Axonyx Reports Data on Effects of Phenserine on the Brains of Alzheimer's Disease Patients; PET Scans Show Increased Brain Neuron Activity and Reduced Amyloid Load.

NEW YORK -- Axonyx Inc. (NASDAQ: AXYX) today reported on data showing an increase in brain glucose metabolism and reduction of brain amyloid levels in the memory and cognition areas in brains of mild-to-moderate Alzheimer's disease (AD) patients treated with Phenserine 15mg twice daily (BID) for 13-weeks. The data will be included in an oral presentation by Prof. Dr. Agneta Nordberg, MD, PhD of the Karolinska Institute, Stockholm, Sweden, on Friday, April 21st, 2006 at the 9th International Geneva/Springfield Symposium on Advances in Alzheimer Therapy.

A double-blind, placebo-controlled pilot study, using Positron Emission Tomography (PET), examined the effects of Phenserine treatment on the brains of 20 AD patients (Phenserine 15mg BID, 10 patients; and placebo, 10 patients). PET is an imaging technique that provides information about physiological and biochemical processes. Two different aspects brain changes were assessed; 1) Changes in brain glucose metabolism using 18F-fluorodeoxyglucose (FDG), and 2) Changes in the level of brain amyloid load using (11C)-PIB (Pittsburgh Compound B).

There was a statistically significant increase in glucose metabolism as compared to baseline in the frontal and parietal cortical areas in the brains of Phenserine patients, while the placebo group did not show any significant changes from baseline. These observed changes were highly correlated with the statistically significant improvement in the Digit Symbol test of attention, an ability that resides in the frontal cortex. The accumulation of FDG is a direct measure of the metabolic activity of neurons and is known to change in parallel with neuronal function. Patients with AD have characteristic reductions in FDG measurements of regional brain activity, which are progressive and correlate to dementia severity.

Baseline PIB PET scans showed a statistically significant increase in retention in the most AD relevant brain regions compared to age matched healthy historical controls, thus confirming that the included patients were suffering from AD. PET studies with the amyloid-imaging ligand (11C)-PIB have shown a difference in PIB retention in brains of AD patients compared to healthy controls. A trend to a decreased amyloid load was observed in Phenserine treated patients as compared to baseline whereas the placebo group did not change. In addition, an inverse correlation was found between glucose metabolism and amyloid load, confirming historical published data. The deposition of beta-amyloid is one of the key pathological features of AD. Tracking the beta-amyloid load in the brains of AD patients with PET is a promising strategy for imaging the specific disease process.

"This is the first time that a treatment for AD is being studied using the amyloid imaging compound where an effect has been measured," said Prof. Dr. Agneta Nordberg, MD, PhD of the Karolinska Institute, "The results to date are promising and we look forward to the further analyses of the scans and spinal fluid and at the end of 6 months of treatment."

While these data are the result of an interim analysis conducted after 13 weeks of double blind treatment, the Company believes that these data provide encouraging signals associated with metabolic and potential amyloid reducing effects of Phenserine. The study is continuing and the patients will be evaluated again following a total of 6 months of treatment. Additional analyses of the above PET scan data are currently being undertaken, and an examination of the spinal fluid of these patients is planned.

About Phenserine

Phenserine is a highly selective inhibitor of acetylcholinesterase (AchE-I), an enzyme that breaks down the neurotransmitter acetylcholine, a neurotransmitter important to memory and cognitive function. Unlike other AchE-I's, which only suppress the activity of the enzyme, Phenserine has been shown to have two mechanisms of action: (1) the inhibition of the AChE enzyme, and (2) inhibition of the synthesis of A beta - a protein thought to be a potential cause of Alzheimer's disease and its progression.

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. 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) - 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 filing, will be approved by the FDA 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.