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Biotech / Medical : Gliatech (GLIA) -- Ignore unavailable to you. Want to Upgrade?

To: Dr. John M. de Castro who wrote (1422)	3/1/2000 11:46:00 PM
From: Mike McFarland	Read Replies (1) \| Respond to of 2001

misc Alzheimers I know that folks mostly own Gliatech for the Adcon line and H3 program, but thought I'd post these misc fibril info I came across tonight. Might be a repeat, start here: Message 12862711 J Neurochem 2000 Mar;74(3):1017-25 Amyloid beta and amylin fibrils induce increases in proinflammatory cytokine and chemokine production by THP-1 cells and murine microglia. Yates SL, Burgess LH, Kocsis-Angle J, Antal JM, Dority MD, Embury PB, Piotrkowski AM, Brunden KR Gliatech Inc., Cleveland, Ohio 44122, USA. yatess@gliatech.com [Medline record in process] Activated microglia surrounding amyloid beta-containing senile plaques synthesize interleukin-1, an inflammatory cytokine that has been postulated to contribute to Alzheimer's disease pathology. Studies have demonstrated that amyloid beta treatment causes increased cytokine release in microglia and related cell cultures. The present work evaluates the specificity of this cellular response by comparing the effects of amyloid beta to that of amylin, another amyloidotic peptide. Both lipopolysaccharide-treated THP-1 monocytes and mouse microglia showed significant increases in mature interleukin-1beta release 48 h following amyloid beta or human amylin treatment, whereas nonfibrillar rat amylin had no effect on interleukin-1beta production by THP-1 cells. Lipopolysaccharide-stimulated THP-1 cells treated with amyloid beta or amylin also showed increased release of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-6, as well as the chemokines interleukin-8 and macrophage inflammatory protein-1alpha and -1beta. THP-1 cells incubated with fibrillar amyloid beta or amylin in the absence of lipopolysaccharide also showed significant increases of both interleukin-1beta and tumor necrosis factor-alpha mRNA. Furthermore, treatment of THP-1 cells with amyloid fibrils resulted in an elevated expression of the immediate-early genes c-fos and junB. These studies provide further evidence that fibrillar amyloid peptides can induce signal transduction pathways that initiate an inflammatory response that is likely to contribute to Alzheimer's disease pathology. PMID: 10693932, UI: 20155599 __________________________________ Scientists Uncover Action of a Risk Factor for Alzheimer?s Disease medicine.wustl.edu . "We believe it may be possible to alter the levels of brain apoE with drug therapy," says Paul, who is group vice president of discovery research and clinical investigation at Eli Lilly and Company. "Such drugs should inhibit the deposition of amyloid-beta, prevent fibril formation and promote amyloid removal ? which would have the potential to slow down or even prevent Alzheimer?s disease." Links for newbies: Gliatech R&D gliatech.com The Recap query recap.com

To: Dr. John M. de Castro who wrote (1422)	3/1/2000 11:48:00 PM
From: jeffbas	Read Replies (3) \| Respond to of 2001

John, I am appalled that clinical trials would involve gratuitously cutting people open twice and potentially killing them to take a look. Could that be true? As far as your comment earlier today about getting financing while the iron is hot, GLIA is not in the same boat as other biotech companies whose stocks have gone up 10 times. Its stock is roughly the same price as before the FDA problem. I am not sure that lack of progress means the stock is relatively cheap now or relatively expensive before?