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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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Journal ArticleDOI

Ultrastructural localization of complement membrane attack complex (MAC)-like immunoreactivity in brains of patients with Alzheimer's disease

TL;DR: Immunopositivity was detected in association with lamellated bodies in the neuronal cytoplasm, lipofuscin granules, lysosomes and neurofibrillary tangles, providing further evidence that complement-mediated injury of neurons plays a part in the pathophysiology of AD.
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Aggregation State-Dependent Activation of the Classical Complement Pathway by the Amyloid β Peptide

TL;DR: It is shown that the fibrillar aggregation state of Aβ is precisely correlated with the ability of the peptide to induce the formation of activated fragments of the complement proteins C4 and C3, suggesting that the classical complement pathway provides a mechanism whereby complement‐dependent processes may contribute to neuronal injury in the proximity of fibrilla but not diffuse Aβ deposits in the AD brain.
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Macrophage/microglial-mediated primary demyelination and motor disease induced by the central nervous system production of interleukin-3 in transgenic mice.

TL;DR: Chronic CNS production of low levels of IL-3 promotes the recruitment, proliferation and activation of macrophage/microglial cells in white matter regions with consequent primary demyelination and motor disease.
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Activation of peroxisome proliferator-activated receptor isoforms and inhibition of prostaglandin H(2) synthases by ibuprofen, naproxen, and indomethacin.

TL;DR: The results demonstrate that the mechanisms of action of NSAIDs on these cell systems are different, and propose that the pharmacological effects ofNSAIDs may be related to both their profile of inhibition of PGHS enzymes and the activation of PPARalpha and/or PPARgamma isoforms.
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Oxidative damage in Alzheimer’s disease: the metabolic dimension

TL;DR: In this review, a summary of recent work demonstrating some key abnormalities that may initiate and promote neuronal oxidatave damage are provided.
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