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Journal ArticleDOI

Inflammation and Alzheimer's disease.

TLDR
By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.
About
This article is published in Neurobiology of Aging.The article was published on 2000-05-01. It has received 4319 citations till now. The article focuses on the topics: Alzheimer's disease & Neuroinflammation.

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Structural and functional features of central nervous system lymphatic vessels

TL;DR: In searching for T-cell gateways into and out of the meninges, functional lymphatic vessels lining the dural sinuses are discovered, which may call for a reassessment of basic assumptions in neuroimmunology and sheds new light on the aetiology of neuroinflammatory and neurodegenerative diseases associated with immune system dysfunction.
Journal ArticleDOI

Mechanisms underlying inflammation in neurodegeneration.

TL;DR: There is evidence for a remarkable convergence in the mechanisms responsible for the sensing, transduction, and amplification of inflammatory processes that result in the production of neurotoxic mediators in neurodegenerative diseases.
References
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Journal ArticleDOI

Synthetic Alzheimer amyloid β/A4 peptides enhance production of complement C3 component by cultured microglial cells

TL;DR: The results suggest that complement components found previously in amyloid deposits may be partly derived from reactive microglia preferentially associated with senile plaques in AD brain.
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Aspartate residue 7 in amyloid beta-protein is critical for classical complement pathway activation: implications for Alzheimer's disease pathogenesis.

TL;DR: A molecular model of this interaction has been generated that should be useful in the design of candidate therapeutic inhibitors of CCP activation by amyloid β-protein, supporting a role for gliosis and inflammation in AD pathogenesis.
Journal ArticleDOI

Glucocorticoid toxicity in the hippocampus. Temporal aspects of synergy with kainic acid.

TL;DR: Exposure to corticosterone only during the period prior to KA infusion or only in the aftermath of infusion potentiated damage is examined, which appears to compromise the capacity of hippocampal neurons to survive KA via both rapid effects (manifest within as little as 24 h) as well as through more persistent actions.
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Induction of cyclo-oxygenase 2 in brains of patients with Down's syndrome and dementia of Alzheimer type: specific localization in affected neurones and axons.

Akira Oka, +1 more
- 24 Mar 1997 - 
TL;DR: Findings demonstrated the induction of COX2 in DAT and DS, which may lead to the production of free radicals and may be causally related to neuronal degeneration.
Journal ArticleDOI

Human brain S100β and S100β mRNA expression increases with age: Pathogenic implications for Alzheimer's disease

TL;DR: It is suggested that age-related increases in S100 beta expression are important in the pathogenesis of Alzheimer's disease and may explain in part the increased incidence of this disease with advancing age.
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