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https://www.readbyqxmd.com/read/29782315/tlr4-gene-expression-and-pro-inflammatory-cytokines-in-alzheimer-s-disease-and-in-response-to-hippocampal-deafferentation-in-rodents
#1
Justin Miron, Cynthia Picard, Josée Frappier, Doris Dea, Louise Théroux, Judes Poirier
One important aspect in Alzheimer's disease pathology is the presence of chronic inflammation. Considering its role as a key receptor in the microglial innate immune system, TLR4 was shown to regulate the binding and phagocytosis of amyloid plaques by microglia in several mouse models of amyloidosis, as well as the production of pro-inflammatory cytokines. To our knowledge, TLR4 and its association with cytokines have not been thoroughly examined in the brains of subjects affected with Alzheimer's disease. Using quantitative reverse transcription polymerase chain reaction (qRT-PCR) in postmortem human brains, we observed increased expression for the TLR4 and TNF genes (p = 0...
May 16, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29758264/anti-il17-treatment-ameliorates-down-syndrome-phenotypes-in-mice
#2
Noemí Rueda, Verónica Vidal, Susana García-Cerro, Josep Oriol Narcís, María Llorens-Martín, Andrea Corrales, Sara Lantigua, Marcos Iglesias, Jesús Merino, Ramón Merino, Carmen Martínez-Cué
Down syndrome (DS) is characterized by structural and functional anomalies that are present prenatally and that lead to intellectual disabilities. Later in life, the cognitive abilities of DS individuals progressively deteriorate due to the development of Alzheimer's disease (AD)-associated neuropathology (i.e., β-amyloid (Aβ) plaques, neurofibrillary tangles (NFTs), neurodegeneration, synaptic pathology, neuroinflammation and increased oxidative stress). Increasing evidence has shown that among these pathological processes, neuroinflammation plays a predominant role in AD etiopathology...
May 11, 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29686672/the-inflammatory-continuum-of-traumatic-brain-injury-and-alzheimer-s-disease
#3
REVIEW
Olga N Kokiko-Cochran, Jonathan P Godbout
The post-injury inflammatory response is a key mediator in long-term recovery from traumatic brain injury (TBI). Moreover, the immune response to TBI, mediated by microglia and macrophages, is influenced by existing brain pathology and by secondary immune challenges. For example, recent evidence shows that the presence of beta-amyloid and phosphorylated tau protein, two hallmark features of AD that increase during normal aging, substantially alter the macrophage response to TBI. Additional data demonstrate that post-injury microglia are "primed" and become hyper-reactive following a subsequent acute immune challenge thereby worsening recovery...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29615895/hypertension-accelerates-alzheimer-s-disease-related-pathologies-in-pigs-and-3xtg-mice
#4
Yao-Hsiang Shih, Shih-Ying Wu, Megan Yu, Sheng-Huai Huang, Chu-Wan Lee, Meei-Jyh Jiang, Pao-Yen Lin, Ting-Ting Yang, Yu-Min Kuo
Epidemiological studies suggest there is an association between midlife hypertension and increased risk of late-life Alzheimer's disease (AD). However, whether hypertension accelerates the onset of AD or is a distinct disease that becomes more prevalent with age (comorbidity) remains unclear. This study aimed to test the possible relationship between hypertension and AD pathogenesis. Two animal models were used in this study. For the first model, 7-month-old Lanyu-miniature-pigs were given the abdominal aortic constriction operation to induce hypertension and their AD-related pathologies were assessed at 1, 2, and 3 months after the operation...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29581224/vascular-cognitive-impairment-linked-to-brain-endothelium-inflammation-in-early-stages-of-heart-failure-in-mice
#5
Mateusz G Adamski, Magdalena Sternak, Tasnim Mohaissen, Dawid Kaczor, Joanna M Wierońska, Monika Malinowska, Iwona Czaban, Katarzyna Byk, Kristina S Lyngsø, Kamil Przyborowski, Pernille B L Hansen, Grzegorz Wilczyński, Stefan Chlopicki
BACKGROUND: Although advanced heart failure (HF) is a clinically documented risk factor for vascular cognitive impairment, the occurrence and pathomechanisms of vascular cognitive impairment in early stages of HF are equivocal. Here, we characterize vascular cognitive impairment in the early stages of HF development and assess whether cerebral hypoperfusion or prothrombotic conditions are involved. METHODS AND RESULTS: Tgαq*44 mice with slowly developing isolated HF triggered by cardiomyocyte-specific overexpression of G-αq*44 protein were studied before the end-stage HF, at the ages of 3, 6, and 10 months: before left ventricle dysfunction; at the stage of early left ventricle diastolic dysfunction (with preserved ejection fraction); and left ventricle diastolic/systolic dysfunction, respectively...
