- Staff St. Louis Business Journal
Researchers at Washington University's medical school have measured a significant difference between the brains of patients with an inherited form of Alzheimer's disease and healthy family members who don't carry a mutation for Alzheimer's.
A new study found that research subjects with genetic mutations that cause early-onset Alzheimer’s make about 20 percent more of a specific form of amyloid beta, a protein fragment known as amyloid beta 42, than family members without the Alzheimer’s mutation, Washington University officials report.
Amyloid beta builds up into plaques in the brain that researchers believe cause memory loss and other cognitive problems found in Alzheimer's patients. Different forms of amyloid beta are formed by normal brain metabolism.
The Washington U scientists also found signs that amyloid beta 42 drops out of the cerebrospinal fluid much quicker than other forms of amyloid beta, possibly because amyloid beta 42 is being deposited on brain amyloid plaques.
“These results indicate how much we should target amyloid beta 42 with Alzheimer’s drugs,” Dr. Randall Bateman, professor of neurology, said in a statement. “We are hopeful that this and other research will lead to preventive therapies to delay or even possibly prevent Alzheimer’s disease.”
Bateman, metabolism expert Bruce Patterson and biomedical engineer Donald Elbert have applied for a patent on the diagnostic use of their new model of amyloid beta metabolism, university officials said.
The new study was published June 12 in Science Translational Medicine. Read more about the study here.
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