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Microglia alzheimer's disease

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https://www.readbyqxmd.com/read/28205565/entorhinal-cortex-dysfunction-can-be-rescued-by-inhibition-of-microglial-rage-in-an-alzheimer-s-disease-mouse-model
#1
Chiara Criscuolo, Veronica Fontebasso, Silvia Middei, Martina Stazi, Martine Ammassari-Teule, Shirley ShiDu Yan, Nicola Origlia
The Entorhinal cortex (EC) has been implicated in the early stages of Alzheimer's disease (AD). In particular, spreading of neuronal dysfunction within the EC-Hippocampal network has been suggested. We have investigated the time course of EC dysfunction in the AD mouse model carrying human mutation of amyloid precursor protein (mhAPP) expressing human Aβ. We found that in mhAPP mice plasticity impairment is first observed in EC superficial layer and further affected with time. A selective impairment of LTP was observed in layer II horizontal connections of EC slices from 2 month old mhAPP mice, whereas at later stage of neurodegeneration (6 month) basal synaptic transmission and LTD were also affected...
February 13, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28203202/plasma-exosomes-spread-and-cluster-around-%C3%AE-amyloid-plaques-in-an-animal-model-of-alzheimer-s-disease
#2
Tingting Zheng, Jiali Pu, Yanxing Chen, Yanfang Mao, Zhangyu Guo, Hongyu Pan, Ling Zhang, Heng Zhang, Binggui Sun, Baorong Zhang
Exosomes, a type of extracellular vesicle, have been shown to be involved in many disorders, including Alzheimer's disease (AD). Exosomes may contribute to the spread of misfolded proteins such as amyloid-β (Aβ) and α-synuclein. However, the specific diffusion process of exosomes and their final destination in brain are still unclear. In the present study, we isolated exosomes from peripheral plasma and injected them into the hippocampus of an AD mouse model, and investigated exosome diffusion. We found that injected exosomes can spread from the dentate gyrus (DG) to other regions of hippocampus and to the cortex...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28197669/clearance-of-cerebral-a%C3%AE-in-alzheimer-s-disease-reassessing-the-role-of-microglia-and-monocytes
#3
REVIEW
Leah Zuroff, David Daley, Keith L Black, Maya Koronyo-Hamaoui
Deficiency in cerebral amyloid β-protein (Aβ) clearance is implicated in the pathogenesis of the common late-onset forms of Alzheimer's disease (AD). Accumulation of misfolded Aβ in the brain is believed to be a net result of imbalance between its production and removal. This in turn may trigger neuroinflammation, progressive synaptic loss, and ultimately cognitive decline. Clearance of cerebral Aβ is a complex process mediated by various systems and cell types, including vascular transport across the blood-brain barrier, glymphatic drainage, and engulfment and degradation by resident microglia and infiltrating innate immune cells...
February 14, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28197095/increase-of-trem2-during-aging-of-an-alzheimer-s-disease-mouse-model-is-paralleled-by-microglial-activation-and-amyloidosis
#4
Matthias Brendel, Gernot Kleinberger, Federico Probst, Anna Jaworska, Felix Overhoff, Tanja Blume, Nathalie L Albert, Janette Carlsen, Simon Lindner, Franz Josef Gildehaus, Laurence Ozmen, Marc Suárez-Calvet, Peter Bartenstein, Karlheinz Baumann, Michael Ewers, Jochen Herms, Christian Haass, Axel Rominger
Heterozygous missense mutations in the triggering receptor expressed on myeloid cells 2 (TREM2) have been reported to significantly increase the risk of developing Alzheimer's disease (AD). Since TREM2 is specifically expressed by microglia in the brain, we hypothesized that soluble TREM2 (sTREM2) levels may increase together with in vivo biomarkers of microglial activity and amyloidosis in an AD mouse model as assessed by small animal positron-emission-tomography (μPET). In this cross-sectional study, we examined a strong amyloid mouse model (PS2APP) of four age groups by μPET with [(18)F]-GE180 (glial activation) and [(18)F]-florbetaben (amyloidosis), followed by measurement of sTREM2 levels and amyloid levels in the brain...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28197094/protein-tyrosine-phosphatase-1b-ptp1b-a-potential-target-for-alzheimer-s-therapy
