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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

Induced expression of neuronal membrane attack complex and cell death by Alzheimer's β-amyloid peptide

TL;DR: It is suggested that A beta activates neuronal complement cascade to induce MAC, and a deficiency of endogenous complement regulatory proteins, e.g., CD59, may increase the vulnerability of neurons to complement-mediated cytotoxicity.
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Complement interactions with amyloid β1–42: A nidus for inflammation in AD brains

TL;DR: Solubilization of bound complement proteins and immunoblotting reveal that aggregated Aβ1–42 binds larger amounts of complement proteins C1q, C4, C3, C5 and C6, than Aggregated A β1–40, Aβ 1–28 and Aβ 17–43, and the binding of C3 requires complement activation, unlike CIq and C4.
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β-amyloid induction of gelatinase B secretion in cultured microglia: inhibition by dexamethasone and indomethacin

TL;DR: Aβ(l-38) and Aβ(1–40) were effective in stimulating MMP-9 activity in a dose-dependent fashion, and co-treatment with INDO or DEX resulted in a 54% and 66% inhibition, respectively, of Ap( 1–40)-stimulated M MP-9 production in microglia.
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Inducible nitric oxide synthase (iNOS)-like immunoreactivity in argyrophilic, tau-positive astrocytes in progressive supranuclear palsy.

TL;DR: It is indicated that TAF-bearing astrocytes may be a major source of excessive NO in PSP brains, and that after the induction of iNOS by unknown stimulating factors, T AF- bearing astroCytes produce an excessive amount of NO that exceeds the detoxification capability of SOD.
Journal Article

Evolution of blood coagulation and fibrinolysis.

TL;DR: The data suggest that the blood coagulation and complement cascades are descendants of an ancestral defence system that served the dual role of immobilization and destruction of invading bacteria and the prevention of loss of body fluids.
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