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https://www.readbyqxmd.com/read/28930663/the-trem2-apoe-pathway-drives-the-transcriptional-phenotype-of-dysfunctional-microglia-in-neurodegenerative-diseases
#1
Susanne Krasemann, Charlotte Madore, Ron Cialic, Caroline Baufeld, Narghes Calcagno, Rachid El Fatimy, Lien Beckers, Elaine O'Loughlin, Yang Xu, Zain Fanek, David J Greco, Scott T Smith, George Tweet, Zachary Humulock, Tobias Zrzavy, Patricia Conde-Sanroman, Mar Gacias, Zhiping Weng, Hao Chen, Emily Tjon, Fargol Mazaheri, Kristin Hartmann, Asaf Madi, Jason D Ulrich, Markus Glatzel, Anna Worthmann, Joerg Heeren, Bogdan Budnik, Cynthia Lemere, Tsuneya Ikezu, Frank L Heppner, Vladimir Litvak, David M Holtzman, Hans Lassmann, Howard L Weiner, Jordi Ochando, Christian Haass, Oleg Butovsky
Microglia play a pivotal role in the maintenance of brain homeostasis but lose homeostatic function during neurodegenerative disorders. We identified a specific apolipoprotein E (APOE)-dependent molecular signature in microglia from models of amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and Alzheimer's disease (AD) and in microglia surrounding neuritic β-amyloid (Aβ)-plaques in the brains of people with AD. The APOE pathway mediated a switch from a homeostatic to a neurodegenerative microglia phenotype after phagocytosis of apoptotic neurons...
September 19, 2017: Immunity
https://www.readbyqxmd.com/read/28927263/molecular-and-cellular-basis-of-neurodegeneration-in-alzheimer-s-disease
#2
Sangyun Jeong
The most common form of senile dementia is Alzheimer's disease (AD), which is characterized by the extracellular deposition of amyloid beta-peptide (Abeta) plaques and the intracellular formation of neurofibrillary tangles (NFTs) in the cerebral cortex. Tau abnormalities are commonly observed in many neurodegenerative diseases including AD, Parkinson's disease, and Pick's disease. Interestingly, tau-mediated formation of NFTs in AD brains shows better correlation with cognitive impairment than Abeta plaque accumulation; pathological tau alone is sufficient to elicit frontotemporal dementia, but it does not cause AD...
September 20, 2017: Molecules and Cells
https://www.readbyqxmd.com/read/28926757/mn-ii-based-t1-and-t2-potential-mri-contrast-agent-appended-with-tryptamine-recognition-moiety-for-a%C3%AE-plaques
#3
Neeraj Rastogi, Nidhi Tyagi, Ovender Singh, B S Hemanth Kumar, Udai P Singh, Kaushik Ghosh, Raja Roy
We report the synthesis and characterization of manganese(II) complexes having pentadentate ligands L1 (2,6-bis(1-(2-phenyl-2-(pyridin-2-yl)hydrazono)ethyl)pyridine), L2 (methyl 2,6-bis((E)-1-(2-phenyl-2-(pyridin-2yl)hydrazono)ethyl)isonicotinate), L3 (N-(2-(1H-indol-3-yl)ethyl)-2,6-bis((E)-1-(2-phenyl-2-(pyridin2yl)hydrazono)ethyl)isonicotiamide) and their application as dual contrast agents for simultaneous T1 and T2 weighted magnetic resonance imaging. Single crystal analysis of all the complexes [Mn(II)L1, Mn(II)L2 and Mn(II)L3] confirm the formation of novel seven-coordinate manganese complexes with an inner sphere water and perchlorate ion...
September 5, 2017: Journal of Inorganic Biochemistry
https://www.readbyqxmd.com/read/28926133/synthesis-of-thiophene-based-optical-ligands-that-selectively-detect-tau-pathology-in-alzheimer%C3%A2-s-disease
#4
Peter Nilsson, Hamid Shirani, Hanna Appelqvist, Marcus Bäck, Therese Klingstedt, Nigel Cairns
The accumulation of protein aggregates is associated with many devastating neurodegenerative diseases and the development of molecular ligands able to detect these pathological hallmarks is essential. Here, we report the synthesis of thiophene based optical ligands, denoted bi-thiophene-vinyl-benzothiazoles (bTVBTs) that can be utilized for selective assignment of tau aggregates in brain tissue with Alzheimer´s disease (AD) pathology. The ability of the ligands to selectively distinguish tau deposits from the other AD associated pathological hallmark, senile plaques consisting of aggregated amyloid-β (Aβ) peptide, were reduced when the chemical composition of the ligands were altered, verifying that specific molecular interactions between the ligands and the aggregates are necessary for the selective detection of tau deposits...
