Alzheimer disease: Transition Therapeutics begins Phase II testing of its drug

By Margarita Snegireva. Transition Therapeutics Inc. will get a $5 million milestone payment for Phase II testing of its Alzheimer's drug, ELND005 from Ireland's Elan Corp.

The clinical study of about 340 patients in North America will last about 18 months, Elan said in a statement.

In connection with the initiation of the Phase II clinical study, Transition will also issue former shareholders of Ellipsis Neurotherapeutics Inc 174,123 common shares at a price of $10.86 per share, the company said.

Alzheimer's disease ( AD ), also called Alzheimer disease , and simply known as Alzheimer's, is a neurodegenerative disease that, in its most common form, is found in people over the age of 65. Approximately 24 million people worldwide have dementia of which the majority (~60%) is due to Alzheimer's. 

Clinical signs of Alzheimer's disease are characterized by progressive cognitive deterioration, together with declining activities of daily living and by neuropsychiatric symptoms or behavioral changes. It is the most common type of dementia. Plaques which contain misfolded peptides called amyloid beta (Aβ) are formed in the brain many years before the clinical signs of Alzheimer's are observed. Together, these plaques and neurofibrillary tangles form the pathological hallmarks of the disease. These features can only be discovered at autopsy and help to confirm the clinical diagnosis. Medications can help reduce the symptoms of the disease, but they cannot change the course of the underlying pathology.

The ultimate cause of Alzheimer's is unknown. Genetic factors are clearly indicated as dominant mutations in three different genes that account for the small number of cases of familial, early-onset AD have been identified. For the more common form of late onset AD, ApoE is the only clearly established susceptibility gene. All four genes can contain mutations or variants that confer increased risk for AD, but account for only 30% of the genetic picture of AD. These four genes have in common the fact that mutations in each lead to the excessive accumulation in the brain of Aβ, the main component of the senile plaques that litter the brains of AD patients.

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