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https://www.readbyqxmd.com/read/27921029/nanoscale-structure-and-spectroscopic-probing-of-a%C3%AE-1-40-fibril-bundle-formation
#1
Katarzyna M Psonka-Antonczyk, Per Hammarström, Leif B G Johansson, Mikael Lindgren, Bjørn T Stokke, K Peter R Nilsson, Sofie Nyström
Amyloid plaques composed of fibrillar Amyloid-β (Aβ) are hallmarks of Alzheimer's disease. However, Aβ fibrils are morphologically heterogeneous. Conformation sensitive luminescent conjugated oligothiophenes (LCOs) are versatile tools for monitoring such fibril polymorphism in vivo and in vitro. Biophysical methods applied on in vitro generated Aβ fibrils, stained with LCOs with different binding and fluorescence properties, can be used to characterize the Aβ fibrillation in depth, far beyond that possible for in vivo generated amyloid plaques...
2016: Frontiers in Chemistry
https://www.readbyqxmd.com/read/27917428/ftir-imaging-of-the-molecular-burden-around-a%C3%AE-deposits-in-an-early-stage-3-tg-app-psp1-tau-mouse-model-of-alzheimer-s-disease
#2
Artur Dawid Surowka, Michael Pilling, Alex Henderson, Herve Boutin, Lidan Christie, Magdalena Szczerbowska-Boruchowska, Peter Gardner
Alzheimer's disease is one of the major causes of dementia in the elderly. The disease is caused by the misfolding of water soluble alpha-helical proteins, which leads to the accumulation of β-sheets in the form of amyloid plaques, which can subsequently affect surrounding tissue areas by oxidative stress neurotoxicity. The aim of the present study was to design a novel methodology to analyze the extent to the neuronal burden around protein-rich Aβ plaques suspected to affect molecular components by oxidative stress induced by inflammatory states...
December 5, 2016: Analyst
https://www.readbyqxmd.com/read/27917270/effect-of-creatine-supplementation-on-cognitive-performance-and-apoptosis-in-a-rat-model-of-amyloid-beta-induced-alzheimer-s-disease
#3
Malek Alimohammadi-Kamalabadi, Mohammadreza Eshraghian, Mohammad-Reza Zarindast, Abbas Aliaghaei, Hamideh Pishva
OBJECTIVES: Neuroprotective effect of creatine (Cr) against β-amyloid (Aβ) is reported in an in vitro study. This study investigated the effect of Cr supplementation on β-amyloid toxicity in vivo. MATERIALS AND METHODS: Thirty two, male Wistar rats were divided into 4 groups. During ten weeks of study, control group went through no surgical or dietary intervention. At the 4th week of study Sham group had a hippocampal normal saline injection, while Aβ and AβCr groups had an β-amyloid injection in the hippocampus...
November 2016: Iranian Journal of Basic Medical Sciences
https://www.readbyqxmd.com/read/27917152/amyloid-dysmetabolism-relates-to-reduced-glucose-uptake-in-white-matter-hyperintensities
#4
Lisa Flem Kalheim, Per Selnes, Atle Bjørnerud, Christopher Coello, Kjetil Vegge, Tormod Fladby
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder and cause of dementia and is characterized by amyloid plaques and neurofibrillary tangles. AD has traditionally been considered to primarily affect gray matter, but multiple lines of evidence also indicate white matter (WM) pathology and associated small-vessel cerebrovascular disease. WM glucose delivery and metabolism may have implications for local tissue integrity, and [(18)F]-fluorodeoxyglucose positron emission tomography (FDG-PET) may be helpful to assess neuroglial and axonal function in WM...
2016: Frontiers in Neurology
https://www.readbyqxmd.com/read/27915995/lack-of-p-glycoprotein-results-in-impairment-of-removal-of-beta-amyloid-and-increased-intraparenchymal-cerebral-amyloid-angiopathy-after-active-immunization-in-a-transgenic-mouse-model-of-alzheimer-s-disease
#5
Sascha Brückmann, Anja Brenn, Markus Grube, Katharina Niedrig, Silva Holtfreter, Oliver von Bohlen Und Halbach, Martin Groschup, Markus Keller, Silke Vogelgesang
Immunization against beta-amyloid (Aβ) reduces cerebral Aβ deposits and improves cognitive capacities in transgenic mouse models, and thus has been considered a promising disease-modifying therapeutic approach for Alzheimer's disease (AD). Although clinical trials in AD patients have yielded evidence for clearance of parenchymal Aβ plaques, Aβ increases in blood vessels of treated patients. We hypothesize that an age-related decline in the mechanisms that clear Aβ from the brain might be at least in part responsible for the failure to purge and re-distribute Aβ...
