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Alzheimers and inflammation

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https://www.readbyqxmd.com/read/28914166/repeated-iron-soot-exposure-and-nose-to-brain-transport-of-inhaled-ultrafine-particles
#1
Laurie E Hopkins, Emilia A Laing, Janice L Peake, Dale Uyeminami, Savannah M Mack, Xueting Li, Suzette Smiley-Jewell, Kent E Pinkerton
Particulate exposure has been implicated in the development of a number of neurological maladies such as multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's disease, and idiopathic Parkinson's disease. Only a few studies have focused on the olfactory pathway as a portal through which combustion-generated particles may enter the brain. The primary objective of this study was to define the deposition, uptake, and transport of inhaled ultrafine iron-soot particles in the nasal cavities of mice to determine whether combustion-generated nanoparticles reach the olfactory bulb via the olfactory epithelium and nerve fascicles...
January 1, 2017: Toxicologic Pathology
https://www.readbyqxmd.com/read/28912710/key-aging-associated-alterations-in-primary-microglia-response-to-beta-amyloid-stimulation
#2
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/28906270/microbiota-and-neurodegenerative-diseases
#3
Moira Marizzoni, Stefania Provasi, Annamaria Cattaneo, Giovanni B Frisoni
PURPOSE OF REVIEW: Despite the extensive research carried out in the past decades, the current pathophysiological notions of neurodegenerative disease as well as effective treatments to reduce their progression are largely unknown. Alterations of the human microbiota, the plethora of different microscopic organisms that our body hosts, have been linked to neurodegenerative disease risk, onset and progression. This review summarizes the current knowledge on the possible role of microbiota in neurodegenerative disorders and briefly discusses strategies to restore microbiota homeostasis...
September 12, 2017: Current Opinion in Neurology
https://www.readbyqxmd.com/read/28899014/slow-wave-sleep-disruption-increases-cerebrospinal-fluid-amyloid-%C3%AE-levels
#4
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/28891528/2-2-benzofuranyl-2-imidazoline-2-bfi-improved-the-impairments-in-ad-rat-models-by-inhibiting-oxidative-stress-inflammation-and-apoptosis
#5
Ji-Sha Tian, Qi-Jin Zhai, Ying Zhao, Rui Chen, Lian-Dong Zhao
Alzheimer's Disease (AD) is one of the commonest neural degeneration in aging population, and has become a global health challenge. 2-(2-benzofuranyl)-2-imidazoline (2-BFI) was reported to effectively improved the damage of patients with neuropathological disorders. In the present study, we investigated the effect of 2-BFI on the improvement of antioxidative, inflammation, and apoptosis in AD rats. Sprague-Dawley rats (2 months old, n=40) were used in this study and after injection of Aβ1-42 into hippocampal CA1 (Cornu Ammonis) region, the rats were given high, moderate and low dose of 2-BFI though intraperitoneal (i...
2017: Journal of Integrative Neuroscience
https://www.readbyqxmd.com/read/28890695/acute-hypoxia-induced-an-imbalanced-m1-m2-activation-of-microglia-through-nf-%C3%AE%C2%BAb-signaling-in-alzheimer-s-disease-mice-and-wild-type-littermates
#6
Feng Zhang, Rujia Zhong, Song Li, Zhenfa Fu, Cheng Cheng, Huaibin Cai, Weidong Le
Alzheimer's disease (AD) is the most common neurodegenerative disease mainly caused by abnormal tau phosphorylation, amyloid β (Aβ) deposition and neuroinflammation. As an important environmental factor, hypoxia has been reported to aggravate AD via exacerbating Aβ and tau pathologies. However, the link between hypoxia and neuroinflammation, especially the changes of pro-inflammatory M1 or anti-inflammation M2 microglia phenotypes in AD, is still far from being clearly investigated. Here, we evaluated the activation of microglia in the brains of APP(swe)/PS1(dE9) transgenic (Tg) mice and their wild type (Wt) littermates, after a single episode of acute hypoxia (24 h) exposure...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28890476/old-and-new-inflammation-and-infection-hypotheses-of-alzheimer-s-disease-focus-on-microglia-aging-for-chronic-neuroinflammation
#7
Zhou Wu, Hiroshi Nakanishi
No abstract text is available yet for this article.
