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Biotech / Medical : Ligand (LGND) Breakout! -- Ignore unavailable to you. Want to Upgrade?

To: NeuroInvestment who wrote (29940)	1/7/2000 2:37:00 PM
From: Torben Noerup Nielsen	Respond to of 32384

Thanks, I appreciate the clarification. I thought that registration was now one-step. One thing I do remember is that there are some differences between what can be sold OTC and what requires a prescription. I also know of a pain killer that is OTC in France, but banned in the Scandinavian countries. Thanks again, Torben

To: NeuroInvestment who wrote (29940)	1/7/2000 3:12:00 PM
From: celeryroot.com	Respond to of 32384

Henry thanks very much for the clarification for those of you who dont know Dr. Tracy (neuroinvestment) writes and excellent newsletter ...you might want to visit his site www.neuroinvestment.com

To: NeuroInvestment who wrote (29940)	1/14/2000 9:01:00 AM
From: Henry Niman	Respond to of 32384

Any comments in J of Neuroscience artucle on using PPARgamma agonists for treating Alzheimer's Disease: J Neurosci 2000 Jan 15;20(2):558-67 Inflammatory mechanisms in Alzheimer's disease: inhibition of beta-amyloid-stimulated proinflammatory responses and neurotoxicity by PPARgamma agonists. Combs CK, Johnson DE, Karlo JC, Cannady SB, Landreth GE. Alzheimer Research Laboratory, Departments of Neurosciences and Neurology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA. [Medline record in process] Alzheimer's disease (AD) is characterized by the extracellular deposition of beta-amyloid fibrils within the brain and the subsequent association and phenotypic activation of microglial cells associated with the amyloid plaque. The activated microglia mount a complex local proinflammatory response with the secretion of a diverse range of inflammatory products. Nonsteroidal anti-inflammatory drugs (NSAIDs) are efficacious in reducing the incidence and risk of AD and significantly delaying disease progression. A recently appreciated target of NSAIDs is the ligand-activated nuclear receptor peroxisome proliferator-activated receptor gamma PPARgamma). PPARgamma is a DNA-binding transcription factor whose transcriptional regulatory actions are activated after agonist binding. We report that NSAIDs, drugs of the thiazolidinedione class, and the natural ligand prostaglandin J2 act as agonists for PPARgamma and inhibit the beta-amyloid-stimulated secretion of proinflammatory products by microglia and monocytes responsible for neurotoxicity and astrocyte activation. The activation of PPARgamma also arrested the differentiation of monocytes into activated macrophages. PPARgamma agonists were shown to inhibit the stimulated expression of the cytokine genes interleukin-6 and tumor necrosis factor alpha. Furthermore, PPARgamma agonists inhibited the expression of cyclooxygenase-2. These data provide direct evidence that PPARgamma plays a critical role in regulating the inflammatory responses of microglia and monocytes to beta-amyloid. We argue that the efficacy of NSAIDs in the treatment of AD may be a consequence of their actions on PPARgamma rather than on their canonical targets the cyclooxygenases. Importantly, the efficacy of these agents in inhibiting a broad range of inflammatory responses suggests PPARgamma agonists may provide a novel therapeutic approach to AD. PMID: 10632585, UI: 20098930