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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.
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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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DNA microarray analysis of the aging brain.

TL;DR: The use of DNA microarrays generates panels of hundreds of transcriptional biomarkers of molecular aging, providing a new tool to measure biological age on a tissue-specific basis and suggesting that genomic approaches may be useful in understanding the molecular basis of the aging process in experimental animals.
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DAP12 Stabilizes the C-terminal Fragment of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) and Protects against LPS-induced Pro-inflammatory Response.

TL;DR: It is shown that DAP12 stabilizes the C-terminal fragment of TREM2 (TREM2-CTF), a substrate for γ-secretase, which regulates inflammatory responses in microglia, thereby protecting against excessive pro-inflammatory responses.
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Trafficking CD11b-Positive Blood Cells Deliver Therapeutic Genes to the Brain of Amyloid-Depositing Transgenic Mice

TL;DR: Observations support the feasibility of testing autologous monocytes for application of therapeutic genes in human CNS disease and support the results from bone marrow grafts that circulating CD11b+ cells can enter the CNS without requiring the use of lethal irradiation.
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Combined volumetry and DTI in subcortical structures of mild cognitive impairment and Alzheimer's disease patients.

TL;DR: Combining different MRI modalities can allow identifying sensitive indicators of the subtle pathogenic mechanisms that occur in subcortical areas of AD patients, including hippocampus, amygdala, and in the right caudate.
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Microglia Lacking E Prostanoid Receptor Subtype 2 Have Enhanced Aβ Phagocytosis yet Lack Aβ-Activated Neurotoxicity

TL;DR: It is shown that ablation of E prostanoid receptor subtype 2 (EP2) significantly increased microglial-mediated clearance of Aβ peptides from AD brain sections and enhanced microglian Aβ phagocytosis in cell culture, and that lack of EP2 completely suppressed Aβ-activated microglia-mediated paracrine neurotoxicity.
References
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Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs

TL;DR: Experiments with guinea-pig lung suggest that some of the therapeutic effects of sodium salicylate and aspirin-like drugs are due to inhibition of the synthesis of prostaglandins.
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TGF-beta signal transduction.

TL;DR: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms and mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
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An endotoxin-induced serum factor that causes necrosis of tumors

TL;DR: It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.
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Chemokines — Chemotactic Cytokines That Mediate Inflammation

TL;DR: This review introduces the burgeoning family of cytokines, with special emphasis on their role in the pathophysiology of disease and their potential as targets for therapy.
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An Antidiabetic Thiazolidinedione Is a High Affinity Ligand for Peroxisome Proliferator-activated Receptor γ (PPARγ)

TL;DR: It is reported that thiazolidinediones are potent and selective activators of peroxisome proliferator-activated receptor γ (PPARγ), a member of the nuclear receptor superfamily recently shown to function in adipogenesis, and raised the intriguing possibility that PPARγ is a target for the therapeutic actions of this class of compounds.
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