March 26, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29552013/differential-phagocytic-properties-of-cd45-low-microglia-and-cd45-high-brain-mononuclear-phagocytes-activation-and-age-related-effects
#6
Srikant Rangaraju, Syed Ali Raza, Noel Xiang'An Li, Ranjita Betarbet, Eric B Dammer, Duc Duong, James J Lah, Nicholas T Seyfried, Allan I Levey
In the central nervous system (CNS), microglia are innate immune mononuclear phagocytes (CNS MPs) that can phagocytose infectious particles, apoptotic cells, neurons, and pathological protein aggregates, such as Aβ in Alzheimer's disease (AD). While CD11b+ CD45low microglia account for the majority of CNS MPs, a small population of CD11b+ CD45high CNS MPs is also recognized in AD that surround Aβ plaques. These transcriptionally and pathologically unique CD45high cells have unclear origin and undefined phagocytic characteristics...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29522854/chronic-amyloid-%C3%AE-oligomer-infusion-evokes-sustained-inflammation-and-microglial-changes-in-the-rat-hippocampus-via-nlrp3
#7
Csaba Fekete, Csaba Vastagh, Ádám Dénes, Erik Hrabovszky, Gábor Nyiri, Imre Kalló, Zsolt Liposits, Miklós Sárvári
Microglia are instrumental for recognition and elimination of amyloid β1-42 oligomers (AβOs), but the long-term consequences of AβO-induced inflammatory changes in the brain are unclear. Here, we explored microglial responses and transciptome-level inflammatory signatures in the rat hippocampus after chronic AβO challenge. Middle-aged Long Evans rats received intracerebroventricular infusion of AβO or vehicle for 4 weeks, followed by treatment with artificial CSF or MCC950 for the subsequent 4 weeks...
March 6, 2018: Neuroscience
https://www.readbyqxmd.com/read/29471781/solid-lipid-curcumin-particles-provide-greater-anti-amyloid-anti-inflammatory-and-neuroprotective-effects-than-curcumin-in-the-5xfad-mouse-model-of-alzheimer-s-disease
#8
Panchanan Maiti, Leela Paladugu, Gary L Dunbar
BACKGROUND: Neuroinflammation and the presence of amyloid beta protein (Aβ) and neurofibrillary tangles are key pathologies in Alzheimer's disease (AD). As a potent anti-amyloid and anti-inflammatory natural polyphenol, curcumin (Cur) could be potential therapies for AD. Unfortunately, poor solubility, instability in physiological fluids, and low bioavailability limit its clinical utility. Recently, different lipid modifications in the formulae of Cur have been developed that would enhance its therapeutic potential...
February 23, 2018: BMC Neuroscience
https://www.readbyqxmd.com/read/29467614/safety-and-efficacy-of-scanning-ultrasound-treatment-of-aged-app23-mice
#9
Gerhard Leinenga, Jürgen Götz
Deposition of amyloid-β (Aβ) peptide leads to amyloid plaques that together with tau deposits characterize the brains of patients with Alzheimer's disease (AD). In modeling this pathology, transgenic animals such as the APP23 strain, that expresses a mutant form of the amyloid precursor protein found in familial cases of AD, have been instrumental. In previous studies, we have shown that repeated treatments with ultrasound in a scanning mode (termed scanning ultrasound or SUS) were effective in removing Aβ and restoring memory functions, without the need for a therapeutic agent such as an Aβ antibody...
2018: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29454581/emerging-roles-of-microglial-cathepsins-in-neurodegenerative-disease
#10
REVIEW
Jessica R Lowry, Andis Klegeris
Alzheimer's disease (AD) is one of the leading causes of dementia, and its prevalence is expected to increase dramatically due to the aging global population. Microglia-driven neuroinflammation may contribute to the progression of AD. Microglia, the immune cells of the central nervous system (CNS), become chronically activated by the pathological proteins of AD including amyloid-β peptides (Aβ). Such adversely activated microglia secrete mediators that promote inflammation and damage neurons. Cathepsins are proteases that are expressed by all brain cell types, and most of them are found both intra- and extra-cellularly...
