標(biāo)題: Titlebook: Alzheimer’s Disease Research; What Has Guided Rese Christian Behl Book 2023 The Editor(s) (if applicable) and The Author(s), under exclusiv [打印本頁] 作者: iniquity 時(shí)間: 2025-3-21 19:57
書目名稱Alzheimer’s Disease Research影響因子(影響力)
作者: FIN 時(shí)間: 2025-3-21 21:47 作者: 鎮(zhèn)壓 時(shí)間: 2025-3-22 00:59
,Alzheimer’s Disease Research After 1945: The Recommencement,ative disorders. In addition to Alzheimer’s, several other types of dementia exist. Alzheimer’s disease?research officially set off with the introduction of the label “Alzheimer’s disease” in 1910, but similar neurodegenerative processes had already been described years before..The restart of Alzhei作者: Ancestor 時(shí)間: 2025-3-22 07:19 作者: 蕨類 時(shí)間: 2025-3-22 12:22 作者: foliage 時(shí)間: 2025-3-22 16:18
,The , of Alzheimer’s Disease,itatory neurotransmitter in the vertebrate nervous system. This neurotransmitter displays its activities via different types of receptors localized at the nerve cell membrane. Physiologically, glutamate and its receptors (especially the so-called NMDA type) are involved in higher brain functions suc作者: Charitable 時(shí)間: 2025-3-22 19:07
,Biochemistry and Genetics Point Out a Prime Suspect for Causing Alzheimer’s Disease,rsh chemical conditions, the sequence of 24 amino acids of the amyloid beta peptide isolated from cerebrovascular material was unraveled at the UCSD by Georg Glenner and Caine Wong in 1984. Shortly thereafter, the German and Australian researchers Konrad Beyreuther and Colin Masters, respectively, p作者: 情感脆弱 時(shí)間: 2025-3-22 22:50
Getting to the Bottom of It: Amyloid Beta Peptide Is Derived from a Larger Precursor, peptide. A fierce competition commenced?between several research groups during the year 1987 around the further molecular characterization of this peptide..Key findings were the cloning of its precursor protein (APP), the molecular assignment of the APP gene to chromosome 21, and the discovery that作者: 緊張過度 時(shí)間: 2025-3-23 04:36
,Step by Step Toward an Amyloid Beta Peptide-Based Hypothesis of Alzheimer’s Disease,of molecular and cellular findings around this peptide was delivered and, consequently, in 1992 the . was presented. This hypothesis assigned the amyloid beta protein the role as initial trigger standing at the beginning of a cascade of pathogenic events. In the 15?years from 1984 to 1999, the puzzl作者: 外向者 時(shí)間: 2025-3-23 09:29 作者: Offensive 時(shí)間: 2025-3-23 13:37 作者: 令人苦惱 時(shí)間: 2025-3-23 17:28 作者: 在駕駛 時(shí)間: 2025-3-23 21:49 作者: 頌揚(yáng)本人 時(shí)間: 2025-3-24 01:08 作者: 牛馬之尿 時(shí)間: 2025-3-24 04:28
The , Has to Deliver, Finally, increasing and the disease been acknowledged as a major health problem. More than 2000 clinical trials targeting different mechanisms were performed, and no breakthrough therapy showing convincing clinical benefit in patients could be found so far. Numerous hypotheses were formulated in the attempt作者: 赦免 時(shí)間: 2025-3-24 08:21
Beyond ,, ,, ,, and ,: What Else Does the Genome Tell Us?,up of genetic familial disease cases, and they are dominantly inherited (full penetrance; early-onset autosomal-dominant Alzheimer’s disease). Independently of these “Alzheimer genes”, in 1993, the gene coding for the apolipoprotein E (APOE) was presented as an Alzheimer’s risk gene with high penetr作者: Decibel 時(shí)間: 2025-3-24 10:43 作者: seroma 時(shí)間: 2025-3-24 18:53
Is the Persistence of the , a Result of Constant Confirmation Bias?,of researchers who?challenge it. The current “defect” of the . is that its supporters see their ultimate proof in the clinical success of clearing amyloid beta from the brain of affected individuals. However, so far, removal of the peptide did not result in a convincing clinical benefit or breakthro作者: Pruritus 時(shí)間: 2025-3-24 20:35 作者: 完成 時(shí)間: 2025-3-25 02:19
