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Amyloid aging microglia

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https://www.readbyqxmd.com/read/28282924/autophagy-and-microglia-novel-partners-in-neurodegeneration-and-aging
#1
REVIEW
Ainhoa Plaza-Zabala, Virginia Sierra-Torre, Amanda Sierra
Autophagy is emerging as a core regulator of Central Nervous System (CNS) aging and neurodegeneration. In the brain, it has mostly been studied in neurons, where the delivery of toxic molecules and organelles to the lysosome by autophagy is crucial for neuronal health and survival. However, we propose that the (dys)regulation of autophagy in microglia also affects innate immune functions such as phagocytosis and inflammation, which in turn contribute to the pathophysiology of aging and neurodegenerative diseases...
March 9, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28253987/metabolic-syndrome-and-the-cellular-phase-of-alzheimer-s-disease
#2
S Pugazhenthi
Alzheimer's disease (AD) is characterized by cognitive dysfunction and progressive neurodegeneration. The major hallmarks of AD pathology are amyloid plaques and neurofibrillary tangles. However, AD often coexists with other brain microvascular lesions caused by comorbidities, including obesity, diabetes, hypertension, and cardiovascular diseases. The risk factors for these comorbidities are collectively referred to as metabolic syndrome (MetS). Clinical AD is preceded by decades of prodromal cellular phase...
2017: Progress in Molecular Biology and Translational Science
https://www.readbyqxmd.com/read/28203202/plasma-exosomes-spread-and-cluster-around-%C3%AE-amyloid-plaques-in-an-animal-model-of-alzheimer-s-disease
#3
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/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/28185874/psychosocial-stress-on-neuroinflammation-and-cognitive-dysfunctions-in-alzheimer-s-disease-the-emerging-role-for-microglia
#5
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/28143566/apoe-genotype-differentially-modulates-effects-of-anti-a%C3%AE-passive-immunization-in-app-transgenic-mice
#6
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/28123027/innate-immunity-stimulation-via-toll-like-receptor-9-ameliorates-vascular-amyloid-pathology-in-tg-swdi-mice-with-associated-cognitive-benefits
#7
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. Depending on their activation state and environment, microglia can be beneficial or detrimental...
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
#8
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
https://www.readbyqxmd.com/read/28087694/iso-%C3%AE-acids-bitter-components-of-beer-prevent-inflammation-and-cognitive-decline-induced-in-a-mouse-model-of-alzheimer-s-disease
#9
Yasuhisa Ano, Atsushi Dhata, Yoshimasa Taniguchi, Ayaka Hoshi, Kazuyuki Uchida, Akihiko Takashima, Hiroyuki Nakayama
Alongside the rapid growth in aging populations worldwide, prevention and therapy for age-related memory decline and dementia are in great demand to maintain a long healthy life. Here we found that iso-α-acids, hop-derived bitter compounds in beer, enhance microglial phagocytosis and suppress inflammation via activation of the peroxisome proliferator-activated receptor (PPAR-γ). In normal mice, oral administration of iso-α-acids led to a significant increase both in CD11b and CD206 double-positive anti-inflammatory type microglia (P<0...
January 13, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28073379/tau-passive-immunization-inhibits-not-only-tau-but-also-a%C3%AE-pathology
#10
Chun-Ling Dai, Yunn Chyn Tung, Fei Liu, Cheng-Xin Gong, Khalid Iqbal
BACKGROUND: Accumulation of hyperphosphorylated tau protein is a histopathological hallmark of Alzheimer's disease (AD) and related tauopathies. Currently, there is no effective treatment available for these progressive neurodegenerative diseases. In recent years, tau immunotherapy has shown great potential in animal models. We report the effect of immunization with tau antibodies 43D against tau 6-18 and 77E9 against tau 184-195 on tau and amyloid-β (Aβ) pathologies and cognition in triple-transgenic (3×Tg)-AD mice at mild to moderate stages of the disease...
