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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.
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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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Electrochemical Analysis of Protein Nitrotyrosine and Dityrosine in the Alzheimer Brain Indicates Region-Specific Accumulation

TL;DR: The results suggest that AD pathogenesis may involve the activation of oxidant-producing inflammatory enzyme systems, including nitric oxide synthase, as well as peroxynitrite scavenger systems.
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Elevated circulating tumor necrosis factor levels in Alzheimer's disease.

TL;DR: Elevated circulating TNF may be derived from the local CNS inflammatory reaction in AD, and may account for some systemic manifestations of AD such as weight loss.
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Nitric oxide neurotoxicity.

TL;DR: It is likely that most of the neurotoxic actions of NO are mediated by peroxynitrite (ONOO-), the reaction product from NO and superoxide anion.
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Transforming growth factor-beta 1 in the rat brain: increase after injury and inhibition of astrocyte proliferation.

TL;DR: The present results indicate that TGF- beta 1 expressed in the lesioned brain plays a role in nerve regeneration by stimulating NGF production and by controlling the extent of astrocyte proliferation and scar formation.
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CNTF protection of oligodendrocytes against natural and tumor necrosis factor-induced death

TL;DR: Ciliary neurotrophic factor (CNTF), a trophic factor found in astrocytes in the central nervous system (CNS), promoted the survival and maturation of cultured oligodendroCytes and protected oligodends from death induced by tumor necrosis factors (apoptosis) but not against complement (necrosis).
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