Book 2023s still not been convincingly proven in the clinics? Are there other hypotheses that might explainthe pathogenesis of this complex brain disease, and if so, why were these perspectives not adequately followed?.In this book, Behl tries to answer these questions. Starting with the historical backgroun作者: 屈尊 時(shí)間: 2025-3-25 07:05 作者: 凝結(jié)劑 時(shí)間: 2025-3-25 09:22 作者: Vasodilation 時(shí)間: 2025-3-25 11:43 作者: 記憶法 時(shí)間: 2025-3-25 18:47 作者: GRIN 時(shí)間: 2025-3-25 23:33 作者: 變態(tài) 時(shí)間: 2025-3-26 02:14 作者: 虛情假意 時(shí)間: 2025-3-26 04:52 作者: 無情 時(shí)間: 2025-3-26 12:05
Getting to the Bottom of It: Amyloid Beta Peptide Is Derived from a Larger Precursor,y?of amyloid beta research. For instance, a link of herpes simplex virus to Alzheimer’s disease was described and a role of nerve cell survival factors (neurotrophic factors) in its pathogenesis was proposed. However, all these additional findings were largely overshadowed by the excitement over amy作者: Inelasticity 時(shí)間: 2025-3-26 13:47
,Step by Step Toward an Amyloid Beta Peptide-Based Hypothesis of Alzheimer’s Disease,on approach targeting amyloid can retrospectively be defined as the hot phase in Alzheimer’s research. Most strikingly, human genetics delivered evidence that mutations in the . gene are linked to dominantly inherited familial forms of the disease. Subsequently, two more genes were identified as Alz作者: 愉快么 時(shí)間: 2025-3-26 20:00
Concerns about the , and Reappraisals, a pathogenetic role, the . has?remained the most influential and field-guiding hypothesis in Alzheimer’s disease research..Even?more than three decades after its introduction, this hypothesis still?asserts its dominance, and amyloid persists as the prime target in the search for a . therapy; clinic作者: 挫敗 時(shí)間: 2025-3-26 23:13
Ignorance or Conspiracy? Or Just an , that Blocks Alternative Ideas?,l incidents, reported or found in the literature, could prove that innovative ideas that do not conform with the dominating view in the field are neglected, blinded out, and not accordingly funded. All of this happened in the public eye and rather obviously. As a consequence, an increasing number of作者: 不能平靜 時(shí)間: 2025-3-27 01:45
In the Slip Stream of Amyloid: The ,ntually leading to the formation of tau fibrils and NFTs, thereby disturbing microtubular structure and function and impacting neuronal signal and synaptic transmission. In postmortem Alzheimer’s tissue, tangles are addressed as remnants of degenerated neurons..The ., also called ., defines the deve作者: Indecisive 時(shí)間: 2025-3-27 06:31 作者: insert 時(shí)間: 2025-3-27 09:49
,Alzheimer’s Research Gains Momentum and Spreads Out,bodies were developed as a therapy approach..Besides all the findings that?further confirmed a pathogenic role of amyloid beta?in particular, the physiological role of APP and its fragments was also?brought back into the discussion. Because of the almost exclusive focus on APP as the (pathological) 作者: HIKE 時(shí)間: 2025-3-27 16:52
The , Has to Deliver, Finally, the pillar in the search for a . therapy. Unfortunately, all the clinical trials aiming to interrupt amyloid beta generation, aggregation, deposition, or its clearance from the brain have?largely failed until 2021..In the last decade, a whole series of anti-amyloid antibodies were tested. With each作者: MAG 時(shí)間: 2025-3-27 18:52
Beyond ,, ,, ,, and ,: What Else Does the Genome Tell Us?,k genes can be largely grouped into three biological categories comprising (1) lipid and cholesterol metabolism and homeostasis, (2) endocytosis, vesicle-mediated transport, trafficking, and (3) immune response..One of the most prominent risk genes identified by GWAS was the gene coding for TREM2 (“作者: doxazosin 時(shí)間: 2025-3-28 01:57 作者: DEFER 時(shí)間: 2025-3-28 05:14 作者: 嗎啡 時(shí)間: 2025-3-28 07:39