September 19, 2017: Chemistry: a European Journal
https://www.readbyqxmd.com/read/28923083/prevention-of-c5ar1-signaling-delays-microglial-inflammatory-polarization-favors-clearance-pathways-and-suppresses-cognitive-loss
#5
Michael X Hernandez, Shan Jiang, Tracy A Cole, Shu-Hui Chu, Maria I Fonseca, Melody J Fang, Lindsay A Hohsfield, Maria D Torres, Kim N Green, Rick A Wetsel, Ali Mortazavi, Andrea J Tenner
BACKGROUND: Pharmacologic inhibition of C5aR1, a receptor for the complement activation proinflammatory fragment, C5a, suppressed pathology and cognitive deficits in Alzheimer's disease (AD) mouse models. To validate that the effect of the antagonist was specifically via C5aR1 inhibition, mice lacking C5aR1 were generated and compared in behavior and pathology. In addition, since C5aR1 is primarily expressed on cells of the myeloid lineage, and only to a lesser extent on endothelial cells and neurons in brain, gene expression in microglia isolated from adult brain at multiple ages was compared across all genotypes...
September 18, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28922846/different-complicated-brain-pathologies-in-monozygotic-twins-with-gerstmann-str%C3%A3-ussler-scheinker-disease
#6
Hiroyuki Honda, Kensuke Sasaki, Hiroshi Takashima, Daisuke Mori, Sachiko Koyama, Satoshi O Suzuki, Toru Iwaki
Gerstmann-Sträussler-Scheinker disease (GSS) is an autosomal, dominantly inherited prion disease. In this study, we present different complicated brain pathologies determined postmortem of monozygotic GSS twin sisters. Case 1 showed cerebellar ataxia at the age of 58 years, and died at 66 years. Case 2 became symptomatic at the age of 75 years, and died at 79 years. There was a 17-year difference in the age of onset between the twins. Postmortem examination revealed numerous prion protein (PrP) plaques in the brains of both cases...
October 1, 2017: Journal of Neuropathology and Experimental Neurology
https://www.readbyqxmd.com/read/28919107/combination-of-a%C3%AE-suppression-and-innate-immune-activation-in-the-brain-significantly-attenuates-amyloid-plaque-deposition
#7
Christophe Verbeeck, Anna Carrano, Paramita Chakrabarty, Joanna L Jankowsky, Pritam Das
Anti-Aβ clinical trials are currently underway to determine whether preventing amyloid deposition will be beneficial in arresting progression of Alzheimer disease. Both clinical and pre-clinical studies suggest that anti-amyloid strategies are only effective if started at very early stages of the disease process in a primary prevention strategy. Because this approach will be difficult to deploy, strategies for secondary prevention aimed at later stages of disease are also needed. In this study, we asked whether combining innate immune activation in the brain with concurrent Aβ suppression could enhance plaque clearance and improve pathological outcomes in mice with moderate amyloid pathology...
September 14, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28917978/sen1500-a-novel-oral-amyloid-%C3%AE-aggregation-inhibitor-attenuates-brain-pathology-in-a-mouse-model-of-alzheimer-s-disease
#8
D Brunner, S Flunkert, J Neddens, S Duller, D I C Scopes, J M Treherne, B Hutter-Paier
INTRODUCTION: Amyloid-β (Aβ) aggregation is thought to be a major pathogenic event underlying the neuropathology of Alzheimer's disease (AD). The development of new drugs inhibiting the Aβ aggregation process is, therefore, important. SEN1500, an orally bioavailable and CNS-penetrant Aβ aggregation inhibitor, has previously been shown to reduce spatial learning and memory deficits in an APP transgenic mouse model. To verify that the pharmacological properties of SEN1500 are not unique to this model, we investigated brain Aβ pathology, neuroinflammation, as well as memory in a different mouse model of AD expressing the human amyloid precursor protein with Swedish and London mutations (APPSL)...
September 13, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28916532/comparison-of-symptomatic-and-asymptomatic-persons-with-primary-age-related-tauopathy
#9
Lilah M Besser, John F Crary, Charles Mock, Walter A Kukull
OBJECTIVE: To conduct a clinicopathologic study to characterize clinical and neuropathologic features associated with cognitive impairment in participants with no neuritic amyloid plaques (primary age-related tauopathy [PART] definite) and sparse neuritic plaques (amyloid sparse). METHODS: Using the National Alzheimer's Coordinating Center database, we identified 377 individuals who were PART definite (n = 170) or amyloid sparse (n = 207), clinically examined within 1 year of death, and autopsied at 1 of 26 National Institute on Aging-funded Alzheimer's Disease Centers...
