Rock Creek Pharmaceuticals Inc. (fka RCPIQ)

[Buddhahead]

Antisense compound may provide new Alzheimer's treatment in Fierce Biotech Research, May 27, 2014 | By Emily Mullin

Excerpt:
"A new antisense compound developed by Saint Louis University scientists restored learning, memory and other behaviors in mice genetically engineered to have Alzheimer's disease.

The compound, antisense oligonucleotide (OL-1), also reduced inflammation in the part of the brain responsible for learning and memory. The finding, which appears in the May issue of the Journal of Alzheimer's Disease, is the second mouse study published by the team that supports the potential therapeutic value of an antisense compound in treating Alzheimer's disease in humans.

Many antisense therapies are approved to treat certain genetic disorders and infections, such as familial hypercholesterolemia, cancer and HIV/AIDS. Antisense is a strand of molecules that bind to messenger RNA, triggering a sequence of cellular events that turn off a certain gene"

Article at:
http://www.fiercebiotechresearch.com/story/antisense-compound-may-provide-new-alzheimers-treatment/2014-05-27

My comments:
Isn't that what Anatabine Citrate does?

Excerpt from PubMed:
"Anatabine lowers Alzheimer's Aß production in vitro and in vivo.
Paris D1, Beaulieu-Abdelahad D, Bachmeier C, Reed J, Ait-Ghezala G, Bishop A, Chao J, Mathura V, Crawford F, Mullan M.
Author information
1Roskamp Institute, 2040 Whit?eld Avenue, Sarasota, FL 34243, USA. [e-mail]
Abstract
Brain Aß accumulation represents a key pathological hallmark in Alzheimer's disease. In this study, we investigated the impact of anatabine, a minor alkaloid present in plants of the Solanacea family on Aß production in vitro using a cell line overexpressing the human amyloid precursor protein (APP) and in vivo using a transgenic mouse model of Alzheimer's disease. In vitro, anatabine lowers Aß1?40 and Aß1?42 levels in a dose dependent manner and reduces sAPPß production without impacting sAPPa levels suggesting that anatabine lowers Aß production by mainly impacting the ß-cleavage of APP. Additionally, we show that anatabine lowers NF?B activation at doses that inhibit Aß production in vitro. Since NF?B is known to regulate BACE-1 expression (the rate limiting enzyme responsible for Aß production), we determined the impact of anatabine on BACE-1 transcription. We show that anatabine inhibits BACE-1 transcription and reduces BACE-1 protein levels in human neuronal like SHSY-5Y cells suggesting that the Aß lowering properties of anatabine are mediated via a regulation of BACE-1 expression. In vivo, we show that an acute treatment with anatabine for four days significantly lowers brain soluble Aß1?40 and Aß1?42 levels in a transgenic mouse model of Alzheimer's disease. Altogether our data suggest that anatabine may represent an interesting compound for regulating brain Aß accumulation."

Article at:
http://www.ncbi.nlm.nih.gov/pubmed/21958873