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https://www.readbyqxmd.com/read/28816110/reduced-beta-amyloid-sensitivity-for-platelet-monocyte-aggregates-in-edta-blood-of-alzheimer-patients
#1
Michaela Defrancesco, Josef Marksteiner, Christian Humpel
Alzheimer´s disease (AD) is a severe neurodegenerative brain disorder characterized by beta-amyloid plaques, Tau pathology, inflammation, neurodegeneration, and cerebrovascular dysfunction. Besides that, alterations in monocytes and platelets have been reported in the blood of Alzheimer patients. In the present study, we measured circulating levels of platelet-monocyte aggregates in EDTA blood of cognitively healthy participants and 40 AD patients, and examined their changes induced by stimulation with beta-amyloid peptides...
August 17, 2017: International Psychogeriatrics
https://www.readbyqxmd.com/read/28815528/alzheimer-disease
#2
Estela Area-Gomez, Eric A Schon
The most widely accepted hypothesis to explain the pathogenesis of Alzheimer disease (AD) is the amyloid cascade, in which the accumulation of extraneuritic plaques and intracellular tangles plays a key role in driving the course and progression of the disease. However, there are other biochemical and morphological features of AD, including altered calcium, phospholipid, and cholesterol metabolism and altered mitochondrial dynamics and function that often appear early in the course of the disease, prior to plaque and tangle accumulation...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28814675/retinal-amyloid-pathology-and-proof-of-concept-imaging-trial-in-alzheimer-s-disease
#3
Yosef Koronyo, David Biggs, Ernesto Barron, David S Boyer, Joel A Pearlman, William J Au, Shawn J Kile, Austin Blanco, Dieu-Trang Fuchs, Adeel Ashfaq, Sally Frautschy, Gregory M Cole, Carol A Miller, David R Hinton, Steven R Verdooner, Keith L Black, Maya Koronyo-Hamaoui
BACKGROUND: Noninvasive detection of Alzheimer's disease (AD) with high specificity and sensitivity can greatly facilitate identification of at-risk populations for earlier, more effective intervention. AD patients exhibit a myriad of retinal pathologies, including hallmark amyloid β-protein (Aβ) deposits. METHODS: Burden, distribution, cellular layer, and structure of retinal Aβ plaques were analyzed in flat mounts and cross sections of definite AD patients and controls (n = 37)...
August 17, 2017: JCI Insight
https://www.readbyqxmd.com/read/28812438/acute-formaldehyde-exposure-induced-early-alzheimer-like-changes-in-mouse-brain
#4
Xudong Liu, Yuchao Zhang, Ruliu Wu, Meng Ye, Yuqing Zhao, Jun Kang, Ping Ma, Jinquan Li, Xu Yang
Alzheimer's disease (AD) is a serious, common, global disease, yet its etiology and pathogenesis are incompletely understood. Although an association between AD and exposure to air pollutants has been discussed, the effects of pollutants on the functioning of the brain remain unclear. The indoor environment is where exposure to formaldehyde (FA) can occur. Whether exposure to FA contributes to the development of AD needs to be investigated. To determine the objective, C57BL/6 mice were exposed daily to FA (0, 0...
August 16, 2017: Toxicology Mechanisms and Methods
https://www.readbyqxmd.com/read/28811745/inhibition-of-inflammation-mediated-through-the-tumor-necrosis-factor-%C3%AE-biochemical-pathway-can-lead-to-favorable-outcomes-in-alzheimer-disease
#5
REVIEW
Daniah Shamim, Michael Laskowski
Tumor necrosis factor α (TNF-α) inhibitors have long been used as disease-modifying agents in immune disorders. Recently, research has shown a role of chronic neuroinflammation in the pathophysiology of neurodegenerative diseases such as Alzheimer disease, and interest has been generated in the use of anti-TNF agents and TNF-modulating agents for prevention and treatment. This article extensively reviewed literature on animal studies testing these agents. The results showed a role for direct and indirect TNF-α inhibition through agents such as thalidomide, 3,6-dithiothalidomide, etanercept, infliximab, exendin-4, sodium hydrosulfide, minocycline, imipramine, and atorvastatin...
2017: Journal of Central Nervous System Disease
https://www.readbyqxmd.com/read/28803064/high-glucose-induces-tau-hyperphosphorylation-through-activation-of-tlr9-p38mapk-pathway
#6
Yue Sun, Qian Xiao, Cheng Luo, Yuxing Zhao, Die Pu, Kexiang Zhao, Jinliang Chen, Meili Wang, Zhiyin Liao
Diabetic encephalopathy (DE) is one of the most common complications of diabetes. The major pathological variations include neurofibrillary tangles (NFTs), which are caused by tau hyperphosphorylation, and senile plaques (SPs) consisting of amyloid β- protein(Aβ) deposits. In recent years, DE research studies have focused on exploring the activation of the inflammatory signaling pathway in immune cells. Toll-like receptor 9 (TLR9) is well known to regulate the inflammatory reactions in immune processes. During the tau hyperphosphorylation process, TLR9 in microglia plays bidirectional roles...
