WordNet

the natural process of laying down a deposit of something (同)deposit
the act of deposing someone; removing a powerful person from a position or office (同)dethronement
(law) a pretrial interrogation of a witness; usually conducted in a lawyers office
(pathology) a waxy translucent complex protein resembling starch that results from degeneration of tissue
a non-nitrogenous food substance consisting chiefly of starch; any substance resembling starch

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〈U〉廃位;(高官などの)免職 / 〈C〉宣誓供述書 / 〈U〉堆積作用;〈C〉堆積物

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1. アミロイドーシスの概要 overview of amyloidosis
2. 免疫グロブリン軽鎖（AL）アミロイドーシスおよび軽鎖重鎖沈着症の病因 pathogenesis of immunoglobulin light chain al amyloidosis and light and heavy chain deposition diseases
3. 免疫グロブリン軽鎖（AL）アミロイドーシス（原発性アミロイドーシス）の臨床像、検査所見、および診断 clinical presentation laboratory manifestations and diagnosis of immunoglobulin light chain al amyloidosis primary amyloidosis
4. 腎アミロイドーシス renal amyloidosis
5. アミロイド心筋症の臨床症状および診断 clinical manifestations and diagnosis of amyloid cardiomyopathy

English Journal

Mammalian target of rapamycin hyperactivity mediates the detrimental effects of a high sucrose diet on Alzheimer's disease pathology.

Orr ME1, Salinas A1, Buffenstein R1, Oddo S2.Author information 1Department of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.2Department of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; Banner Sun Health Research Institute, Sun City, AZ, USA; Department of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, Phoenix, AZ, USA. Electronic address: oddo@email.arizona.edu.AbstractHigh sugar consumption and diabetes increase the risk of developing Alzheimer's disease (AD) by unknown mechanisms. Using an animal model of AD, here we show that high sucrose intake induces obesity with changes in central and peripheral insulin signaling. These pre-diabetic changes are associated with an increase in amyloid-β production and deposition. Moreover, high sucrose ingestion exacerbates tau phosphorylation by increasing Cdk5 activity. Mechanistically, the sucrose-mediated increase in AD-like pathology results from hyperactive mammalian target of rapamycin (mTOR), a key nutrient sensor important in regulating energy homeostasis. Specifically, we show that rapamycin, an mTOR inhibitor, prevents the detrimental effects of sucrose in the brain without altering changes in peripheral insulin resistance. Overall, our data suggest that high sucrose intake and dysregulated insulin signaling, which are known to contribute to the occurrence of diabetes, increase the risk of developing AD by upregulating brain mTOR signaling. Therefore, early interventions to modulate mTOR activity in individuals at high risk of developing diabetes may decrease their AD susceptibility.
Neurobiology of aging.Neurobiol Aging.2014 Jun;35(6):1233-42. doi: 10.1016/j.neurobiolaging.2013.12.006. Epub 2013 Dec 14.
High sugar consumption and diabetes increase the risk of developing Alzheimer's disease (AD) by unknown mechanisms. Using an animal model of AD, here we show that high sucrose intake induces obesity with changes in central and peripheral insulin signaling. These pre-diabetic changes are associated w
PMID 24411482

Aging, cortical injury and Alzheimer's disease-like pathology in the guinea pig brain.

