…『から』・《起原・出所》…『から』[『の』](out of) ・《『名』+『of』+『a』(『an』)+『名』の形で》…のような・《『名』+『of』+『mine』(『yours, his』など独立所有格)の形で》…の…・《時》(1)《副詞句を作って》…に《形容詞句を作って》…の・《時刻》《米》…前(to,《米》before)
- 老年の,老衰の,(特に)もうろくした
- (医学的な)痴呆(ちほう)
UpToDate Contents
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English Journal
- Study on Aβ34 biology and detection in transgenic mice brains.
- Caillava C1, Ranaldi S2, Lauritzen I1, Bauer C1, Fareh J2, Abraham JD2, Checler F3.Author information 1Institut de Pharmacologie Moléculaire et Cellulaire, UMR7275 CNRS/UNS, Team "Fondation pour la Recherche Médicale" and "Labex Distalz", Valbonne, France.2SysDiag CNRS-Bio-Rad, UMR3145, SysDiag,, Montpellier, France.3Institut de Pharmacologie Moléculaire et Cellulaire, UMR7275 CNRS/UNS, Team "Fondation pour la Recherche Médicale" and "Labex Distalz", Valbonne, France. Electronic address: checler@ipmc.cnrs.fr.AbstractThe β-amyloid precursor protein undergoes cleavages by β- and γ-secretasses yielding amyloid-β peptides (Aβ) that accumulate in Alzheimer's disease. Subsequently, Aβ peptides are targets of additional truncations or endoproteolytic cleavages explaining the diversity of Aβ-related fragments recovered in cell media or pathologic human fluids. Here, we focused on Aβ1-34 (Aβ34) that has been detected both in vitro and in vivo and that derives from the hydrolysis of Aβ by β-secretase. We have obtained and fully characterized by immunologic and biochemical approaches, a polyclonal antibody that specifically recognizes the C-terminus of Aβx-34. We present immunohistochemical evidence for the presence of Aβx-34 in the brain of 3xTg mice and Alzheimer's disease-affected human brains. Finally, we demonstrate a neprilysin-mediated degradation process of Aβ34 and the ability of synthetic Aβ34 to protect HEK cells overexpressing either wild type or Swedish-mutated β-amyloid precursor protein from apoptosis.
- Neurobiology of aging.Neurobiol Aging.2014 Jul;35(7):1570-81. doi: 10.1016/j.neurobiolaging.2014.01.011. Epub 2014 Jan 11.
- The β-amyloid precursor protein undergoes cleavages by β- and γ-secretasses yielding amyloid-β peptides (Aβ) that accumulate in Alzheimer's disease. Subsequently, Aβ peptides are targets of additional truncations or endoproteolytic cleavages explaining the diversity of Aβ-related fragments re
- PMID 24495834
- H63D mutation in hemochromatosis alters cholesterol metabolism and induces memory impairment.
- Ali-Rahmani F1, Grigson PS2, Lee S3, Neely E3, Connor JR4, Schengrund CL5.Author information 1Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA, USA; Department of Neurosurgery, The Pennsylvania State University College of Medicine, Hershey, PA, USA.2Department of Neural and Behavioral Sciences, The Pennsylvania State University College of Medicine, Hershey, PA, USA.3Department of Neurosurgery, The Pennsylvania State University College of Medicine, Hershey, PA, USA.4Department of Neurosurgery, The Pennsylvania State University College of Medicine, Hershey, PA, USA. Electronic address: jconnor@hmc.psu.edu.5Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, PA, USA. Electronic address: cxs8@psu.edu.AbstractThe H63D variant of the hemochromatosis (HFE) gene, when expressed in carriers of the apolipoprotein E4 allele, is implicated as a risk factor for earlier onset of Alzheimer's disease (AD). We tested the hypothesis that like expression of apolipoprotein E4, expression of H63D-HFE disrupts cholesterol metabolism contributing to an increase in neurodegeneration and memory deficits. Analysis of SH-SY5Y human neuroblastoma cells transfected to stably express either wild type- (WT) or H63D-HFE indicated about a 50% reduction in cholesterol content in cells expressing H63D-HFE. This was accompanied by a significant decrease in expression of 3-hydroxy-3-methyl-glutaryl-CoA reductase, and a significant increase in expression of cholesterol 24-hydroxylase. Consistent with these studies, H67D-HFE (orthologous to human H63D-HFE) knock-in mice, showed a greater age dependent decline in brain cholesterol than WT-HFE animals and changes in expression of proteins regulating cholesterol metabolism. Brains of aged H67D-HFE mice also exhibited a significant decrease in expression of synapse proteins and a significant increase in caspase-3 expression relative to WT-HFE controls. H67D-HFE mice also had a greater reduction in brain volume and poorer recognition and spatial memory than WT-HFE mice, symptoms associated with AD. These results indicate that the alterations in cholesterol metabolism associated with expression of H63D-HFE may contribute to the development of AD.
- Neurobiology of aging.Neurobiol Aging.2014 Jun;35(6):1511.e1-12. doi: 10.1016/j.neurobiolaging.2013.12.014. Epub 2013 Dec 25.
