Inflammation in Alzheimer disease: driving force, bystander or beneficial response? - Wikidata - awgldk - TriplyDB

Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

http://www.wikidata.org/entity/Q36589042

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TNF signaling inhibition in the CNS: implications for normal brain function and neurodegenerative disease Transthyretin and the brain re-visited: is neuronal synthesis of transthyretin protective in Alzheimer's disease?Pro-inflammatory interleukin-18 increases Alzheimer's disease-associated amyloid-β production in human neuron-like cells MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer Alzheimer's disease; taking the edge off with cannabinoids?Glial Tau Pathology in Tauopathies: Functional Consequences Clinical perspectives of TRAIL: insights into central nervous system disorders Genetics ignite focus on microglial inflammation in Alzheimer's disease Potential Therapeutical Contributions of the Endocannabinoid System towards Aging and Alzheimer's Disease Rodent models of neuroinflammation for Alzheimer's disease ACE overexpression in myelomonocytic cells: effect on a mouse model of Alzheimer's disease Glial cells in (patho)physiology Inflammation and α-synuclein's prion-like behavior in Parkinson's disease--is there a link?Alzheimer's-related peptide amyloid-β plays a conserved role in angiogenesis Therapeutic effects of glatiramer acetate and grafted CD115⁺ monocytes in a mouse model of Alzheimer's disease.Reactive microglia drive tau pathology and contribute to the spreading of pathological tau in the brain.Reduced β-amyloid pathology in an APP transgenic mouse model of Alzheimer's disease lacking functional B and T cells Distinct Contributions of Astrocytes and Pericytes to Neuroinflammation Identified in a 3D Human Blood-Brain Barrier on a Chip Ocular indicators of Alzheimer's: exploring disease in the retina Alzheimer's disease and type 2 diabetes via chronic inflammatory mechanisms Potential mechanisms contributing to sulfatide depletion at the earliest clinically recognizable stage of Alzheimer's disease: a tale of shotgun lipidomics The Potassium Channel KCa3.1 Represents a Valid Pharmacological Target for Astrogliosis-Induced Neuronal Impairment in a Mouse Model of Alzheimer’s Disease Early neurodegeneration progresses independently of microglial activation by heparan sulfate in the brain of mucopolysaccharidosis IIIB mice The Toll-->NFkappaB signaling pathway mediates the neuropathological effects of the human Alzheimer's Abeta42 polypeptide in Drosophila Suppression of Alzheimer's disease-related phenotypes by geranylgeranylacetone in mice Loading into nanoparticles improves quercetin's efficacy in preventing neuroinflammation induced by oxysterols Triptolide preserves cognitive function and reduces neuropathology in a mouse model of Alzheimer's disease Effects of Ranolazine on Astrocytes and Neurons in Primary Culture Pioglitazone improves reversal learning and exerts mixed cerebrovascular effects in a mouse model of Alzheimer's disease with combined amyloid-β and cerebrovascular pathology A computational procedure for functional characterization of potential marker genes from molecular data: Alzheimer's as a case study Cumulative inflammatory load is associated with short leukocyte telomere length in the Health, Aging and Body Composition Study Genetic evidence implicates the immune system and cholesterol metabolism in the aetiology of Alzheimer's disease LRP1 in brain vascular smooth muscle cells mediates local clearance of Alzheimer's amyloid-β.Overexpression of low-density lipoprotein receptor in the brain markedly inhibits amyloid deposition and increases extracellular A beta clearance Cognitive Deficits, Changes in Synaptic Function, and Brain Pathology in a Mouse Model of Normal Aging(1,2,3).Amyloid-beta and mitochondria in aging and Alzheimer's disease: implications for synaptic damage and cognitive decline Role of the macrophage inflammatory protein-1alpha/CC chemokine receptor 5 signaling pathway in the neuroinflammatory response and cognitive deficits induced by beta-amyloid peptide The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice.

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Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

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2006 nî lūn-bûn

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Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

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Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

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Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

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Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

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Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

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Tony Wyss-Coray

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LEF-1, a gene encoding a lymphoid-specific protein with an HMG domain, regulates T-cell receptor alpha enhancer function [corrected]

Assembly and function of a TCR alpha enhancer complex is dependent on LEF-1-induced DNA bending and multiple protein-protein interactions

CCAAT/enhancer binding protein alpha is a regulatory switch sufficient for induction of granulocytic development from bipotential myeloid progenitors

Modulation of transcriptional regulation by LEF-1 in response to Wnt-1 signaling and association with beta-catenin

Autoregulation of the human C/EBP alpha gene by stimulation of upstream stimulatory factor binding.

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Alzheimer's disease