January 10, 2017: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/28060896/isobavachalcone-attenuates-mptp-induced-parkinson-s-disease-in-mice-by-inhibition-of-microglial-activation-through-nf-%C3%AE%C2%BAb-pathway
#11
Haoran Jing, Shaoxia Wang, Min Wang, Wenliang Fu, Chao Zhang, Donggang Xu
Parkinson's disease (PD) is a complex multi-system and age-related neurodegenerative disorder. The intervention targeting neuroinflammation in PD patients is one effective strategy to slow down or inhibit disease progression. Microglia-mediated inflammatory response plays an important role in Parkinson's, Alzheimer's and other cerebral diseases. Isobavachalcone is a main component of Chinese herb medicine Psoralea corylifolia, which function includes immunoregulation, anti-oxidation and the regulation of β-amyloid (Aβ42) deposited in hippocampus in Alzheimer's patients...
2017: PloS One
https://www.readbyqxmd.com/read/28054940/neuroprotective-effects-of-aged-garlic-extract-on-cognitive-dysfunction-and-neuroinflammation-induced-by-%C3%AE-amyloid-in-rats
#12
Nutchareeporn Nillert, Wanassanun Pannangrong, Jariya Umka Welbat, Wunnee Chaijaroonkhanarak, Kittisak Sripanidkulchai, Bungorn Sripanidkulchai
Neuroinflammation is pathological evidence of Alzheimer's disease (AD) that likely starts as a host defense response to the damaging effects of the β-amyloid (Aβ) deposits in the brain. The activation of microglia may promote the neurodegenerative process through the release of proinflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNFα), which may lead to neuronal damage and eventual death. Aged garlic extract (AGE) has been reported to have multiple biological activities, including anti-inflammatory effects...
January 3, 2017: Nutrients
https://www.readbyqxmd.com/read/28039950/ageing-causes-prominent-neurovascular-dysfunction-associated-with-loss-of-astrocytic-contacts-and-gliosis
#13
Jessica Duncombe, Ross J Lennen, Maurits A Jansen, Ian Marshall, Joanna M Wardlaw, Karen Horsburgh
AIMS: Normal neurovascular coupling, mediated by the fine interplay and communication of cells within the neurovascular unit, is critical for maintaining normal brain activity and cognitive function. This study investigated whether, with advancing age there is disruption of neurovascular coupling and specific cellular components of the neurovascular unit, and whether the effects of increasing amyloid (a key feature of Alzheimer's disease) would exacerbate these changes. METHODS: Wild-type mice, in which amyloid deposition is absent, were compared to transgenic APP littermates (TgSwDI) which develop age-dependent increases in amyloid...
December 31, 2016: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/28027926/early-life-stress-lastingly-alters-the-neuroinflammatory-response-to-amyloid-pathology-in-an-alzheimer-s-disease-mouse-model
#14
Lianne Hoeijmakers, Silvie R Ruigrok, Anna Amelianchik, Daniela Ivan, Anne-Marie van Dam, Paul J Lucassen, Aniko Korosi
Exposure to stress during the sensitive period of early-life increases the risk to develop cognitive impairments and psychopathology later in life. In addition, early-life stress (ES) exposure, next to genetic causes, has been proposed to modulate the development and progression of Alzheimer's disease (AD), however evidence for this hypothesis is currently lacking. We here tested whether ES modulates progression of AD-related neuropathology and assessed the possible contribution of neuroinflammatory factors in this...
December 25, 2016: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28007893/young-microglia-restore-amyloid-plaque-clearance-of-aged-microglia
#15
Anna Daria, Alessio Colombo, Gemma Llovera, Heike Hampel, Michael Willem, Arthur Liesz, Christian Haass, Sabina Tahirovic
Alzheimer's disease (AD) is characterized by deposition of amyloid plaques, neurofibrillary tangles, and neuroinflammation. In order to study microglial contribution to amyloid plaque phagocytosis, we developed a novel ex vivo model by co-culturing organotypic brain slices from up to 20-month-old, amyloid-bearing AD mouse model (APPPS1) and young, neonatal wild-type (WT) mice. Surprisingly, co-culturing resulted in proliferation, recruitment, and clustering of old microglial cells around amyloid plaques and clearance of the plaque halo...