2017: Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
https://www.readbyqxmd.com/read/28884281/angiotensin-receptor-blockade-by-inhibiting-glial-activation-promotes-hippocampal-neurogenesis-via-activation-of-wnt-%C3%AE-catenin-signaling-in-hypertension
#8
Shahnawaz Ali Bhat, Ruby Goel, Shubha Shukla, Rakesh Shukla, Kashif Hanif
Hypertension is one of the major risk factors for central nervous system (CNS) disorders like stroke and Alzheimer's disease (AD). On the other hand, CNS diseases like AD have been associated with gliosis and impaired neurogenesis. Further, renin angiotensin system (RAS) is intricately associated with hypertension; however, the accumulating evidences suggest that over-activity of RAS may perpetuate the brain inflammation related with AD. Therefore, in the present study, we examined the effect of hypertension and RAS on glial (astrocytes and microglia) activation and hippocampal neurogenesis in a rat model of chronic hypertension...
September 7, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28882786/exosomal-biomarkers-in-down-syndrome-and-alzheimer-s-disease
#9
REVIEW
Eric D Hamlett, Aurélie Ledreux, Huntington Potter, Heidi J Chial, David Patterson, Joaquin M Espinosa, Brianne M Bettcher, Ann-Charlotte Granholm
Every person with Down syndrome (DS) has the characteristic features of Alzheimer's disease (AD) neuropathology in their brain by the age of forty, and most go on to develop AD dementia. Since people with DS show highly variable levels of baseline function, it is often difficult to identify early signs of dementia in this population. The discovery of blood biomarkers predictive of dementia onset and/or progression in DS is critical for developing effective clinical diagnostics. Our recent studies show that neuron-derived exosomes, which are small extracellular vesicles secreted by most cells in the body, contain elevated levels of amyloid-beta peptides and phosphorylated-Tau that could indicate a preclinical AD phase in people with DS starting in childhood...
September 4, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28879423/transcriptional-effects-of-apoe4-relevance-to-alzheimer-s-disease
#10
REVIEW
Veena Theendakara, Clare A Peters-Libeu, Dale E Bredesen, Rammohan V Rao
The major genetic risk factor for sporadic Alzheimer's disease (AD) is the lipid binding and transporting carrier protein apolipoprotein E, epsilon 4 allele (ApoE4). One of the unsolved mysteries of AD is how the presence of ApoE4 elicits this age-associated, currently incurable neurodegenerative disease. Recently, we showed that ApoE4 acts as a transcription factor and binds to the promoters of genes involved in a range of processes linked to aging and AD disease pathogenesis. These findings point to novel therapeutic strategies for AD and aging, resulting in an extension of human healthspan, the disease-free and functional period of life...
September 6, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28872464/cns-inflammation-and-neurodegeneration
#11
Tanuja Chitnis, Howard L Weiner
There is an increasing recognition that inflammation plays a critical role in neurodegenerative diseases of the CNS, including Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and the prototypic neuroinflammatory disease multiple sclerosis (MS). Differential immune responses involving the adaptive versus the innate immune system are observed at various stages of neurodegenerative diseases, and may not only drive disease processes but could serve as therapeutic targets. Ongoing investigations into the specific inflammatory mechanisms that play roles in disease causation and progression have revealed lessons about inflammation-driven neurodegeneration that can be applied to other neurodegenerative diseases...
