by Agent G

Created on: July 28, 2009

As many as 5.3 million people in the United States are living with Alzheimer disease (AD), and it is the sixth leading cause of death. The annual direct and indirect costs of AD amount to more than $148 billion. (Alzheimer's Association 2009) The Mayo Clinic Study of Aging has estimated that the prevalence of mild cognitive impairment (MCI) is between 13% and 16% of individuals age 70 to 89 years. The Alzheimer's Association estimates that if nothing is done to delay the onset or slow the progression of AD, this single entity will bankrupt the health care system as we know it. (Alzheimer's Association 2009, Doody 2009) Early recognition and interventions can reduce the societal costs of the disease; therefore, it is imperative that geriatric psychiatrists routinely screen patients who display MCI.

Currently there is no treatment available that prevents or stops the deterioration of brain cells in AD-available agents only slow disease progression. The US Food and Drug Administration has approved 5 drugs that slow worsening of symptoms for about 6 to 12 months, on average, for about half of the individuals who take them. These cholinesterase inhibitor therapies mask the symptoms, but do not effectively mitigate the underlying disease. Based on deepening insight into the underlying biology of AD and emerging conceptual frameworks for understanding the disease, researchers have identified treatment strategies such as anti-amyloid beta (Abeta) antibodies that may have the potential to change its course. (Sabbagh 2008, Kellner 2009, Zetterberg 2009) Researchers are currently broadening their goals and seeking to interveve at different paoint in the disease process. On the foreseeable horizon are agents currently in early phase trials that could help delay or slow the pathology, in particular agents that inhibit Abeta 42 protein and Tau formation.

Current AD theory states that subtypes of Abeta clump together into plaques that eventually kill brain cells. Agents in late-stage clinical development target Abeta and its developmental pathway directly in hopes of halting all disease progression and slowing or stopping brain death. Also under investigation in phase 3 clinical trials is a gamma-secretase inhibitor for the treatment of mild to moderate AD. (Wolfe 2008) Secretase inhibition is being tested to see if it can slow the progression associated with AD by inhibiting gamma secretase, an enzyme that can create Abeta. By blocking gamma secretase, there is less

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