- The H63D variant of the hemochromatosis (HFE) gene, when expressed in carriers of the apolipoprotein E4 allele, is implicated as a risk factor for earlier onset of Alzheimer's disease (AD). We tested the hypothesis that like expression of apolipoprotein E4, expression of H63D-HFE disrupts cholestero
- PMID 24439478
- Intravenous ascorbate improves spatial memory in middle-aged APP/PSEN1 and wild type mice.
- Kennard JA1, Harrison FE2.Author information 1Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, United States. Electronic address: John.Kennard@Vanderbilt.edu.2Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, United States.AbstractThe present study investigated the effects of a single intravenous (i.v.) dose of Vitamin C (ascorbate, ASC) on spatial memory in APP/PSEN1 mice, an Alzheimer's disease model. First, we confirmed the uptake time course in ASC-depleted gulo (-/-) mice, which cannot synthesize ASC. Differential tissue uptake was seen based on ASC transporter distribution. Liver (SVCT1 and SVCT2) ASC was elevated at 30, 60 and 120 min post-treatment (125 mg/kg, i.v.), whereas spleen (SVCT2) ASC increased at 60 and 120 min. There was no detectable change in cortical (SVCT2 at choroid plexus, and neurons) ASC within the 2-h interval, although the cortex preferentially retained ASC. APP/PSEN1 and wild type (WT) mice at three ages (3, 9, or 20 months) were treated with ASC (125 mg/kg, i.v.) or saline 45 min before testing on the Modified Y-maze, a two-trial task of spatial memory. Memory declined with age and ASC treatment improved performance in 9-month-old APP/PSEN1 and WT mice. APP/PSEN1 mice displayed no behavioral impairment relative to WT controls. Although dopamine and metabolite DOPAC decreased in the nucleus accumbens with age, and improved spatial memory was correlated with increased dopamine in saline treated mice, acute ASC treatment did not alter monoamine levels in the nucleus accumbens. These data show that the Modified Y-maze is sensitive to age-related deficits, but not additional memory deficits due to amyloid pathology in APP/PSEN1 mice. They also suggest improvements in short-term spatial memory were not due to changes in the neuropathological features of AD or monoamine signaling.
- Behavioural brain research.Behav Brain Res.2014 May 1;264:34-42. doi: 10.1016/j.bbr.2014.01.044. Epub 2014 Feb 5.
- The present study investigated the effects of a single intravenous (i.v.) dose of Vitamin C (ascorbate, ASC) on spatial memory in APP/PSEN1 mice, an Alzheimer's disease model. First, we confirmed the uptake time course in ASC-depleted gulo (-/-) mice, which cannot synthesize ASC. Differential tissue
- PMID 24508240
Japanese Journal
- 三枝 隆博,中谷 嘉文,萩原 麻衣 [他]
- 臨床神経学 = Clinical neurology 54(4), 321-324, 2014-04
- NAID 40020055543
- アルツハイマー病とホモシステイン(<特集>ビタミンB研究委員会 平成24年度シンポジウム「B群ビタミンによる疾患の治療」)
- 濱野 忠則,白藤 法道,栗山 勝,中本 安成
- ビタミン 88(2), 92-96, 2014-02-25
- … Recently, with the increase of aged people in Japan, the number of people with dementia has been markedly increasing. … It was estimated that the number of people with dementia is 4.62 million people in Japan. …
- NAID 110009805256
- Corticobasal syndromeを呈した若年性アルツハイマー病の1剖検例
- 藤井 直樹,若宮 富浩,渡邉 暁博,古谷 博和,佐々木 健介,岩城 徹
- 臨床神経学 53(10), 814-820, 2013
- 症例は51歳男性である．ものわすれで発症．右優位の上肢の巧緻運動障害が進行性に増悪した．MRI画像上，左側優位の側頭・頭頂葉萎縮をみとめた．その後，失行，右側優位のパーキンソン徴候が顕在化し，認知症とともに増悪し，失外套状態となり，59歳誤嚥性肺炎で死亡．剖検をおこない，左優位に大脳が萎縮．大脳皮質全体に老人斑が高頻度にみられ，多くのcotton wool plaqueもみとめた．免疫染色で抗リン …
- NAID 130004505309
Related Links
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- Alzheimer's disease Senile dementia - Alzheimer's type (SDAT), SDAT information center covers Definition, Disorders, Overview, Causes, & Risk Factors, Symptoms & Signs, Diagnosis & Tests, Treatment, Support Groups ...
★リンクテーブル★
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- 英
- senile dementia of Alzheimer type, SDAT
- 同
- アルツハイマー型老人性認知症
- 関
- 認知症
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- 英
- senile dementia of Alzheimer type SDAT
- 関
- アルツハイマー型痴呆
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- (windows)ファイル内容表示(linux -> cat])
- ex. type report_20111118.jp.htm | php a.php > report_20111118.jp.jp.jp.html
- 関
- form、mode、pattern、type specimen、typed
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- 関
- ageing、aging、geriatric、senescence、senescent、senility、senium
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老年認知症、老年痴呆
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- Alzheimer disease、Alzheimer's disease、early-onset Alzheimer disease、late-onset Alzheimer disease、presenile dementia
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- 関
- dementia、dementing、deterioration
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- 関
- form、mode、pattern、type