September 5, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28870559/intranasal-deferoxamine-affects-memory-loss-oxidation-and-the-insulin-pathway-in-the-streptozotocin-rat-model-of-alzheimer-s-disease
#12
J M Fine, A C Forsberg, B M Stroebel, K A Faltesek, D R Verden, K A Hamel, E B Raney, J M Crow, L R Haase, K E Knutzen, K D Kaczmarczek, W H Frey, L R Hanson
Accumulation of metal and the accompanying increase in oxidative stress and inflammation plays an important role in neurodegenerative disease. Deferoxamine (DFO) is a metal chelator found to be beneficial in several animal models of neurodegenerative disease and insult including Alzheimer's disease, Parkinson's disease, stroke, and subarachnoid hemorrhage. In this study, we determine whether intranasally (IN) administered DFO is beneficial in the intracerebroventricular streptozotocin (ICV STZ) rat model of sporadic Alzheimer's disease, which is different from previous models in that it exhibits dysregulation of insulin metabolism as well as oxidative stress and inflammation...
September 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28869479/kynurenine-pathway-metabolites-in-alzheimer-s-disease
#13
Lasse Melvaer Giil, Øivind Midttun, Helga Refsum, Arve Ulvik, Rajiv Advani, A David Smith, Per Magne Ueland
BACKGROUND: Metabolites of tryptophan, produced via the kynurenine pathway (kynurenines), have been linked to Alzheimer's disease (AD) in small cohorts with conflicting results. OBJECTIVE: To compare differences in plasma kynurenine levels between AD and controls and identify potential associations with cognition. METHODS: The study included 65 histopathologically-confirmed AD patients and 65 cognitively-screened controls from the Oxford Project to Investigate Memory and Ageing (OPTIMA) cohort...
August 30, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28867259/early-and-late-cns-inflammation-in-alzheimer-s-disease-two-extremes-of-a-continuum
#14
REVIEW
A Claudio Cuello
In 1990 it was reported that individuals receiving NSAIDs (non-steroidal anti-inflammatory drugs) showed a markedly reduced prevalence of Alzheimer's disease (AD) compared to the overall population. Large epidemiological studies corroborated this assertion and provoked numerous prospective AD clinical trials with a variety of NSAIDs, all of which demonstrated lack of efficacy. It is postulated that the explanation for the success of NSAIDS in preventing AD onset when given at preclinical stages, and for their failure when administered after AD clinical presentation, lies in the changing nature of central nervous system (CNS) inflammation in the decades-long continuum of AD pathology...
August 31, 2017: Trends in Pharmacological Sciences
https://www.readbyqxmd.com/read/28865468/brain-ureido-degenerative-protein-modifications-are-associated-with-neuroinflammation-and-proteinopathy-in-alzheimer-s-disease-with-cerebrovascular-disease
#15
Xavier Gallart-Palau, Aida Serra, Benjamin Sian Teck Lee, Xue Guo, Siu Kwan Sze
BACKGROUND: Brain degenerative protein modifications (DPMs) are associated with the apparition and progression of dementia, and at the same time, Alzheimer's disease with cerebrovascular disease (AD + CVD) is the most prevalent form of dementia in the elder population. Thus, understanding the role(s) of brain DPMs in this dementia subtype may provide novel insight on the disease pathogenesis and may aid on the development of novel diagnostic and therapeutic tools. Two essential DPMs known to promote inflammation in several human diseases are the ureido DPMs (uDPMs) arginine citrullination and lysine carbamylation, although they have distinct enzymatic and non-enzymatic origins, respectively...
September 2, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28863860/discoidin-domain-receptor-inhibition-reduces-neuropathology-and-attenuates-inflammation-in-neurodegeneration-models
#16
Michaeline Hebron, Margo Peyton, Xiaoguang Liu, Xiaokong Gao, Ruochong Wang, Irina Lonskaya, Charbel E-H Moussa
The role of cell surface tyrosine kinase collagen-activated receptors known as discoidin domain receptors (DDRs) is unknown in neurodegenerative diseases. We detect up-regulation in DDRs level in post-mortem Alzheimer and Parkinson brains. Lentiviral shRNA knockdown of DDR1 and DDR2 reduces the levels of α-synuclein, tau, and β-amyloid and prevents cell loss in vivo and in vitro. DDR1 and DDR2 knockdown alters brain immunity and significantly reduces the level of triggering receptor expressed on myeloid cells (TREM)-2 and microglia...