Bates K1, Vink R2, Martins R3, Harvey A4.Author information 1School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, Western Australia, Australia; School of Psychiatry and Clinical Neuroscience, The University of Western Australia, Crawley, Western Australia, Australia; The McCusker Foundation for Alzheimer's Disease Research Inc, Nedlands, Western Australia, Australia. Electronic address: kristyn.bates@uwa.edu.au.2School of Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia.3School of Psychiatry and Clinical Neuroscience, The University of Western Australia, Crawley, Western Australia, Australia; The McCusker Foundation for Alzheimer's Disease Research Inc, Nedlands, Western Australia, Australia; School of Medical Sciences, Edith Cowan University, Joondalup, Western Australia, Australia.4School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, Western Australia, Australia.AbstractAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized histopathologically by the abnormal deposition of the proteins amyloid-beta (Aβ) and tau. A major issue for AD research is the lack of an animal model that accurately replicates the human disease, thus making it difficult to investigate potential risk factors for AD such as head injury. Furthermore, as age remains the strongest risk factor for most of the AD cases, transgenic models in which mutant human genes are expressed throughout the life span of the animal provide only limited insight into age-related factors in disease development. Guinea pigs (Cavia porcellus) are of interest in AD research because they have a similar Aβ sequence to humans and thus may present a useful non-transgenic animal model of AD. Brains from guinea pigs aged 3-48 months were examined to determine the presence of age-associated AD-like pathology. In addition, fluid percussion-induced brain injury was performed to characterize mechanisms underlying the association between AD risk and head injury. No statistically significant changes were detected in the overall response to aging, although we did observe some region-specific changes. Diffuse deposits of Aβ were found in the hippocampal region of the oldest animals and alterations in amyloid precursor protein processing and tau immunoreactivity were observed with age. Brain injury resulted in a strong and sustained increase in amyloid precursor protein and tau immunoreactivity without Aβ deposition, over 7 days. Guinea pigs may therefore provide a useful model for investigating the influence of environmental and non-genetic risk factors on the pathogenesis of AD.
Neurobiology of aging.Neurobiol Aging.2014 Jun;35(6):1345-51. doi: 10.1016/j.neurobiolaging.2013.11.020. Epub 2013 Nov 27.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized histopathologically by the abnormal deposition of the proteins amyloid-beta (Aβ) and tau. A major issue for AD research is the lack of an animal model that accurately replicates the human disease, thus making it diff
PMID 24360504

Neuropep-1 ameliorates learning and memory deficits in an Alzheimer's disease mouse model, increases brain-derived neurotrophic factor expression in the brain, and causes reduction of amyloid beta plaques.

Shin MK1, Kim HG1, Baek SH1, Jung WR1, Park DI1, Park JS2, Jo DG2, Kim KL3.Author information 1Department of Biological Sciences, Sungkyunkwan University, Suwon, Gyeonggi-Do, Korea.2School of Pharmacy, Sungkyunkwan University, Suwon, Gyeonggi-Do, Korea.3Department of Biological Sciences, Sungkyunkwan University, Suwon, Gyeonggi-Do, Korea. Electronic address: kimkl@skku.ac.kr.AbstractAlzheimer's disease (AD) is a neurodegenerative disease characterized by amyloid beta (Aβ) deposits, hyperphosphorylated tau deposition, and cognitive dysfunction. Abnormalities in the expression of brain-derived neurotrophic factor (BDNF), which plays an important role in learning and memory formation, have been reported in the brains of AD patients. A BDNF modulating peptide (Neuropep-1) was previously identified by positional-scanning synthetic peptide combinatorial library. Here we examine the neuroprotective effects of Neuropep-1 on several in vitro neurotoxic insults, and triple-transgenic AD mouse model (3xTg-AD). Neuropep-1 protects cultured neurons against oligomeric Aβ1-42, 1-methyl-4-phenylpyridinium, and glutamate-induced neuronal cell death. Neuropep-1 injection also significantly rescues the spatial learning and memory deficits of 3xTg-AD mice compared with vehicle-treated control group. Neuropep-1 treatment markedly increases hippocampal and cortical BDNF levels. Furthermore, we found that Neuropep-1-injected 3xTg-AD mice exhibit dramatically reduced Aβ plaque deposition and Aβ levels without affecting tau pathology. Neuropep-1 treatment does not alter the expression or activity of full-length amyloid precursor protein, α-, β-, or γ-secretase, but levels of insulin degrading enzyme, an Aβ degrading enzyme, were increased. These findings suggest Neuropep-1 may be a therapeutic candidate for the treatment of AD.
Neurobiology of aging.Neurobiol Aging.2014 May;35(5):990-1001. doi: 10.1016/j.neurobiolaging.2013.10.091. Epub 2013 Oct 29.
Alzheimer's disease (AD) is a neurodegenerative disease characterized by amyloid beta (Aβ) deposits, hyperphosphorylated tau deposition, and cognitive dysfunction. Abnormalities in the expression of brain-derived neurotrophic factor (BDNF), which plays an important role in learning and memory forma
PMID 24268884