February 13, 2001

Neurochem Reports Key Findings on Role of Inflammation in Alzheimer's Disease.

Genetic Predisposition Found for Level of Inflammatory Response in Brain Cells of Mice.

Neurochem Inc. (TSX : NRM) announced the results of a study which examined the genetic predisposition of inflammatory responses of brain cells to amyloid protein, a key element of Alzheimer's Disease (AD). Genetics play a role in the way mice respond to different inflammatory stimuli. The study demonstrates that genetics also play an important role in the way microglia, the brain macrophages, respond to the presence of amyloid (Ab). The results suggest that differences in levels of microglial inflammation, caused by amyloid, are genetically linked and could alter the sequence of events leading to the neurodegeneration in AD. These results were reported at the IBC Conference on Alzheimer's Disease held in Atlanta (Georgia, U.S.) on February 8 th, 2001.

"Alzheimer's Disease continues to challenge the medical community because the exact pathway leading to neurodegeneration in this disease is not well understood," said Louis R. Lamontagne, President and Chief Executive Officer of Neurochem. "This finding is important not only because it adds significant information about the AD mechanism, but it shows that early treatment for those patients who are genetically predisposed to suffer earlier from the inflammatory damages caused by amyloid can have a dramatic effect in halting the disease's progression. Neurochem's expertise in amyloid-based diseases keeps us at the forefront of research in AD. Treating AD before it causes severe and irreversible damage is the goal of our AD therapeutic, which completed a successful phase I clinical trial. Alzhemed™ could not only block amyloid fibrils from forming, but could also block the initial inflammation caused by the very presence of amyloid, which could truly stop the progression of AD."

About the study

Research has shown that the level of inflammatory response to pathogenic stimuli is genetically controlled. In the study presented last week at the IBC Conference, the objective was to determine whether the level of microglial response to Ab is also genetically controlled. In the presence of Ab, activated microglia, the brain phagocytes, induce an inflammatory response leading to the release of neurotoxic factors. Using genetically different strains of mice known to have low or high response to inflammation, researchers analyzed key markers following stimulation with Ab. A morphological analysis of the microglia as well as a measure of inflammatory mediators produced by these cells showed a significant difference in the activation of microglia in one strain compared to the other. This means that there is a genetic predisposition to the neurotoxic effect that amyloid has on microglia. This suggests that differences in the levels of the microglial inflammatory response to amyloid could alter the sequence of events leading to neurodegeneration in AD.

Neurochem's Technologies

Neurochem currently focuses on the development of therapeutic agents for several major diseases characterized by the presence of toxic deposits of amyloid protein. These amyloid deposits, namely amyloid fibrils, are abnormal aggregates of naturally occurring proteins. These fibrillary structures are associated with many diseases grouped under the generic name Amyloidosis. The amyloid deposits build up in specific tissues or organs, such as in Alzheimer's Disease where they form plaques in the brain. Alternatively, the tiny, needle-like amyloid fibril deposits can be widely distributed throughout the body, as in certain systemic diseases such as Secondary Amyloidosis. Amyloid deposit formation is the result of the interactive combination of several components including the sulphated glycosaminoglycans or GAGs, common to all deposits and an amyloid protein, which is specific to each disorder and normally exists in soluble form. When they interact, the protein changes shape and aggregates, thus forming a toxic amyloid deposit.

The Phase II/III clinical trial has been designed as a multicenter, multinational, randomized, double-blind, placebo-controlled, and parallel-design trial.

Neurochem's GAG Mimetics

Neurochem's innovative core technology consists of the design and synthesis of compounds that mimic GAGs properties. These GAGs promote amyloid fibril formation. Neurochem's synthetic compounds compete with the naturally occurring GAGs by binding to the amyloid protein thereby interfering with the formation and deposition of amyloid aggregates. This biochemical "deception" has been proven successful in studies showing the compounds disrupting the formation of beta amyloid, amylin (IAPP), amyloid AL and amyloid A, indicators of Alzheimer's Disease, Diabetes, and of Primary and Secondary Amyloidosis, respectively.

About Neurochem

Neurochem is a leader in the development of novel, proprietary compounds that inhibit the formation, deposition and toxic effects of amyloid fibrils within the body. Neurochem's research team has been working with international amyloid experts on the development of therapeutic cures to amyloid-related diseases, including Alzheimer's Disease, Secondary Amyloidosis, Diabetes Type II and Hemorrhagic Stroke due to Cerebral Amyloid Angiopathy. Neurochem has advanced three drug candidates to clinical trials for Alzheimer's Disease, Secondary Amyloidosis and Hemorrhagic Stroke.

At present, the Company employs over 66 people and is located in Saint-Laurent, Canada (www.neurochem.com).

All of the statements contained in this news release, other than statements of fact which are independently verifiable at the date hereof, are forward-looking statements. Such statements, based as they are on the current expectations of management, inherently involve numerous risks and uncertainties, known and unknown. Some examples of known risks are: the impact of general economic conditions, general conditions in the pharmaceutical industry, changes in the regulatory environment in the jurisdictions in which Neurochem does business, stock market volatility, fluctuations in costs, and changes to the competitive environment due to consolidation or otherwise. Consequently, actual future results may differ materially from the anticipated results expressed in the forward-looking statements.

For further Information, please contact:
Dr. Lise Hébert
Vice President, Corporate Communications
lhebert@neurochem.com

275 Armand-Frappier
Laval (Quebec)
H7V 4A7
Tel: (450) 680-4500
Fax: (450) 680-4501

Our site is best viewed with IE4+ at a resolution of 1024×768.
All contents copyright © 1998-2007 Neurochem Inc.
Terms, Conditions and Legal Notice.