October 15, 2017: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/28862075/shedding-light-on-designing-potential-meprin-%C3%AE-inhibitors-through-ligand-based-robust-validated-computational-approaches-a-proposal-to-chemists
#17
Nilanjan Adhikari, Sk Abdul Amin, Balaram Ghosh, Tarun Jha
Human meprin (EC 3.4.24.18) is a member of the metzincin superfamily. It correlates with matrix metalloproteinases and ADAMs (a disintegrin and metalloproteinase domain). Overexpression of meprin β is implicated in fibrosis, inflammatory diseases, and cancers. However, selective meprin β inhibition is crucial to reduce cancer metastasis and adverse effects in inflammation. It also plays critical roles in modulating several interleukins and growth factors. Moreover, meprin β cleaves amyloid precursor protein (APP), thought to be involved in the progression of Alzheimer's disease...
September 1, 2017: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/28855816/identification-of-novel-inhibitors-against-cyclin-dependent-kinase-9-cyclin-t1-complex-as-anti-cancer-agent
#18
Afzal Hussain, Chandan Kumar Verma, Usha Chouhan
Cell cycle consists of different types of phases, transition from G1, S, G2, M. Inhibition of associated CDKs like CDK9/Cyclin T1 complex, which are indirectly involved in the Cell cycle progression in the form of transcription elongation, reduces diverse diseases such as Cardiac Hypertrophy, Alzheimer's, Cancer, AIDS and Inflammation. Glide tool of the Schrodinger software has been used for performing Structure Based Virtual Screening and Docking against Drug Bank and MDPI database. The best hits were identified which go and bind in the active site of the target where ATP binds for the activity...
September 2017: Saudi Journal of Biological Sciences
https://www.readbyqxmd.com/read/28854940/diesel-engine-exhaust-accelerates-plaque-formation-in-a-mouse-model-of-alzheimer-s-disease
#19
Maja Hullmann, Catrin Albrecht, Damiën van Berlo, Miriam E Gerlofs-Nijland, Tina Wahle, Agnes W Boots, Jean Krutmann, Flemming R Cassee, Thomas A Bayer, Roel P F Schins
BACKGROUND: Increasing evidence from toxicological and epidemiological studies indicates that the central nervous system is an important target for ambient air pollutants. We have investigated whether long-term inhalation exposure to diesel engine exhaust (DEE), a dominant contributor to particulate air pollution in urban environments, can aggravate Alzheimer's Disease (AD)-like effects in female 5X Familial AD (5XFAD) mice and their wild-type female littermates. Following 3 and 13 weeks exposures to diluted DEE (0...
August 30, 2017: Particle and Fibre Toxicology
https://www.readbyqxmd.com/read/28844606/ampk-activation-role-in-the-signaling-pathways-of-neuroinflammation-and-neurodegeneration
#20
REVIEW
Christina Alves Peixoto, Wilma Helena de Oliveira, Shyrlene Meiry da Racho Araújo, Ana Karolina Santana Nunes
Adenosine monophosphate-activated protein kinase (AMPK) is an evolutionarily conserved sensor of cellular energy status and has been reported to be involved in chronic inflammatory disorders. AMPK is expressed in immune cells, such as dendritic cells, macrophages, lymphocytes and neutrophils, and is an important regulator of inflammatory responses through the regulation of complex signaling networks in part by inhibiting downstream cascade pathways, such as nuclear factor kB, which is a key regulator of innate immunity and inflammation, as well as acting as a negative regulator of toll-like receptors...
August 24, 2017: Experimental Neurology
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