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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.

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.

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
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