February 15, 2018: Brain Research Bulletin
https://www.readbyqxmd.com/read/29425372/sleep-deprivation-and-csf-biomarkers-for-alzheimer-disease
#11
Martin Olsson, Johan Ärlig, Jan Hedner, Kaj Blennow, Henrik Zetterberg
Study Objective: To investigate the cumulative effect of 5 consecutive nights of partial sleep deprivation on a panel of cerebrospinal fluid (CSF) biomarkers in healthy adults. Methods: A randomized, cross-over study conducted at the University of Gothenburg. The participants (N=13) were healthy adults (20-40 years of age) with a normal sleeping pattern. The participants underwent a baseline sleep period consisting of 5 nights with 8h spent in bed. A subsequent period with partial sleep deprivation (PSD) consisted of 5 nights of maximum 4h of sleep per night...
February 7, 2018: Sleep
https://www.readbyqxmd.com/read/29385576/aging-exacerbates-neuroinflammatory-outcomes-induced-by-acute-ozone-exposure
#12
Christina R Tyler, Shahani Noor, Tamara Young, Valeria Rivero, Bethany Sanchez, Selita Lucas, Kevin K Caldwell, Erin D Milligan, Matthew J Campen
The role of environmental stressors, particularly exposure to air pollution, in the development of neurodegenerative disease remains underappreciated. We examined the neurological effects of acute ozone (O3) exposure in aged mice, where increased blood brain barrier (BBB) permeability may confer vulnerability to neuroinflammatory outcomes. C57BL/6 male mice, aged 8-10 weeks or 12 - 18 months were exposed to either filtered air (FA) or 1.0 ppm O3 for 4 hours; animals received a single IP injection of sodium fluorescein (FSCN) 20 hours post-exposure...
January 27, 2018: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/29301654/the-additive-effect-of-aging-on-sepsis-induced-cognitive-impairment-and-neuroinflammation
#13
Rodrigo Olivieri, Monique Michels, Bruna Pescador, Pricila Ávila, Mariane Abatti, Luana Cucker, Henrique Burger, Diogo Dominguini, João Quevedo, Felipe Dal-Pizzol
Systemic inflammation is emerging as a significant driver of cognitive decline in the aged and vulnerable brain. In sepsis survivors animals low-grade brain inflammation occurs, suggesting that sepsis is able to induce in microglia a primed-like state. The purpose of this study is to analyze the role of sepsis-induced brain inflammation in the progression of the physiological process of brain aging. Wistar rats 2month-old were subjected to sepsis and 60 and 90days after were submitted to the new object recognition test and brain was removed to the determination of cytokines, myeloperoxidase (MPO) activity, amyloid-beta peptide (Aβ) and immunohistochemistry markers of microglial activation...
January 15, 2018: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29297157/astroglial-responses-to-amyloid-beta-progression-in-a-mouse-model-of-alzheimer-s-disease
#14
Malin Olsen, Ximena Aguilar, Dag Sehlin, Xiaotian T Fang, Gunnar Antoni, Anna Erlandsson, Stina Syvänen
PURPOSE: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (Aβ) deposition, hyperphosphorylation of tau, and neuroinflammation. Astrocytes, the most abundant glial cell type in the nervous system, respond to neurodegenerative disorders through astrogliosis, i.e., converting to a reactive inflammatory state. The aim of this study was to investigate how in vivo quantification of astrogliosis using positron emission tomography (PET) radioligand deuterium-L-[11 C]deprenyl ([11 C]DED), binding to enzyme monoamine oxidase-B (MAO-B) which is overexpressed in reactive astrocytes during AD, corresponds to expression of glial fibrillary acidic protein (GFAP) and vimentin, i...
January 2, 2018: Molecular Imaging and Biology: MIB: the Official Publication of the Academy of Molecular Imaging
https://www.readbyqxmd.com/read/29275160/role-of-the-peripheral-innate-immune-system-in-the-development-of-alzheimer-s-disease
#15
REVIEW
Aurélie Le Page, Gilles Dupuis, Eric H Frost, Anis Larbi, Graham Pawelec, Jacek M Witkowski, Tamas Fulop
Alzheimer's disease is one of the most devastating neurodegenerative diseases. The exact cause of the disease is still not known although many scientists believe in the beta amyloid hypothesis which states that the accumulation of the amyloid peptide beta (Aβ) in brain is the initial cause which consequently leads to pathological neuroinflammation. However, it was recently shown that Aβ may have an important role in defending the brain against infections. Thus, the balance between positive and negative impact of Aβ may determine disease progression...