#5
Marcelo N N Vieira, Natalia M Lyra E Silva, Sergio T Ferreira, Fernanda G De Felice
Despite significant advances in current understanding of mechanisms of pathogenesis in Alzheimer's disease (AD), attempts at drug development based on those discoveries have failed to translate into effective, disease-modifying therapies. AD is a complex and multifactorial disease comprising a range of aberrant cellular/molecular processes taking part in different cell types and brain regions. As a consequence, therapeutics for AD should be able to block or compensate multiple abnormal pathological events. Here, we examine recent evidence that inhibition of protein tyrosine phosphatase 1B (PTP1B) may represent a promising strategy to combat a variety of AD-related detrimental processes...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28193696/astrocytic-orosomucoid-2-modulates-microglial-activation-and-neuroinflammation
#6
Myungjin Jo, Jong-Heon Kim, Gyunjee Song, Minchul Seo, Eun Mi Hwang, Kyoungho Suk
Orosomucoid (ORM) is an acute-phase protein that belongs to the immunocalin subfamily, a group of small-molecule binding proteins with immunomodulatory functions. Little is known about the role of ORM proteins in the central nervous system. The aim of the present study was to investigate the brain expression of ORM and its role in neuroinflammation. Expression of Orm2, but not Orm1 or Orm3, was highly induced in the mouse brain after systemic injection of lipopolysaccharide (LPS). Plasma levels of ORM2 were also significantly higher in patients with cognitive impairment than in normal subjects...
February 13, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28191738/the-role-of-neuroinflammation-and-amyloid-in-cognitive-impairment-in-an-app-ps1-transgenic-mouse-model-of-alzheimer-s-disease
#7
Shenghua Zhu, Junhui Wang, Yanbo Zhang, Jue He, Jiming Kong, Jun-Feng Wang, Xin-Min Li
AIMS: Both amyloid deposition and neuroinflammation appear in the early course of Alzheimer's disease (AD). However, the progression of neuroinflammation and its relationship with amyloid deposition and behavioral changes have not been fully elucidated. A better understanding the role of neuroinflammation in AD might extend our current knowledge to therapeutic intervention possibilities. METHODS: This study systematically characterized changes in behavioral abnormalities in APP/PS1 transgenic mice...
February 12, 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/28185874/psychosocial-stress-on-neuroinflammation-and-cognitive-dysfunctions-in-alzheimer-s-disease-the-emerging-role-for-microglia
#8
REVIEW
Sami Piirainen, Andrew Youssef, Cai Song, Allan V Kalueff, Gary E Landreth, Tarja Malm, Li Tian
Chronic psychosocial stress is increasingly recognized as a risk factor for late-onset Alzheimer's disease (LOAD) and associated cognitive deficits. Chronic stress also primes microglia and induces inflammatory responses in the adult brain, thereby compromising synapse-supportive roles of microglia and deteriorating cognitive functions during aging. Substantial evidence demonstrates that failure of microglia to clear abnormally accumulating amyloid-beta (Aβ) peptide contributes to neuroinflammation and neurodegeneration in AD...
February 6, 2017: Neuroscience and Biobehavioral Reviews
https://www.readbyqxmd.com/read/28183245/ykl-40-as-a-potential-biomarker-and-a-possible-target-in-therapeutic-strategies-of-alzheimer-s-disease
#9
Paweł Muszyński, Magdalena Groblewska, Agnieszka Kulczyńska-Przybik, Alina Kułakowska, Barbara Mroczko
BACKGROUND: Growing body of evidence suggests that pathogenesis of Alzheimer's disease (AD), a progressing neurodegenerative condition, is not limited to the neuronal compartment, but also involves various immunological mechanisms. Insoluble Aβ aggregates in the brain can induce the activation of microglia, resulting in synthesis of proinflammatory mediators, which further can stimulate astrocytic expression of YKL-40. Therefore, the aim of the current review is to present up-to-date data about the role of YKL-40 as a biomarker of AD as well as the possibility of therapeutic strategies targeting neuroinflammation...
