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Experimental Drug Ketasyn(TM) (AC-1202) Treats Alzheimer's as Diabetes of the Brain

by Medindia Content Team on  June 27, 2007 at 5:18 PM Drug News   - G J E 4
Experimental Drug Ketasyn(TM) (AC-1202) Treats Alzheimer's as Diabetes of the Brain
Accera, Inc. announced today that recent data from its Phase IIb study in Alzheimer's disease (AD) support findings showing that AD may effectively be thought of and treated as diabetes of the brain.
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AD is widely believed to be caused by the accumulation of amyloid beta plaques in the brain, yet recent research from Brown University has shown that inducing insulin resistance in the brains of mice gives rise to some of the behavioral and pathological symptoms of AD. AD may therefore be thought of as brain-specific "type 3 diabetes," an idea that is further supported by brain images of AD patients showing decreased glucose metabolism.

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All cells in the body require glucose, which is controlled with the aid of the hormone insulin. In type 2 diabetes, which accounts for 90% of the 180 million diabetes cases worldwide according to the World Health Organization, certain cells become resistant to insulin and therefore cannot take in enough glucose. When brain cells become insulin-resistant, as happens in AD, inadequate glucose leads to damage that results in impaired memory and cognition and brain shrinkage.

Because these metabolic defects in the brain often appear 10 to 20 years earlier than other AD symptoms, targeting them may allow for earlier treatment of the disease. Based on this hypothesis, Accera is developing the AD drug, Ketasyn(TM) (AC-1202), which provides glucose-deprived brain cells with an alternative energy source. Ketasyn is converted by the liver into ketone bodies, which brain cells can use for energy even when their ability to metabolize glucose is impaired.

Dr. Samuel Henderson, Executive Director of Research at Accera, said, "While many drugs currently under development for AD target production and clearance of amyloid beta plaques, our approach is to address a much earlier event. Declines in glucose use are visible decades before there is extensive amyloid deposition and decades before clinical signs of dementia are evident. We hope that our early intervention in this process will have a significant impact on the disease."

Accera recently completed Phase IIb clinical trial that confirmed Ketasyn's safety and efficacy as measured by improvement in ADAS-Cog scores, the FDA's gold standard measure for efficacy in cognition and short-term memory. As in earlier studies, Ketasyn was particularly effective in a subgroup lacking the APOE4 genotype, which represents half of the Alzheimer's population.

APOE4 is a known major risk factor for late onset AD, which is the most common form of the disease. Interestingly, other treatments aimed at tackling the "type 3 diabetes" hypothesis have yielded similar results: AD patients lacking the APOE4 genotype have responded positively to an insulin-sensitizing drug, and to direct exposure to insulin, while patients expressing the APOE4 genotype showed little or no response.

"The different responses in people of varying APOE4 status with Ketasyn and other treatments indicates that APOE4 is altering something fundamental about brain metabolism," said Dr. Henderson. "These findings are consistent with studies demonstrating differential insulin sensitivity based on APOE4 status. Our study has provided us with valuable insights for our future research."

Accera plans to initiate a pivotal, Phase III multi-center clinical trial in early 2008 in mild-to-moderate Alzheimer's patients who do not have the APOE4 genotype. This study will focus on several measures of efficacy, including ADAS-Cog, safety and the role of insulin regulation in Alzheimer's disease.

Source: PR Newswire
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How come you can't go into the brain, and have a nerons inplanted in the stem cell,and have it though out the formula that will KILL the amyloid beta plaques..Thanks
guest Saturday, August 11, 2007

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