December 1, 2016: Current Alzheimer Research
https://www.readbyqxmd.com/read/27914799/computational-approach-for-the-assessment-of-inhibitory-potency-against-beta-amyloid-aggregation
#6
Marek Bajda, Sławomir Filipek
Beta-amyloid (Aβ) plaques are one of the hallmarks of Alzheimer's disease. Their presence in the brain leads to neurodegeneration and memory decline. Therefore, search for new drugs able to decrease formation of such deposits is of great interest. Our previously developed multifunctional compounds inhibited transformation of monomers into fibrils. Herein, we describe the computational approach for the assessment of inhibitory activity against Aβ aggregation. The influence of novel inhibitors on amyloid Aβ17-42 was studied by employing of molecular docking and all-atom molecular dynamics simulations...
November 24, 2016: Bioorganic & Medicinal Chemistry Letters
https://www.readbyqxmd.com/read/27911317/alzheimer-s-disease-histological-and%C3%A2-behavioral-manifestations-in%C3%A2-transgenic-mice-correlate-with%C3%A2-specific%C3%A2-gut-microbiome-state
#7
Liang Shen, Lu Liu, Hong-Fang Ji
Alzheimer's disease (AD) is a neurodegenerative brain disease and is the most common form of dementia. In recent years, many studies indicated the association of gut microbiota changes with metabolic diseases. However, the gut microbiota of AD has not been investigated. The present study aims to compare the gut microbiota in APP/PS1 transgenic mice of AD and C57/Bl6 wild-type (WT) mice by pyrosequencing the V3 and V4 regions of the bacterial 16S ribosomal RNA genes. The 3-, 6-, and 8-month-old APP/PS1 and WT mice were used to explore the effects of age on the gut microbiota...
November 28, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/27911312/increased-transforming-growth-factor-%C3%AE-2-in-the-neocortex-of-alzheimer-s-disease-and-dementia-with-lewy-bodies-is%C3%A2-correlated-with-disease-severity-and%C3%A2-soluble-a%C3%AE-42-load
#8
Joyce R Chong, Yuek Ling Chai, Jasinda H Lee, David Howlett, Johannes Attems, Clive G Ballard, Dag Aarsland, Paul T Francis, Christopher P Chen, Mitchell K P Lai
BACKGROUND: Of the three transforming growth factor (TGF)-β isoforms known, TGFβ1 deficits have been widely reported in Alzheimer's disease (AD) and studied as a potential therapeutic target. In contrast, the status of TGFβ2, which has been shown to mediate amyloid-β (Aβ)-mediated neuronal death, are unclear both in AD and in Lewy body dementias (LBD) with differential neuritic plaque and neurofibrillary tangle burden. OBJECTIVE: To measure neocortical TGFβ2 levels and their correlations with neuropathological and clinical markers of disease severity in a well-characterized cohort of AD as well as two clinical subtypes of LBD, dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), known to manifest relatively high and low Aβ plaque burden, respectively...
November 28, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/27911291/a-metal-free-method-for-producing-mri-contrast-at-amyloid-%C3%AE
#9
Silvia Hilt, Tang Tang, Jeffrey H Walton, Madhu Budamagunta, Izumi Maezawa, Tamás Kálai, Kálmán Hideg, Vikrant Singh, Heike Wulff, Qizhi Gong, Lee-Way Jin, Angelique Louie, John C Voss
Alzheimer's disease (AD) is characterized by depositions of the amyloid-β (Aβ) peptide in the brain. The disease process develops over decades, with substantial neurological loss occurring before a clinical diagnosis of dementia can be rendered. It is therefore imperative to develop methods that permit early detection and monitoring of disease progression. In addition, the multifactorial pathogenesis of AD has identified several potential avenues for AD intervention. Thus, evaluation of therapeutic candidates over lengthy trial periods also demands a practical, noninvasive method for measuring Aβ in the brain...
