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Amyloid aging microglia

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 (AβO), 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. AβO infusion evoked a sustained inflammatory response including activation of NF-κB, triggered microglia activation and increased the expression of pattern recognition and phagocytic receptors...
March 6, 2018: Neuroscience
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
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
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
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
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
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
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-[11C]deprenyl ([11C]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
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
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...
December 12, 2017: Brain, Behavior, and Immunity
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
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
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
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
Sara van Duijn, Marjolein Bulk, Sjoerd G van Duinen, Rob J A Nabuurs, Mark A van Buchem, Louise van der Weerd, Remco Natté
Abnormal iron distribution in the isocortex is increasingly recognized as an in vivo marker for Alzheimer's disease (AD). However, the contribution of iron accumulation to the AD pathology is still poorly understood. In this study, we investigated: 1) frontal cortical iron distribution in AD and normal aging and 2) the relation between iron distribution and degree of AD pathology. We used formalin fixed paraffin embedded frontal cortex from 10 AD patients, 10 elder, 10 middle aged, and 10 young controls and visualized iron with a modified Perl's histochemical procedure...
2017: Journal of Alzheimer's Disease: JAD
Cheryl E G Leyns, Jason D Ulrich, Mary B Finn, Floy R Stewart, Lauren J Koscal, Javier Remolina Serrano, Grace O Robinson, Elise Anderson, Marco Colonna, David M Holtzman
Variants in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) were recently found to increase the risk for developing Alzheimer's disease (AD). In the brain, TREM2 is predominately expressed on microglia, and its association with AD adds to increasing evidence implicating a role for the innate immune system in AD initiation and progression. Thus far, studies have found TREM2 is protective in the response to amyloid pathology while variants leading to a loss of TREM2 function impair microglial signaling and are deleterious...
October 24, 2017: Proceedings of the National Academy of Sciences of the United States of America
Lianne Hoeijmakers, Gideon F Meerhoff, Janneke W de Vries, Silvie R Ruigrok, Anne-Marie van Dam, Fred van Leuven, Aniko Korosi, Paul J Lucassen
In Alzheimer's disease, the hippocampus is characterized by abundant deposition of amyloid peptides (amyloid β [Aβ]) and neuroinflammation. Adult hippocampal neurogenesis (AHN) is a form of plasticity that contributes to cognition and can be influenced by either or both pathology and neuroinflammation. Their interaction has been studied before in rapidly progressing transgenic mouse models with strong overexpression of amyloid precursor protein (APP) and/or presenilin 1. So far, changes in AHN and neuroinflammation remain poorly characterized in slower progressing models at advanced age, which approach more closely sporadic Alzheimer's disease...
January 2018: Neurobiology of Aging
Botond Penke, Ferenc Bogár, Lívia Fülöp
Protein dyshomeostasis is the common mechanism of neurodegenerative diseases such as Alzheimer's disease (AD). Aging is the key risk factor, as the capacity of the proteostasis network declines during aging. Different cellular stress conditions result in the up-regulation of the neurotrophic, neuroprotective amyloid precursor protein (APP). Enzymatic processing of APP may result in formation of toxic Aβ aggregates (β-amyloids). Protein folding is the basis of life and death. Intracellular Aβ affects the function of subcellular organelles by disturbing the endoplasmic reticulum-mitochondria cross-talk and causing severe Ca2+-dysregulation and lipid dyshomeostasis...
October 10, 2017: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
Francisco R López-Picón, Anniina Snellman, Olli Eskola, Semi Helin, Olof Solin, Merja Haaparanta-Solin, Juha O Rinne
Rationale: Neuroinflammation has been associated with different neurological diseases including Alzheimer's disease (AD). In AD, the translocator protein 18kDa (TSPO) is overexpressed in the activated microglia that surround the β-amyloid plaques. In the current longitudinal study, using a mouse model of AD, we evaluated the association between β-amyloid deposition and neuroinflammation in AD. Methods: To monitor the longitudinal changes in β-amyloid deposition and neuroinflammation, we used in vivo PET imaging and ex vivo autoradiography with (11)C-PIB and a TSPO tracer, (18)F-GE-180, in the APP23 mouse model of AD...
October 6, 2017: Journal of Nuclear Medicine: Official Publication, Society of Nuclear Medicine
Athanasios Metaxas, Ramanan Vaitheeswaran, Katrine T Jensen, Camilla Thygesen, Laura Ilkjaer, Sultan Darvesh, Bente Finsen
Background Although mood and sleep disturbances are nearly universal among patients with Alzheimer's disease (AD), brain structures involved in non-cognitive processing remain under characterized in terms of AD pathology. Objectives This study was designed to evaluate hallmarks of AD pathology in the brainstem of the APPswe/PS1dE9 mouse model of familial AD. Methods Fresh-frozen sections from female, 12 month old, transgenic and control B6C3 mice (n=6/genotype) were examined for amyloid burden and neurofibrillary alterations, by using 6E10 immunohistochemistry and the Gallyas silver stain, respectively...
October 4, 2017: Current Alzheimer Research
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