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

By T. Wyss‐Coray. Nature Medicine, 2006

1,237 citations recorded by the source corpus.

Subfields: Cell Biology, Genetics, Physiology

View Paper: https://www.semanticscholar.org/paper/b819bb09590f1c15b873fbdab84f2b2a0a323a2c

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Citations in the corpus

A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines (2012, background): “This activation is thought to result from the glial reaction to the events related to the ongoing deposition of Aβ [16–18].”
Molecular Inflammation: Underpinnings of Aging and Age-related Diseases (2008, background): “…the onset of AD pathology, including members of the complement pathway; cytokines and chemokines, such as IL-1β, IL-6, TNF-α and TGF-β; coagulation factors; acute-phase reactive proteins, such as α-2-macroglobulin and α1-ACT; reactive astrocytes; and activated microglia cells (Wyss-coray, 2006).”
TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models (2015, background): “2015 Vol. 212 No. 3 287–295 www.jem.org/cgi/doi/10.1084/jem.20142322 287 Brief Definit ive Report It has historically been debated whether inflammation plays an active role in Alzheimer’s disease (AD) pathogenesis or is ancillary to other AD pathologies (Wyss-Coray, 2006).”
Inflammation in Alzheimer disease-a brief review of the basic science and clinical literature. (2012, background): “Microglia also contribute to a healthy CNS by attacking and removing potential pathogens and detritus, and by secreting tissue rebuilding factors (Wyss-Coray 2006).”
CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer (2009, background): “We therefore tested whether fibrillar β-amyloid peptide (1-42) (Aβ1-42) could activate TLR4-TLR6 signaling via CD36.”
Role of inflammation in the pathogenesis of osteoarthritis: latest findings and interpretations (2013, background): “Two additional degenerative diseases common with advancing age and associated with innate immune activation and low-grade inflammation are age-related macular degeneration [Telander, 2011] and Alzheimer’s disease [Wyss-Coray, 2006].”
Interleukin-6, a Major Cytokine in the Central Nervous System (2012, background): “This is not unexpected as activated microglia can efficiently phagocytize beta-amyloid peptide and delay pathology course in transgenic models [184-186].”
Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “On one hand, activation of astrocytes was often viewed as part of the neuroinflammatory neurotoxic response (152, 264); on the other hand, it was shown that in brain slices from AD mice, astrocytes migrated and degraded amyloid plaques (265) in an apolipoprotein E-dependent manner (121).”
Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, neutral): “, 2001) leading to disease progression (Akiyama et al., 2000; Wyss-Coray, 2006).”
A meta-analysis of cytokines in Alzheimer's disease. (2010, neutral): “With evidence reviewed elsewhere (12-15,19,150) demon-”
FoxO transcription factors in the maintenance of cellular homeostasis during aging. (2008, background): “As the expression of certain genes associated with inflammation is increased during aging (reviewed by [81]), it is tempting to speculate that FoxO factors could also maintain tissue homeostasis by preventing uncontrolled inflammatory responses.”
Inflammation: The Common Pathway of Stress-Related Diseases (2017, background): “An array of elevated inflammatory mediators including TNFα, IL-1, PGE2, NF-κB, COX-2 and MCP-1 has been detected from patients with AD (Wyss-Coray, 2006; Comi et al., 2010) and correlated with the amount of Aβ and the severity of AD pathogenesis (Hoshino et al., 2009; Chen et al., 2012).”