Axonyx Reports Data on Effects of Phenserine on the Brains of Alzheimer's Disease Patients; PET Scans Show Increased Brain Neur

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.