,Driving Forces of Alzheimer’s Research Directions,or newcomers in a research area, it might look more promising to follow the supported and acknowledged mainstream, meaning the dominating view, rather than going down a controversial path. This certainly applies to some developments in the field of Alzheimer’s research in the last three decades, res作者: 外觀 時(shí)間: 2025-3-28 11:38
https://doi.org/10.1007/978-3-662-39472-4ature from already about 1500?years ago. Several forms of dementia exist, and it was owed to the German?psychiatrist Emil Kraepelin who in 1910 gave Alois Alzheimer’s clinical and pathological observations the name “Alzheimersche Krankheit,” Alzheimer’s disease.作者: 強(qiáng)制令 時(shí)間: 2025-3-28 16:42 作者: hypnotic 時(shí)間: 2025-3-28 20:24 作者: famine 時(shí)間: 2025-3-29 02:56 作者: 提名的名單 時(shí)間: 2025-3-29 06:09 作者: 山頂可休息 時(shí)間: 2025-3-29 09:03 作者: CHAR 時(shí)間: 2025-3-29 14:50
https://doi.org/10.1007/978-3-642-92571-9logy of this peptide derived from the brain of Alzheimer’s patients and from individuals with a trisomy 21 pointed toward the smallest human chromosomes, chromosome 21. The biochemical characterization of the amyloid beta peptide was the beginning of a new era in Alzheimer’s disease research.作者: Harpoon 時(shí)間: 2025-3-29 18:05 作者: 粉筆 時(shí)間: 2025-3-29 19:49 作者: 狼群 時(shí)間: 2025-3-30 01:09 作者: CESS 時(shí)間: 2025-3-30 05:47
https://doi.org/10.1007/978-3-642-85287-9l incidents, reported or found in the literature, could prove that innovative ideas that do not conform with the dominating view in the field are neglected, blinded out, and not accordingly funded. All of this happened in the public eye and rather obviously. As a consequence, an increasing number of作者: Insensate 時(shí)間: 2025-3-30 11:09
https://doi.org/10.1007/978-3-642-85287-9ntually leading to the formation of tau fibrils and NFTs, thereby disturbing microtubular structure and function and impacting neuronal signal and synaptic transmission. In postmortem Alzheimer’s tissue, tangles are addressed as remnants of degenerated neurons..The ., also called ., defines the deve作者: guardianship 時(shí)間: 2025-3-30 14:41 作者: Cholesterol 時(shí)間: 2025-3-30 18:45
https://doi.org/10.1007/978-3-662-29093-4bodies were developed as a therapy approach..Besides all the findings that?further confirmed a pathogenic role of amyloid beta?in particular, the physiological role of APP and its fragments was also?brought back into the discussion. Because of the almost exclusive focus on APP as the (pathological) 作者: 半導(dǎo)體 時(shí)間: 2025-3-30 22:58 作者: Abrupt 時(shí)間: 2025-3-31 04:54 作者: irreparable 時(shí)間: 2025-3-31 06:01 作者: lymphedema 時(shí)間: 2025-3-31 10:40
https://doi.org/10.1007/978-3-662-29092-7o further increase in the amount of confirmatory data.. is a phenomenon that often occurs in science and it is also observable in Alzheimer’s research, in concert with less balanced and biased discussions. It is very hard to argue against a leading hypothesis that is equipped with, at first sight, c作者: Ascribe 時(shí)間: 2025-3-31 14:41
Die Verrenkungen im Schultergelenke,or newcomers in a research area, it might look more promising to follow the supported and acknowledged mainstream, meaning the dominating view, rather than going down a controversial path. This certainly applies to some developments in the field of Alzheimer’s research in the last three decades, res作者: majestic 時(shí)間: 2025-3-31 20:40
explainthe pathogenesis of this complex brain disease, and if so, why were these perspectives not adequately followed?.In this book, Behl tries to answer these questions. Starting with the historical backgroun978-3-031-31572-5978-3-031-31570-1作者: Budget 時(shí)間: 2025-4-1 01:37
https://doi.org/10.1007/978-3-662-39472-4ted. Age is one major risk factor for the disease and, therefore, it is anticipated that the number of patients will constantly rise as life expectancy keeps increasing?generally. Since the invention of the label “Alzheimer’s disease,” researchers in academia and the pharmaceutical industry worldwid