August 9, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28802038/trem2-maintains-microglial-metabolic-fitness-in-alzheimer-s-disease
#7
Tyler K Ulland, Wilbur M Song, Stanley Ching-Cheng Huang, Jason D Ulrich, Alexey Sergushichev, Wandy L Beatty, Alexander A Loboda, Yingyue Zhou, Nigel J Cairns, Amal Kambal, Ekaterina Loginicheva, Susan Gilfillan, Marina Cella, Herbert W Virgin, Emil R Unanue, Yaming Wang, Maxim N Artyomov, David M Holtzman, Marco Colonna
Elevated risk of developing Alzheimer's disease (AD) is associated with hypomorphic variants of TREM2, a surface receptor required for microglial responses to neurodegeneration, including proliferation, survival, clustering, and phagocytosis. How TREM2 promotes such diverse responses is unknown. Here, we find that microglia in AD patients carrying TREM2 risk variants and TREM2-deficient mice with AD-like pathology have abundant autophagic vesicles, as do TREM2-deficient macrophages under growth-factor limitation or endoplasmic reticulum (ER) stress...
August 10, 2017: Cell
https://www.readbyqxmd.com/read/28801921/autophagy-impairment-by-caspase-1-dependent-inflammation-mediates-memory-loss-in-response-to-%C3%AE-amyloid-peptide-accumulation
#8
Lourdes Álvarez-Arellano, Martha Pedraza-Escalona, Tonali Blanco-Ayala, Nohemí Camacho-Concha, Javier Cortés-Mendoza, Leonor Pérez-Martínez, Gustavo Pedraza-Alva
β-Amyloid peptide accumulation in the cortex and in the hippocampus results in neurodegeneration and memory loss. Recently, it became evident that the inflammatory response triggered by β-Amyloid peptides promotes neuronal cell death and degeneration. In addition to inflammation, β-Amyloid peptides also induce alterations in neuronal autophagy, eventually leading to neuronal cell death. Thus, here we evaluated whether the inflammatory response induced by the β-Amyloid peptides impairs memory via disrupting the autophagic flux...
August 12, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/28800454/tau-protein-aggregation-in-alzheimer-s-disease-an-attractive-target-for-the-development-of-novel-therapeutic-agents
#9
Marie Jouanne, Sylvain Rault, Anne-Sophie Voisin-Chiret
Alzheimer's Disease (AD) is a neurodegenerative brain disorder in which many biological dysfunctions are involved. Among them, two main types of lesions were discovered and widely studied: the amyloid plaques and the neurofibrillary tangles (NFTs). These two lesions are caused by the dysfunction and the accumulation of two proteins which are, respectively, the beta-amyloid peptide and the tau protein. The process that leads these two proteins to aggregate is complex and is the subject of current studies. After a brief description of the aggregation mechanisms, we will provide an overview of new therapeutic agents targeting the different dysfunctions and toxic species found during aggregation...
July 29, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28800329/chronic-verubecestat-treatment-suppresses-amyloid-accumulation-in-advanced-aged-tg2576-a%C3%AE-ppswe-mice-without-inducing-microhemorrhage
#10
Stephanie Villarreal, Fuqiang Zhao, Lynn A Hyde, Daniel Holder, Thomas Forest, Marie Sondey, Xia Chen, Cyrille Sur, Eric M Parker, Matthew E Kennedy
Verubecestat is a potent BACE1 enzyme inhibitor currently being investigated in Phase III trials for the treatment of mild-to-moderate and prodromal Alzheimer's disease. Multiple anti-amyloid immunotherapies have been dose-limited by adverse amyloid related imaging abnormalities such as vasogenic edema (ARIA-E) and microhemorrhage (ARIA-H) observed in human trials and mice. Verubecestat was tested in a 12-week nonclinical study for the potential to exacerbate microhemorrhage (ARIA-H) profiles in 18-22-month-old post-plaque Tg2576-AβPPswe mice...