November 26, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/27909447/stem-cell-therapy-a-prospective-treatment-for-alzheimer-s-disease
#10
REVIEW
Ji Han Lee, Il-Hoan Oh, Hyun Kook Lim
Alzheimer's disease (AD) without cure remains as a serious health issue in the modern society. The major neuropathological alterations in AD are characterized by chronic neuroinflammation and neuronal loss due to neurofibrillary tangles (NFTs) of abnormally hyperphosphorylated tau, plaques of β-amyloid (Aβ) and various metabolic dysfunctions. Due to the multifaceted nature of AD pathology and our limited understanding on its etiology, AD is difficult to be treated with currently available pharmaceuticals...
November 2016: Psychiatry Investigation
https://www.readbyqxmd.com/read/27906438/cholinesterase-inhibitors-and-non-steroidal-anti-inflammatory-drugs-as-alzheimer-s-disease-therapies-an-updated-umbrella-review-of-systematic-reviews-and-meta-analyses
#11
C-H Wang, L-S Wang, N Zhu
OBJECTIVE: Alzheimer's Disease (AD) is a major neurological disorder marked by an amyloid-beta plaque and neurofibrillary tau-tangle depositions in the brain. Cognitive dysfunction is the key manifestation of AD. In this study, we conducted an umbrella review of meta-analyses on the risk factors and therapeutics targeting cognitive impairment and AD. MATERIALS AND METHODS: We searched PubMed from January 2000-August, 2016, and screened systematic reviews and meta-analyses of studies that examined the effects of cholinesterase inhibitors in AD patients...
November 2016: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/27906174/therapeutic-advantage-of-pro-electrophilic-drugs-to-activate-the-nrf2-are-pathway-in-alzheimer-s-disease-models
#12
Stuart A Lipton, Tayebeh Rezaie, Anthony Nutter, Kevin M Lopez, James Parker, Kunio Kosaka, Takumi Satoh, Scott R McKercher, Eliezer Masliah, Nobuki Nakanishi
Alzheimer's disease (AD) is characterized by synaptic and neuronal loss, which occurs at least partially through oxidative stress induced by oligomeric amyloid-β (Aβ)-peptide. Carnosic acid (CA), a chemical found in rosemary and sage, is a pro-electrophilic compound that is converted to its active form by oxidative stress. The active form stimulates the Keap1/Nrf2 transcriptional pathway and thus production of phase 2 antioxidant enzymes. We used both in vitro and in vivo models. For in vitro studies, we evaluated protective effects of CA on primary neurons exposed to oligomeric Aβ...
December 1, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27905353/-twenty-five-years-of-the-amyloid-hypothesis-of-alzheimer-disease-advances-failures-and-new-perspectives
#13
O S Levin, E E Vasenina
Amyloid hypothesis of Alzheimer's disease (AD) has been long the primary one. During the 25-year history the concept has been dramatically changed. Accumulation of β-amyloid is associated not only with the disruption of its synthesis (as it seemed after the discovery of genetic mechanisms of some familial cases of AD) but rather with the disruption of its clearance and elimination from the brain tissue via the microcirculatory system. It has been recognized that soluble oligomers of β-amyloid, but not senile plaques that consisted of insoluble conjugates described by A...
2016: Zhurnal Nevrologii i Psikhiatrii Imeni S.S. Korsakova
https://www.readbyqxmd.com/read/27904493/beta-2-adrenergic-receptor-activation-enhances-neurogenesis-in-alzheimer-s-disease-mice
#14
Gao-Shang Chai, Yang-Yang Wang, Amina Yasheng, Peng Zhao
Impaired hippocampal neurogenesis is one of the early pathological features of Alzheimer's disease. Enhancing adult hippocampal neurogenesis has been pursued as a potential therapeutic strategy for Alzheimer's disease. Recent studies have demonstrated that environmental novelty activates β2-adrenergic signaling and prevents the memory impairment induced by amyloid-β oligomers. Here, we hypothesized that β2-adrenoceptor activation would enhance neurogenesis and ameliorate memory deficits in Alzheimer's disease...
October 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/27904476/impairment-of-the-nerve-growth-factor-pathway-driving-amyloid-accumulation-in-cholinergic-neurons-the-incipit-of-the-alzheimer-s-disease-story
#15
REVIEW
Viviana Triaca, Pietro Calissano
The current idea behind brain pathology is that disease is initiated by mild disturbances of common physiological processes. Overtime, the disruption of the neuronal homeostasis will determine irreversible degeneration and neuronal apoptosis. This could be also true in the case of nerve growth factor (NGF) alterations in sporadic Alzheimer's disease (AD), an age-related pathology characterized by cholinergic loss, amyloid plaques and neurofibrillary tangles. In fact, the pathway activated by NGF, a key neurotrophin for the metabolism of basal forebrain cholinergic neurons (BFCN), is one of the first homeostatic systems affected in prodromal AD...