February 8, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/28164764/neuroinflammation-and-alzheimer-s-disease-implications-for-microglial-activation
#10
Francesca Regen, Julian Hellmann-Regen, Erica Costantini, Marcella Reale
Microglial activation is a hallmark of neuroinflammation, seen in most acute and chronic neuropsychiatric conditions. With growing knowledge about microglia functions in surveying the brain for alterations, microglial activation is increasingly discussed in the context of disease progression and pathogenesis of Alzheimer's disease (AD). Underlying molecular mechanisms, however, remain largely unclear. While proper microglial function is essentially required for its scavenging duties, local activation of the brain's innate immune cells also brings about many less advantageous changes, such as reactive oxygen species (ROS) production, secretion of proinflammatory cytokines or degradation of neuroprotective retinoids, and may thus unnecessarily put surrounding healthy neurons in danger...
February 3, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28163132/aging-leads-to-altered-microglial-function-that-reduces-brain-resiliency-increasing-vulnerability-to-neurodegenerative-diseases
#11
Paula C Bickford, Antwoine Flowers, Bethany Grimmig
Aging is the primary risk factor for many neurodegenerative diseases. Thus, understanding the basic biological changes that take place with aging that lead to the brain being less resilient to disease progression of neurodegenerative diseases such as Parkinson's disease or Alzheimer's disease or insults to the brain such as stroke or traumatic brain injuries. Clearly this will not cure the disease per se, yet increasing the ability of the brain to respond to injury could improve long term outcomes. The focus of this review is examining changes in microglia with age and possible therapeutic interventions involving the use of polyphenol rich dietary supplements...
February 2, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28157094/treadmill-exercise-exerts-neuroprotection-and-regulates-microglial-polarization-and-oxidative-stress-in-a-streptozotocin-induced-rat-model-of-sporadic-alzheimer-s-disease
#12
Yujiao Lu, Yan Dong, Donovan Tucker, Ruimin Wang, Mohammad Ejaz Ahmed, Darrell Brann, Quanguang Zhang
Recent work has suggested that exercise may be beneficial in preventing or ameliorating symptoms of several neurological disorders, although the mechanism is not entirely understood. The current study was designed to examine the potential beneficial effect of treadmill exercise upon cognitive function in a streptozotocin (STZ)-induced rat model of Alzheimer's disease (AD). Animals underwent treadmill exercise (30 min/day, 5 days/week) for 4 weeks after bilateral STZ intracerebroventricular injection (2.4 mg/kg)...
February 1, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28154566/histological-architecture-underlying-brain-immune-cell-cell-interactions-and-the-cerebral-response-to-systemic-inflammation
#13
Atsuyoshi Shimada, Sanae Hasegawa-Ishii
Although the brain is now known to actively interact with the immune system under non-inflammatory conditions, the site of cell-cell interactions between brain parenchymal cells and immune cells has been an open question until recently. Studies by our and other groups have indicated that brain structures such as the leptomeninges, choroid plexus stroma and epithelium, attachments of choroid plexus, vascular endothelial cells, cells of the perivascular space, circumventricular organs, and astrocytic endfeet construct the histological architecture that provides a location for intercellular interactions between bone marrow-derived myeloid lineage cells and brain parenchymal cells under non-inflammatory conditions...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28150942/identification-of-inhibitors-of-cd36-amyloid-beta-binding-as-potential-agents-for-alzheimer-s-disease
#14
Deborah Doens, Pedro A Valiente, Adelphe M Mfuh, Anh X T Vo, Adilia Tristan, Lizmar Carreño, Mario Quijada, Vu T Nguyen, George Perry, Oleg V Larionov, Ricardo Lleonart, Patricia L Fernández
Neuroinflammation is one of the hallmarks of Alzheimer's disease pathology. Amyloid β has a central role in microglia activation and the subsequent secretion of inflammatory mediators that are associated with neuronal toxicity. The recognition of amyloid β by microglia depends on the expression of several receptors implicated in the clearance of amyloid and in cell activation. CD36 receptor expressed on microglia interacts with fibrils of amyloid inducing the release of proinflammatory cytokines and amyloid internalization...