August 8, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28799137/ethanol-alters-app-processing-and-aggravates-alzheimer-associated-phenotypes
#11
Daochao Huang, Mengjiao Yu, Shou Yang, Dandan Lou, Weitao Zhou, Lingling Zheng, Zhe Wang, Fang Cai, Weihui Zhou, Tingyu Li, Weihong Song
The majority of Alzheimer's disease (AD) cases are sporadic with unknown causes. Many dietary factors including excessive alcohol intake have been reported to increase the risk to develop AD. The effect of alcohol on cognitive functions and AD pathogenesis remains elusive. In this study, we investigated the relationship between ethanol exposure and Alzheimer's disease. Cell cultures were treated with ethanol at different dosages for different durations up to 48 h and an AD model mouse was fed with ethanol for 4 weeks...
August 10, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28795133/performance-of-18-f-flutemetamol-amyloid-imaging-against-the-neuritic-plaque-component-of-cerad-and-the-current-2012-nia-aa-recommendations-for-the-neuropathologic-diagnosis-of-alzheimer-s-disease
#12
Stephen Salloway, Jose E Gamez, Upinder Singh, Carl H Sadowsky, Teresa Villena, Marwan N Sabbagh, Thomas G Beach, Ranjan Duara, Adam S Fleisher, Kirk A Frey, Zuzana Walker, Arvinder Hunjan, Yavir M Escovar, Marc E Agronin, Joel Ross, Andrea Bozoki, Mary Akinola, Jiong Shi, Rik Vandenberghe, Milos D Ikonomovic, Paul F Sherwin, Gill Farrar, Adrian P L Smith, Christopher J Buckley, Dietmar Rudolf Thal, Michelle Zanette, Craig Curtis
INTRODUCTION: Performance of the amyloid tracer [(18)F]flutemetamol was evaluated against three pathology standard of truth (SoT) measures including neuritic plaques (CERAD "original" and "modified" and the amyloid component of the 2012 NIA-AA guidelines). METHODS: After [(18)F]flutemetamol imaging, 106 end-of-life patients who died underwent postmortem brain examination for amyloid plaque load. Blinded positron emission tomography scan interpretations by five independent electronically trained readers were compared with pathology measures...
2017: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
https://www.readbyqxmd.com/read/28790893/brain-and-peripheral-atypical-inflammatory-mediators-potentiate-neuroinflammation-and-neurodegeneration
#13
REVIEW
Duraisamy Kempuraj, Ramasamy Thangavel, Govindhasamy P Selvakumar, Smita Zaheer, Mohammad E Ahmed, Sudhanshu P Raikwar, Haris Zahoor, Daniyal Saeed, Prashant A Natteru, Shankar Iyer, Asgar Zaheer
Neuroinflammatory response is primarily a protective mechanism in the brain. However, excessive and chronic inflammatory responses can lead to deleterious effects involving immune cells, brain cells and signaling molecules. Neuroinflammation induces and accelerates pathogenesis of Parkinson's disease (PD), Alzheimer's disease (AD) and Multiple sclerosis (MS). Neuroinflammatory pathways are indicated as novel therapeutic targets for these diseases. Mast cells are immune cells of hematopoietic origin that regulate inflammation and upon activation release many proinflammatory mediators in systemic and central nervous system (CNS) inflammatory conditions...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28790170/dimerization-of-the-transmembrane-domain-of-amyloid-precursor-protein-is-determined-by-residues-around-the-gamma-secretase-cleavage-sites
#14
Yan Yan, Ting-Hai Xu, Kaleeckal G Harikumar, Laurence J Miller, Karsten Melcher, H Eric Xu
One of the hallmarks of Alzheimer's disease (AD) is the formation of extracellular amyloid plaques that consist mainly of abnormally aggregated forms of amyloid β (Aβ) peptides. These peptides are generated by γ-secretase-catalyzed cleavage of a dimeric membrane-bound C-terminal fragment (C99) of the amyloid precursor protein (APP). While C99 homodimerization has been linked to Aβ; production and changes in the aggregation-determining Aβ42/Aβ40 ratio, the motif through which C99 dimerizes has remained controversial...
August 8, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28790016/tau-imaging-in-neurodegeneration
#15
REVIEW
Gérard N Bischof, Heike Endepols, Thilo van Eimeren, Alexander Drzezga
Pathological cerebral aggregations of proteins are suggested to play a crucial role in the development of neurodegenerative disorders. For example, aggregation of the protein ß-amyloid in form of extracellular amyloid-plaques as well as intraneuronal depositions of the protein tau in form of neurofibrillary tangles represent hallmarks of Alzheimer's disease (AD). Recently, novel tracers for in vivo molecular imaging of tau-aggregates in the brain have been introduced, complementing existing tracers for imaging amyloid-plaques...