December 21, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/29246456/scavenger-receptor-a-deficiency-impairs-immune-response-of-microglia-and-astrocytes-potentiating-alzheimer-s-disease-pathophysiology
#16
Francisca Cornejo, Marianne Vruwink, Claudia Metz, Paola Muñoz, Nicole Salgado, Joaquín Poblete, María Estela Andrés, Jaime Eugenín, Rommy von Bernhardi
Late onset Alzheimer disease's (LOAD) main risk factor is aging. Although it is not well known which age-related factors are involved in its development, evidence points out to the involvement of an impaired amyloid-β (Aβ) clearance in the aged brain among possible causes. Glial cells are the main scavengers of the brain, where Scavenger Receptor class A (SR-A) emerges as a relevant player in AD because of its participation in Aβ uptake and in the modulation of glial cell inflammatory response. Here, we show that SR-A expression is reduced in the hippocampus of aged animals and APP/PS1 mice...
March 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29230021/markers-of-microglia-in-post-mortem-brain-samples-from-patients-with-alzheimer-s-disease-a-systematic-review
#17
REVIEW
K E Hopperton, D Mohammad, M O Trépanier, V Giuliano, R P Bazinet
Neuroinflammation is proposed as one of the mechanisms by which Alzheimer's disease pathology, including amyloid-β plaques, leads to neuronal death and dysfunction. Increases in the expression of markers of microglia, the main neuroinmmune cell, are widely reported in brains from patients with Alzheimer's disease, but the literature has not yet been systematically reviewed to determine whether this is a consistent pathological feature. A systematic search was conducted in Medline, Embase and PsychINFO for articles published up to 23 February 2017...
February 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29217476/sumo1-impact-on-alzheimer-disease-pathology-in-an-amyloid-depositing-mouse-model
#18
Erin Knock, Shinsuke Matsuzaki, Hironori Takamura, Kanayo Satoh, Grace Rooke, Kyung Han, Hong Zhang, Agnieszka Staniszewski, Taiichi Katayama, Ottavio Arancio, Paul E Fraser
Small ubiquitin-related modifiers (SUMOs) conjugated or bound to target proteins can affect protein trafficking, processing and solubility. SUMOylation has been suggested to play a role in the amyloid plaque and neurofibrillary tangle pathology of Alzheimer disease (AD) and related neurodegenerative diseases. The current study examines the impact of SUMO1 on processing of the amyloid precursor protein (APP) leading to the production and deposition of the amyloid-β (Aβ) peptide. An in vivo model of these pathways was developed by the generation of double transgenic mice over-expressing human SUMO1 and a mutant APP...
February 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29189146/transforming-growth-factor-beta-type-i-role-in-neurodegeneration-implications-for-alzheimer%C3%A2-s-disease
#19
Lisbell D Estrada, Luciana Oliveira-Cruz, Daniel Cabrera
Alzheimer's disease is a neurodegenerative condition affecting millions of people worldwide. Alzheimer's symptoms include memory loss and cognitive decline. Pathologically, the hallmarks of Alzheimer´s are the presence of Amyloid beta-plaques, neurofibrillary tangles, and neuronal loss. Unfortunately, no cure is presently available and current treatments are only symptomatic. Transforming growth factor beta type I (TGF-β1) is a trophic factor involved in neuronal development and synaptic plasticity...
November 28, 2017: Current Protein & Peptide Science
https://www.readbyqxmd.com/read/29178139/phagocytic-clearance-of-presynaptic-dystrophies-by-reactive-astrocytes-in-alzheimer-s-disease
#20
Angela Gomez-Arboledas, Jose C Davila, Elisabeth Sanchez-Mejias, Victoria Navarro, Cristina Nuñez-Diaz, Raquel Sanchez-Varo, Maria Virtudes Sanchez-Mico, Laura Trujillo-Estrada, Juan Jose Fernandez-Valenzuela, Marisa Vizuete, Joan X Comella, Elena Galea, Javier Vitorica, Antonia Gutierrez
Reactive astrogliosis, a complex process characterized by cell hypertrophy and upregulation of components of intermediate filaments, is a common feature in brains of Alzheimer's patients. Reactive astrocytes are found in close association with neuritic plaques; however, the precise role of these glial cells in disease pathogenesis is unknown. In this study, using immunohistochemical techniques and light and electron microscopy, we report that plaque-associated reactive astrocytes enwrap, engulf and may digest presynaptic dystrophies in the hippocampus of amyloid precursor protein/presenilin-1 (APP/PS1) mice...
March 2018: Glia
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