February 15, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28143566/apoe-genotype-differentially-modulates-effects-of-anti-a%C3%AE-passive-immunization-in-app-transgenic-mice
#15
Joanna E Pankiewicz, Jairo Baquero-Buitrago, Sandrine Sanchez, Jennifer Lopez-Contreras, Jungsu Kim, Patrick M Sullivan, David M Holtzman, Martin J Sadowski
BACKGROUND: APOE genotype is the foremost genetic factor modulating β-amyloid (Aβ) deposition and risk of sporadic Alzheimer's disease (AD). Here we investigated how APOE genotype influences response to anti-Aβ immunotherapy. METHODS: APPSW/PS1dE9 (APP) transgenic mice with targeted replacement of the murine Apoe gene for human APOE alleles received 10D5 anti-Aβ or TY11-15 isotype control antibodies between the ages of 12 and 15 months. RESULTS: Anti-Aβ immunization decreased both the load of fibrillar plaques and the load of Aβ immunopositive plaques in mice of all APOE backgrounds...
January 31, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28131016/rod-shaped-microglia-morphology-is-associated-with-aging-in-2-human-autopsy-series
#16
Adam D Bachstetter, Eseosa T Ighodaro, Yasmin Hassoun, Danah Aldeiri, Janna H Neltner, Ela Patel, Erin L Abner, Peter T Nelson
A subtype of microglia is defined by the morphological appearance of the cells as rod shaped. Little is known about this intriguing cell type, as there are only a few case reports describing rod-shaped microglia in the neuropathological literature. Rod-shaped microglia were shown recently to account for a substantial proportion of the microglia cells in the hippocampus of both demented and cognitively intact aged individuals. We hypothesized that aging could be a defining feature in the occurrence of rod-shaped microglia...
January 5, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28129888/alzheimer-s-disease-innate-immunity-gone-awry
#17
Theodore B VanItallie
Inflammation is an immune activity designed to protect the host from pathogens and noxious agents. In its low-intensity form, presence of an inflammatory process must be inferred from appropriate biomarkers. Occult neuroinflammation is not just secondary to Alzheimer's disease (AD) but may contribute to its pathogenesis and promote its progression. A leaky blood-brain barrier (BBB) has been observed in early AD and may play a role in its initiation and development. Studies of the temporal evolution of AD's biomarkers have shown that, in AD, the brain's amyloid burden correlates poorly with cognitive decline...
January 11, 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28124586/high-glucose-enhances-neurotoxicity-and-inflammatory-cytokine-secretion-by-stimulated-human-astrocytes
#18
Manpreet Bahniwal, Jonathan P Little, Andis Klegeris
BACKGROUND: Chronic neuroinflammation caused by activation of microglia and astrocytes in the brain contributes to neuronal loss and disease progression in Alzheimer's disease (AD). Recent research has identified type 2 diabetes mellitus (T2DM) as a risk factor for AD. High blood glucose (hyperglycemia) and the phenomenon of insulin resistance are being considered as the major factors contributing to an increased risk of AD. However, the mechanisms involved in this interaction remain unclear...
January 16, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28123027/innate-immunity-stimulation-via-toll-like-receptor-9-ameliorates-vascular-amyloid-pathology-in-tg-swdi-mice-with-associated-cognitive-benefits
#19
Henrieta Scholtzova, Eileen Do, Shleshma Dhakal, Yanjie Sun, Shan Liu, Pankaj D Mehta, Thomas Wisniewski
: Alzheimer's disease (AD) is characterized by the presence of parenchymal amyloid-β (Aβ) plaques, cerebral amyloid angiopathy (CAA) and neurofibrillary tangles. Currently there are no effective treatments for AD. Immunotherapeutic approaches under development are hampered by complications related to ineffectual clearance of CAA. Genome-wide association studies have demonstrated the importance of microglia in AD pathogenesis. Microglia are the primary innate immune cells of the brain...
January 25, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28122877/an-early-and-late-peak-in-microglial-activation-in-alzheimer-s-disease-trajectory
#20
Zhen Fan, David J Brooks, Aren Okello, Paul Edison
Amyloid-β deposition, neuroinflammation and tau tangle formation all play a significant role in Alzheimer's disease. We hypothesized that there is microglial activation early on in Alzheimer's disease trajectory, where in the initial phase, microglia may be trying to repair the damage, while later on in the disease these microglia could be ineffective and produce proinflammatory cytokines leading to progressive neuronal damage. In this longitudinal study, we have evaluated the temporal profile of microglial activation and its relationship between fibrillar amyloid load at baseline and follow-up in subjects with mild cognitive impairment, and this was compared with subjects with Alzheimer's disease...
January 24, 2017: Brain: a Journal of Neurology
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