October 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/27900387/a-modification-specific-peptide-based-immunization-approach-using-crm197-carrier-protein-development-of-a-selective-vaccine-against-pyroglutamate-a%C3%AE-peptides
#16
Valérie Vingtdeux, Haitian Zhao, Pallavi Chandakkar, Christopher M Acker, Peter Davies, Philippe Marambaud
Strategies aimed at reducing cerebral accumulation of the amyloid-β (Aβ) peptides have therapeutic potential in Alzheimer's disease (AD). Aβ immunization has proven to be effective at promoting Aβ clearance in animal models but adverse effects have hampered its clinical evaluation. The first anti-Aβ immunization clinical trial, which assessed a full-length Aβ1-42 vaccine, increased the risk of encephalitis most likely because of autoimmune pro-inflammatory T helper 1 (Th1) response against all forms of Aβ...
November 28, 2016: Molecular Medicine
https://www.readbyqxmd.com/read/27898114/vibration-induced-emission-vie-for-imaging-amyloid-%C3%AE-fibrils
#17
Wei-Tao Dou, Wei Chen, Xiao-Peng He, Jianhua Su, He Tian
This paper discusses the use of N,N'-disubstituted-dihydrodibenzo[a,c]phenazines with typical Vibration-Induced-Emission (VIE) properties for imaging amyloid β (Aβ) fibrils, which are a signature of neurological disorders such as Alzheimer's disease. A water-soluble VIEgen with a red fluorescence emission shows a pronounced, blue-shifted emission with Aβ peptide monomers and fibrils. The enhancement in blue fluorescence can be ascribed to the restriction of the molecular vibration by selectively binding to Aβ...
November 29, 2016: Faraday Discussions
https://www.readbyqxmd.com/read/27895978/cytokines-and-cytokine-receptors-involved-in-the-pathogenesis-of-alzheimer-s-disease
#18
Tomone Nagae, Kiho Araki, Yuki Shimoda, Lucia I Sue, Thomas G Beach, Yoshihiro Konishi
Inflammatory mechanisms are implicated in the pathology of Alzheimer's disease (AD). However, it is unclear whether inflammatory alterations are a cause or consequence of neurodegeneration leading to dementia. Clarifying this issue would provide valuable insight into the early diagnosis and therapeutic management of AD. To address this, we compared the mRNA expression profiles of cytokines in the brains of AD patients with "non-demented individuals with AD pathology" and non-demented healthy control (ND) individuals...
August 2016: Journal of Clinical & Cellular Immunology
https://www.readbyqxmd.com/read/27895577/fus1-ko-mouse-as-a-model-of-oxidative-stress-mediated-sporadic-alzheimer-s-disease-circadian-disruption-and-long-term-spatial-and-olfactory-memory-impairments
#19
Guillermo Coronas-Samano, Keeley L Baker, Winston J T Tan, Alla V Ivanova, Justus V Verhagen
Insufficient advances in the development of effective therapeutic treatments of sporadic Alzheimer's Disease (sAD) to date are largely due to the lack of sAD-relevant animal models. While the vast majority of models do recapitulate AD's hallmarks of plaques and tangles by virtue of tau and/or beta amyloid overexpression, these models do not reflect the fact that in sAD (unlike familial AD) these genes are not risk factors per se and that other mechanisms like oxidative stress, metabolic dysregulation and inflammation play key roles in AD etiology...
2016: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/27891223/is-apoe-%C3%A9-4-a-good-biomarker-for-amyloid-pathology-in-late-onset-alzheimer-s-disease
#20
REVIEW
Maowen Ba, Min Kong, Xiaofeng Li, Kok Pin Ng, Pedro Rosa-Neto, Serge Gauthier
Amyloid plaques are pathological hallmarks of Alzheimer's Disease (AD) and biomarkers such as cerebrospinal fluid (CSF) β-amyloid 1-42 (Aβ1-42) and amyloid positron emission tomographic (PET) imaging are important in diagnosing amyloid pathology in vivo. ɛ4 allele of the Apolipoprotein E gene (ApoE ɛ 4), which is a major genetic risk factor for late onset AD, is an important genetic biomarker for AD pathophysiology. It has been shown that ApoE ɛ 4 is involved in Aβ deposition and formation of amyloid plaques...
2016: Translational Neurodegeneration
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