September 15, 2017: Neurology
https://www.readbyqxmd.com/read/28912896/investigation-of-the-safety-of-focused-ultrasound-induced-blood-brain-barrier-opening-in-a-natural-canine-model-of-aging
#10
Meaghan Anne O'Reilly, Ryan Matthew Jones, Edward Barrett, Anthony Schwab, Elizabeth Head, Kullervo Hynynen
Rationale: Ultrasound-mediated opening of the Blood-Brain Barrier(BBB) has shown exciting potential for the treatment of Alzheimer's disease(AD). Studies in transgenic mouse models have shown that this approach can reduce plaque pathology and improve spatial memory. Before clinical translation can occur the safety of the method needs to be tested in a larger brain that allows lower frequencies be used to treat larger tissue volumes, simulating clinical situations. Here we investigate the safety of opening the BBB in half of the brain in a large aged animal model with naturally occurring amyloid deposits...
2017: Theranostics
https://www.readbyqxmd.com/read/28912710/key-aging-associated-alterations-in-primary-microglia-response-to-beta-amyloid-stimulation
#11
Cláudia Caldeira, Carolina Cunha, Ana R Vaz, Ana S Falcão, Andreia Barateiro, Elsa Seixas, Adelaide Fernandes, Dora Brites
Alzheimer's disease (AD) is characterized by a progressive cognitive decline and believed to be driven by the self-aggregation of amyloid-β (Aβ) peptide into oligomers and fibrils that accumulate as senile plaques. It is widely accepted that microglia-mediated inflammation is a significant contributor to disease pathogenesis; however, different microglia phenotypes were identified along AD progression and excessive Aβ production was shown to dysregulate cell function. As so, the contribution of microglia to AD pathogenesis remains to be elucidated...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28906375/correlations-between-clinical-characteristics-and-neuroimaging-in-chinese-patients-with-subtypes-of-frontotemporal-lobe-degeneration
#12
Zhihong Shi, Shuai Liu, Ying Wang, Shuling Liu, Tong Han, Li Cai, Yuying Zhou, Shuo Gao, Yong Ji
The aim of the study was to obtain an overview of the clinical and neuroimaging features of Chinese patients with subtypes of frontotemporal lobe degeneration (FTLD).We evaluated the demographic features, clinical presentation, and lobe atrophy depicted by magnetic resonance imaging (MRI) in 133 patients with FTLD. Two positron emission tomography (PET) scans were performed at baseline: [C]Pittsburgh compound B PET to assess amyloid-β plaque load and [F]fluorodeoxyglucose (FDG) PET to assess glucose metabolism...
September 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28906268/new-pet-markers-for-the-diagnosis-of-dementia
#13
Pierre Payoux, Anne Sophie Salabert
PURPOSE OF REVIEW: To present the new PET markers that could become in the coming years, relevant to advanced clinical approaches to dementia diagnosis, drug trials, and treatment strategies and discuss their advantages and limitations. RECENT FINDINGS: The most advanced new PET tracers are the markers of the amyloid plaques, the τ compounds and the tracers of the translocator protein as markers of neuroinflammation. The main advantages but also the weaknesses of each of these markers are discussed...
September 12, 2017: Current Opinion in Neurology
https://www.readbyqxmd.com/read/28900428/c-reactive-protein-binds-to-cholesterol-crystals-and-co-localizes-with-the-terminal-complement-complex-in-human-atherosclerotic-plaques
#14
Katrine Pilely, Stefano Fumagalli, Anne Rosbjerg, Ninette Genster, Mikkel-Ole Skjoedt, Carlo Perego, Angela M R Ferrante, Maria-Grazia De Simoni, Peter Garred
Inflammation is a part of the initial process leading to atherosclerosis and cholesterol crystals (CC), found in atherosclerotic plaques, which are known to induce complement activation. The pentraxins C-reactive protein (CRP), long pentraxin 3 (PTX3), and serum amyloid P component (SAP) are serum proteins associated with increased risk of cardiovascular events and these proteins have been shown to interact with the complement system. Whether the pentraxins binds to CC and mediate downstream complement-dependent inflammatory processes remains unknown...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28899417/serotonin-augmentation-therapy-by-escitalopram-has-minimal-effects-on-amyloid-%C3%AE-levels-in-early-stage-alzheimer-s-like-disease-in-mice
#15
Christian Ulrich von Linstow, Jonas Waider, Manuela Grebing, Athanasios Metaxas, Klaus Peter Lesch, Bente Finsen
BACKGROUND: Dysfunction of the serotonergic (5-HTergic) system has been implicated in the cognitive and behavioural symptoms of Alzheimer's disease (AD). Accumulation of toxic amyloid-β (Aβ) species is a hallmark of AD and an instigator of pathology. Serotonin (5-HT) augmentation therapy by treatment with selective serotonin reuptake inhibitors (SSRIs) in patients with AD has had mixed success in improving cognitive function, whereas SSRI administration to mice with AD-like disease has been shown to reduce Aβ pathology...