March 1, 2017: EMBO Journal
https://www.readbyqxmd.com/read/28003160/regulatory-factor-x1-depresses-apoe-dependent-a%C3%AE-uptake-by-mirna-124-in-microglial-response-to-oxidative-stress
#16
Chen-Zhuo Feng, Jin-Bo Yin, Jian-Jun Yang, Lin Cao
Decreased proteolytic clearance of soluble amyloid β (Aβ) in microglia affects Aβ accumulation on Alzheimer's disease progression. However, the potential molecular mechanism by which microglial Aβ uptake is regulated remains unclear. In this study, we identified a microRNA, miR-124, that was down-regulated in aging with a function in regulating apolipoprotein E (ApoE)-dependent Aβ uptake by targeting regulatory factor X1 (RFX1) transcripts on BV2 microglia cell. Decreased expression of miRNA-124 in BV2 cells exposed to mild hydrogen peroxide increased RFX1 protein level and decreased the expression of ApoE, a gene which has been suggested to enhance cellular Aβ uptake in microglia...
March 6, 2017: Neuroscience
https://www.readbyqxmd.com/read/27980116/innate-immunity-stimulation-via-toll-like-receptor-9-ameliorates-vascular-amyloid-pathology-in-tg-swdi-mice-with-associated-cognitive-benefits
#17
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-beta (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, and depending on their activation state and environment can have beneficial or detrimental effects...
December 15, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27929004/gamma-frequency-entrainment-attenuates-amyloid-load-and-modifies-microglia
#18
Hannah F Iaccarino, Annabelle C Singer, Anthony J Martorell, Andrii Rudenko, Fan Gao, Tyler Z Gillingham, Hansruedi Mathys, Jinsoo Seo, Oleg Kritskiy, Fatema Abdurrob, Chinnakkaruppan Adaikkan, Rebecca G Canter, Richard Rueda, Emery N Brown, Edward S Boyden, Li-Huei Tsai
Changes in gamma oscillations (20-50 Hz) have been observed in several neurological disorders. However, the relationship between gamma oscillations and cellular pathologies is unclear. Here we show reduced, behaviourally driven gamma oscillations before the onset of plaque formation or cognitive decline in a mouse model of Alzheimer's disease. Optogenetically driving fast-spiking parvalbumin-positive (FS-PV)-interneurons at gamma (40 Hz), but not other frequencies, reduces levels of amyloid-β (Aβ)1-40 and Aβ 1-42 isoforms...
December 7, 2016: Nature
https://www.readbyqxmd.com/read/27878757/targeting-ccr3-to-reduce-amyloid-%C3%AE-production-tau-hyperphosphorylation-and-synaptic-loss-in-a-mouse-model-of-alzheimer-s-disease
#19
Chunyan Zhu, Bing Xu, Xiaohong Sun, Qiwen Zhu, Yi Sui
The majority of Alzheimer's disease (AD) patients have a late onset, and chronic neuroinflammation, characterized by glial activation and secretion of pro-inflammatory cytokines and chemokines, plays a role in the pathogenesis of AD. The chemokine CCL11 has been shown to be a causative factor of cognitive decline in the process of aging, but little is known whether it is involved in the pathogenesis of AD. In the present study, we showed that CCR3, the receptor for CCL11, was expressed by hippocampal neurons and treatment of primary hippocampal neuronal cultures (14 days in vitro) with CCL11 resulted in activation of cyclin-dependent kinase 5 and glycogen synthase kinase-3β, associated with elevated tau phosphorylation at multiple sites...
November 23, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27830533/analysis-of-the-impact-of-cd200-on-phagocytosis
#20
Anthony Lyons, Aedín M Minogue, Raasay S Jones, Orla Fitzpatrick, Janis Noonan, Veronica A Campbell, Marina A Lynch
One factor that impacts on microglial activation is the interaction between the ubiquitously expressed CD200 and CD200R, which is expressed only on microglia in the brain. Decreased signalling through CD200R, when CD200 expression is reduced, results in microglial activation and may, at least in part, explain the increased cell activity that is observed with age, in models of Alzheimer's and Parkinson's disease as well as in the human diseases. There is evidence of increased microglial activation in CD200-deficient mice, and isolated microglia prepared from these mice are more reactive to inflammatory stimuli like Toll-like receptor 2 and 4 agonists, and interferon-γ...
November 9, 2016: Molecular Neurobiology
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