Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders

Nature reviews. Neuroscience, Journal Year: 2011, Volume and Issue: 12(12), P. 723 - 738

Published: Nov. 3, 2011

Language: Английский

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Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases

Molecular Neurobiology, Journal Year: 2015, Volume and Issue: 53(2), P. 1181 - 1194

Published: Jan. 19, 2015

Language: Английский

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Adverse childhood experiences, allostasis, allostatic load, and age-related disease

Physiology & Behavior, Journal Year: 2011, Volume and Issue: 106(1), P. 29 - 39

Published: Aug. 27, 2011

Language: Английский

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From stress to inflammation and major depressive disorder: A social signal transduction theory of depression.

Psychological Bulletin, Journal Year: 2014, Volume and Issue: 140(3), P. 774 - 815

Published: Jan. 13, 2014

Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically plausible, multilevel theory that describes neural, physiologic, molecular, genomic mechanisms link experiences of social-environmental with internal biological processes drive depression pathogenesis. Central to signal transduction is hypothesis threat adversity up-regulate components immune system involved in inflammation. The key mediators response, called proinflammatory cytokines, can turn elicit profound changes behavior, which include initiation depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, social-behavioral withdrawal. This highly conserved response critical survival during times actual physical or injury. However, also be activated by modern-day social, symbolic, imagined threats, leading an increasingly phenotype may phenomenon driving pathogenesis recurrence, well overlap several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, neurodegeneration. Insights from thus shed light on important questions how develops, why it frequently recurs, strongly predicted early stress, often co-occurs anxiety certain disease conditions. work suggest new opportunities preventing treating targeting

Language: Английский

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Inflammation as a central mechanism in Alzheimer's disease

Alzheimer s & Dementia Translational Research & Clinical Interventions, Journal Year: 2018, Volume and Issue: 4(1), P. 575 - 590

Published: Jan. 1, 2018

Abstract Alzheimer's disease (AD) is a progressive neurodegenerative disorder that characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques neurofibrillary tangles. Over last decade, sustained immune response in brain has emerged as third pathology AD. The activation brain's resident macrophages (microglia) other cells been demonstrated to exacerbate both tau may serve link pathogenesis disorder. In following review, we provide an overview inflammation AD detailed coverage number microglia‐related signaling mechanisms have implicated Additional information on microglia cytokines are also reviewed. We review potential connection risk factors for how they be related inflammatory mechanisms.

Language: Английский

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Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes

Translational Neurodegeneration, Journal Year: 2020, Volume and Issue: 9(1)

Published: Nov. 26, 2020

Abstract Neuroinflammation is associated with neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s and amyotrophic lateral sclerosis. Microglia astrocytes are key regulators of inflammatory responses in the central nervous system. The activation microglia heterogeneous traditionally categorized neurotoxic (M1-phenotype A1-phenotype astrocytes) or neuroprotective (M2-phenotype A2-phenotype astrocytes). However, this dichotomized classification may not reflect various phenotypes astrocytes. relationship between these activated glial cells also very complicated, phenotypic distribution can change, based on progression diseases. A better understanding roles diseases essential for developing effective therapies. In review, we discuss response focusing contributions their relationship. addition, biomarkers to measure neuroinflammation studies therapeutic drugs that modulate neuroinflammation.

Language: Английский

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The role of inflammation in epilepsy

Nature Reviews Neurology, Journal Year: 2010, Volume and Issue: 7(1), P. 31 - 40

Published: Dec. 7, 2010

Language: Английский

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Inflammation and tumor progression: signaling pathways and targeted intervention

Signal Transduction and Targeted Therapy, Journal Year: 2021, Volume and Issue: 6(1)

Published: July 12, 2021

Abstract Cancer development and its response to therapy are regulated by inflammation, which either promotes or suppresses tumor progression, potentially displaying opposing effects on therapeutic outcomes. Chronic inflammation facilitates progression treatment resistance, whereas induction of acute inflammatory reactions often stimulates the maturation dendritic cells (DCs) antigen presentation, leading anti-tumor immune responses. In addition, multiple signaling pathways, such as nuclear factor kappa B (NF-kB), Janus kinase/signal transducers activators transcription (JAK-STAT), toll-like receptor (TLR) cGAS/STING, mitogen-activated protein kinase (MAPK); factors, including cytokines (e.g., interleukin (IL), interferon (IFN), necrosis (TNF)-α), chemokines C-C motif chemokine ligands (CCLs) C-X-C (CXCLs)), growth factors vascular endothelial (VEGF), transforming (TGF)-β), inflammasome; well metabolites prostaglandins, leukotrienes, thromboxane, specialized proresolving mediators (SPM), have been identified pivotal regulators initiation resolution inflammation. Nowadays, local irradiation, recombinant cytokines, neutralizing antibodies, small-molecule inhibitors, DC vaccines, oncolytic viruses, TLR agonists, SPM developed specifically modulate in cancer therapy, with some these already undergoing clinical trials. Herein, we discuss crosstalk between processes. We also highlight potential targets for harnessing cancer.

Language: Английский

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Interactions between the microbiota, immune and nervous systems in health and disease

Nature Neuroscience, Journal Year: 2017, Volume and Issue: 20(2), P. 145 - 155

Published: Jan. 16, 2017

Language: Английский

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Microglia in Alzheimer’s disease

The Journal of Cell Biology, Journal Year: 2017, Volume and Issue: 217(2), P. 459 - 472

Published: Dec. 1, 2017

Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature Alzheimer’s disease (AD). Human genetics data point to key role for pathogenesis AD. The majority risk genes AD are highly expressed (and many selectively expressed) by brain. There mounting evidence that protect against incidence AD, as impaired microglial activities altered responses β-amyloid associated with increased risk. On other hand, there also abundant activated can be harmful neurons. Microglia mediate synapse loss engulfment synapses, likely via complement-dependent mechanism; they exacerbate tau pathology secrete inflammatory factors injure neurons directly or neurotoxic astrocytes. Gene expression profiles indicate multiple states neurodegenerative settings, which might explain disparate roles development progression pathology.

Language: Английский

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