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Researcher Reports Data on Effects of Posiphen(TM) on Human Neuronal Stem Cells; Posiphen May Support Stem Cell Transplantation in Alzheimer's Disease.


NEW YORK -- Axonyx Inc. (NASDAQ NASDAQ
 in full National Association of Securities Dealers Automated Quotations

U.S. market for over-the-counter securities. Established in 1971 by the National Association of Securities Dealers (NASD), NASDAQ is an automated quotation system that reports on
: AXYX) today announced the results of an independent study showing that Posiphen increased the ability of transplanted human neuronal stem cells (HNSC HNSC House National Security Committee ) to differentiate into neurons in APP transgenic mice, a model of Alzheimer's disease (AD) in humans. The research was reported by Kiminobu Sugaya, Ph.D., Professor of Molecular Biology, Biomolecular Sciences Center, University of Central Florida “UCF” redirects here. For other uses, see UCF (disambiguation).
UCF is a member institution of the State University System of Florida. UCF was founded in 1963 as Florida Technological University with the goal of providing highly trained personnel to support the Kennedy
, Orlando, Florida at the 9th International Geneva/Springfield Symposium on Advances in Alzheimer's Disease held April 19 - 22, 2006 in Geneva Geneva, canton and city, Switzerland
Geneva (jənē`və), Fr. Genève, canton (1990 pop. 373,019), 109 sq mi (282 sq km), SW Switzerland, surrounding the southwest tip of the Lake of Geneva.
, Switzerland.

Dr. Sugaya's research showed that when APP transgenic mice had been pre-treated with Posiphen, transplanted HNSC start to differentiate into neurons in the brain area where they are needed. When HNSC were transplanted into the brains of APP transgenic mice in the absence of Posiphen, HNSC did not differentiate into neurons. Dr. Sugaya attributed this effect to Posiphen's ability to decrease the synthesis of amyloid precursor protein Amyloid precursor protein (APP) is an integral membrane protein expressed in many tissues and concentrated in the synapses of neurons. Its primary function is not known, though it has been implicated as a regulator of synapse formation[2] and neural plasticity.  (APP). Posiphen may support and augment production of the new neurons through the suppression of APP production in the brain. The differentiation of stem cells into functioning neurons is critical to the success of stem cell therapy stem cell therapy Cell therapy Molecular medicine A technology in which a person's own cells–eg, neuronal stem cells are triggered to revert to their primitive embryonic form, then redifferentiate into mature cells of various organs  of AD.

"Although a better understanding of the mechanisms of APP function HNSC biology may be needed", stated Dr. Kiminobu Sugaya, "regulation of APP levels by a combination of Posiphen and stem cell treatments Medical researchers believe that stem cell treatments have the potential to change the face of human disease and alleviate suffering. A number of stem cell treatments already exist, although most are still experimental and/or costly, with the notable exception of bone marrow  could be a promising strategy to treat AD."

About Posiphen(TM)

Posiphen is in Phase I clinical development by Axonyx for the potential treatment of AD progression and is the positive isomer isomer (ī`səmər), in chemistry, one of two or more compounds having the same molecular formula but different structures (arrangements of atoms in the molecule). Isomerism is the occurrence of such compounds.  of Phenserine. Posiphen treatment, similar to Phenserine, has been shown to lower secreted and cellular APP and secreted Amyloid beta (A beta) levels in neuronal cells in culture as well as in vivo studies in mice, where brain levels of both APP and A beta were significantly and dose-dependently lowered by Posiphen over a wide range of doses that were well tolerated.

About Alzheimer's Disease

Alzheimer's disease is typified by a progressive impairment in memory, cognition and emotional disturbances that result from the dysfunction and death of neurons in the brain. This pathology is considered, in part, to be the result of the over production and accumulation of beta amyloid amyloid /am·y·loid/ (am´i-loid)
1. starchlike; amylaceous.

2. the pathologic, extracellular, waxy, amorphous substance deposited in amyloidosis, being composed of fibrils in bundles or in a meshwork of polypeptide
 (A beta) in and between neurons. Beta amyloid, a result of the cleavage of APP, subsequently aggregates to form plaques that are a microscopic hallmark of AD and have been postulated to have a causative role in AD.

About Axonyx

Axonyx Inc. is a U.S.-based biopharmaceutical company engaged in the acquisition and development of proprietary pharmaceutical compounds for the treatment of Central Nervous System disorders Nervous system disorders

A satisfactory classification of diseases of the nervous system should include not only the type of reaction (congenital malformation, infection, trauma, neoplasm, vascular diseases, and degenerative, metabolic, toxic, or deficiency
. The Company currently has three compounds in development for Alzheimer's disease; Phenserine - a potential symptomatic and disease progression treatment of mild to moderate Alzheimer's disease (AD); Posiphen(TM) - a potential disease progression treatment for AD now in Phase I; and BisNorCymcerine (BNC (hardware) BNC - A connector for coaxial cable such as that used for some video connections and RG58 "cheapernet" connections. A BNC connector has a bayonet-type shell with two small knobs on the female connector which lock into spiral slots in the male connector when it is twisted ) - a potential symptomatic treatment of severe AD in the pre-Investigational New Drug (IND) stage.

This press release may contain forward-looking statements or predictions. These statements represent our judgment to date, and are subject to risks and uncertainties that could materially affect the Company, including those risks and uncertainties described in the documents Axonyx files from time to time with the SEC, specifically Axonyx's annual report on Form 10-K. Specifically, with respect to our drug candidates Phenserine, Posiphen(TM) and BisNorCymserine, Axonyx cannot assure that: any preclinical studies or clinical trials, whether ongoing or conducted in the future, will prove successful, and if successful, that the results can be replicated; safety and efficacy profiles of any of its drug candidates will be established, or if established, will remain the same, be better or worse in future clinical trials, if any; pre-clinical results related to cognition and the regulation of beta-APP and/or amyloid beta will be substantiated by ongoing or future clinical trials, if any, or that any of its drug candidates will be able to improve the signs or symptoms of their respective clinical indication or slow the progression of Alzheimer's disease; any of its drug candidates will support an NDA (Non Disclosure Agreement) An agreement signed between two parties that have to disclose confidential information to each other in order to do business. In general, the NDA states why the information is being divulged and stipulates that it cannot be used for any  filing, will be approved by the FDA FDA
abbr.
Food and Drug Administration


FDA,
n.pr See Food and Drug Administration.

FDA,
n.pr the abbreviation for the Food and Drug Administration.
 or its equivalent, or if approved, will prove competitive in the market; Axonyx will be able to successfully out-license any of its drug candidates; Axonyx will be able to successfully in-license any additional compounds; or that Axonyx will have or obtain the necessary financing to support its drug development programs. Axonyx cannot assure that it will be successful with regard to identifying a (sub-) licensing partner for any of its compounds. Axonyx undertakes no obligation to publicly release the result of any revisions to such forward-looking statements that may be made to reflect events or circumstances after the date hereof or to reflect the occurrence of unanticipated events.
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Date:Apr 24, 2006
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