August 5, 2017: Methods: a Companion to Methods in Enzymology
https://www.readbyqxmd.com/read/28779977/an-a%C3%AE-3-10-klh-vaccine-reduced-alzheimer-s-disease-like-pathology-and-had-a-sustained-effect-in-tg-appswe-psen1de9-mice
#16
Yuan Meng, Li Ding, Hui-Yi Zhang, Wen-Chao Yin, Yi Yan, Yun-Peng Cao
Alzheimer's disease is a neurodegenerative disease that affects many patients worldwide. The amyloid cascade hypothesis has been adopted by most researchers as the mechanism underlying Alzheimer's disease. Aβ plaques have been considered the core factor in the neurotoxic effect in Alzheimer's disease, though some controversy remains. Further effort is necessary to elucidate the mechanism and to develop effective treatments. Previous studies have indicated that eliminating Aβ plaques could improve synaptic plasticity and cognitive function...
August 2, 2017: Brain Research
https://www.readbyqxmd.com/read/28776187/alzheimer-s-disease-related-amyloid-%C3%AE-1-42-peptide-induces-the-loss-of-human-sperm-function
#17
R S Tavares, S Martins, T Almeida-Santos, A P Sousa, J Ramalho-Santos, O A da Cruz E Silva
Characteristically identified as the main component of senile plaques present in patients suffering from Alzheimer's disease, Aβ has been detected in human testis and reproductive fluids, but its effect on spermatozoa has not been addressed. The present study evaluated whether the most toxic and aggregant amyloid precursor protein (APP)-proteolytic product, amyloid-β1-42 (Aβ1-42), was capable of affecting sperm functionality. Normozoospermic samples were either exposed to different Aβ1-42 doses or to the untreated and scrambled controls for a maximum of 48 h at 37 °C and 5%CO2, and motility, viability and mitochondrial status were evaluated...
August 3, 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/28771976/hdac3-negatively-regulates-spatial-memory-in-a-mouse-model-of-alzheimer-s-disease
#18
Xiaolei Zhu, Sulei Wang, Linjie Yu, Jiali Jin, Xing Ye, Yi Liu, Yun Xu
The accumulation and deposition of beta-amyloid (Aβ) is a key neuropathological hallmark of Alzheimer's disease (AD). Histone deacetylases (HDACs) are promising therapeutic targets for the treatment of AD, while the specific HDAC isoforms associated with cognitive improvement are poorly understood. In this study, we investigate the role of HDAC3 in the pathogenesis of AD. Nuclear HDAC3 is significantly increased in the hippocampus of 6- and 9-month-old APPswe/PS1dE9 (APP/PS1) mice compared with that in age-matched wild-type C57BL/6 (B6) mice...
August 3, 2017: Aging Cell
https://www.readbyqxmd.com/read/28770113/potential-roles-of-exosomal-micrornas-as-diagnostic-biomarkers-and-therapeutic-application-in-alzheimer-s-disease
#19
REVIEW
Jian-Jiao Chen, Bin Zhao, Jie Zhao, Shao Li
Exosomes are bilipid layer-enclosed vesicles derived from endosomes and are released from neural cells. They contain a diversity of proteins, mRNAs, and microRNAs (miRNAs) that are delivered to neighboring cells and/or are transported to distant sites. miRNAs released from exosomes appear to be associated with multiple neurodegenerative conditions linking to Alzheimer's disease (AD) which is marked by hyperphosphorylated tau proteins and accumulation of Aβ plaques. Exciting findings reveal that miRNAs released from exosomes modulate the expression and function of amyloid precursor proteins (APP) and tau proteins...
2017: Neural Plasticity
https://www.readbyqxmd.com/read/28769785/amyloid-%C3%AE-induced-redistribution-of-transcriptional-factor-eb-and-lysosomal-dysfunction-in-primary-microglial-cells
#20
Xingzhi Guo, Peng Tang, Li Chen, Peng Liu, Chen Hou, Xin Zhang, Yue Liu, Li Chong, Xiaoqing Li, Rui Li
Impaired clearance of Amyloid β (Aβ) by microglia in the brain may be associated with the senile plaque formation, a pathological hallmark relevant to Alzheimer's disease. Microglial cells in the brain are not able to efficiently degrade Aβ, suggesting that microglial lysosome impairment may occur. However, the mechanism of Aβ-induced impairment of microglia remains poorly understood. We observed the effects of Aβ on the trafficking of nuclear transcriptional factor EB (TFEB), a master regulator of lysosome biogenesis, and the expression of a downstream osteoporosis-associated transmembrane protein 1 (OSTM1), a vital molecule involved in lysosome acidification in primary microglial cells...
2017: Frontiers in Aging Neuroscience
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