September 12, 2017: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/28899014/slow-wave-sleep-disruption-increases-cerebrospinal-fluid-amyloid-%C3%AE-levels
#16
Yo-El S Ju, Sharon J Ooms, Courtney Sutphen, Shannon L Macauley, Margaret A Zangrilli, Gina Jerome, Anne M Fagan, Emmanuel Mignot, John M Zempel, Jurgen A H R Claassen, David M Holtzman
See Mander et al. (doi:10.1093/awx174) for a scientific commentary on this article.Sleep deprivation increases amyloid-β, suggesting that chronically disrupted sleep may promote amyloid plaques and other downstream Alzheimer's disease pathologies including tauopathy or inflammation. To date, studies have not examined which aspect of sleep modulates amyloid-β or other Alzheimer's disease biomarkers. Seventeen healthy adults (age 35-65 years) without sleep disorders underwent 5-14 days of actigraphy, followed by slow wave activity disruption during polysomnogram, and cerebrospinal fluid collection the following morning for measurement of amyloid-β, tau, total protein, YKL-40, and hypocretin...
August 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28898051/effect-of-alzheimer-familial-chromosomal-mutations-on-the-amyloid-fibril-interaction-with-different-pet-tracers-insight-from-molecular-modeling-studies
#17
Kanagasabai Balamurugan, Natarajan Arul Murugan, Bengt Långström, Agneta Nordberg, Hans Ågren
Alzheimer's disease (AD) is the most common neurodegenerative disorder. Along with an increasing number of elderly worldwide it poses a great challenge for the society and healthcare. Although sporadic AD is the common form of AD, 2-3% of the AD cases are expected to be due to mutations in the beta region of the amyloid precursor protein which is referred to as autosomal dominant AD (ADAD). These mutations may cause changes in the secondary structure of the amyloid beta fibrils and may alter the fibrillization rate leading to changes in the disease development and could also affect the binding to tracers used in diagnosis...
September 12, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28890893/proximate-mediators-of-microvascular-dysfunction-at-the-blood-brain-barrier-neuroinflammatory-pathways-to-neurodegeneration
#18
REVIEW
Barry W Festoff, Ravi K Sajja, Luca Cucullo
Current projections are that by 2050 the numbers of people aged 65 and older with Alzheimer's disease (AD) in the US may increase threefold while dementia is projected to double every 20 years reaching ~115 million by 2050. AD is clinically characterized by progressive dementia and neuropathologically by neuronal and synapse loss, accumulation of amyloid plaques, and neurofibrillary tangles (NFTs) in specific brain regions. The preclinical or presymptomatic stage of AD-related brain changes may begin over 20 years before symptoms occur, making development of noninvasive biomarkers essential...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28890316/iron-biochemistry-is-correlated-with-amyloid-plaque-morphology-in-an-established-mouse-model-of-alzheimer-s-disease
#19
Neil D Telling, James Everett, Joanna F Collingwood, Jon Dobson, Gerrit van der Laan, Joseph J Gallagher, Jian Wang, Adam P Hitchcock
A signature characteristic of Alzheimer's disease (AD) is aggregation of amyloid-beta (Aβ) fibrils in the brain. Nevertheless, the links between Aβ and AD pathology remain incompletely understood. It has been proposed that neurotoxicity arising from aggregation of the Aβ1-42 peptide can in part be explained by metal ion binding interactions. Using advanced X-ray microscopy techniques at sub-micron resolution, we investigated relationships between iron biochemistry and AD pathology in intact cortex from an established mouse model over-producing Aβ...
August 24, 2017: Cell Chemical Biology
https://www.readbyqxmd.com/read/28889269/copper-and-alzheimer-s-disease
#20
Zoe K Mathys, Anthony R White
Alzheimer's disease (AD) is the most common form of adult neurode-generation and is characterised by progressive loss of cognitive function leading to death. The neuropathological hallmarks include extracellular amyloid plaque accumulation in affected regions of the brain, formation of intraneuronal neurofibrillary tangles, chronic neuroinflammation, oxidative stress, and abnormal biometal homeostasis. Of the latter, major changes in copper (Cu) levels and localisation have been identified in AD brain, with accumulation of Cu in amyloid deposits, together with deficiency of Cu in some brain regions...
2017: Advances in Neurobiology
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