Beta amyloid could attack red blood cell
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Work in the late 1990s showed fragments of beta amyloid could actually attack red blood cell membranes and cause them to destruct, says Dr. Hill, neuroscientist at the Medical College of Georgia and Veterans Affairs Medical Center in Augusta. "And, there is some evidence that red blood cells of Alzheimer's patients have been damaged so we think red blood cells are more fragile in some Alzheimer's patients allowing them to be more likely to break open.
Although the XmnI polymorphism's (which can significantly increase fetal hemoglobin expression in adults) protection mechanism is not clear, the researchers found in certain circumstances, adult hemoglobin bound better to beta amyloid, so if there are higher levels of fetal hemoglobin, there may not be as much interaction and subsequent injury, Dr. Hill says.
To determine the impact of the genetic mutation on Alzheimer's risk, studies need to be done on more Alzheimer's patients and their families, including taking blood levels of fetal hemoglobin, says Dr. Rodney T. Perry, UAB molecular geneticist and a study corresponding author. "More studies are needed to confirm the physiologic basis of the interaction," says Dr. Perry who already is working with Dr. Hill to submit a grant to pursue more answers. If they document higher fetal hemoglobin levels in healthy family members with the XmnI polymorphism, the hypothesis that it is providing some sort of protective measure is more likely, says Dr. Perry. Also the amount of disease protection has yet to be determined, he notes. "It may be a small protection."
Either way, the role needs pursuing, Dr. Perry says. "It helps in trying to fill in the pieces of the puzzle of what is going on in the pathogenesis and different etiologies of the disease, how it may come about." If they are right, the findings could open the doors to treatment approaches that increase fetal hemoglobin levels, Dr. Hill says. One such drug, hydroxyurea, already is used to treat sickle cells patients because fetal hemoglobin will not sickle.
Alzheimer's Donation
Donate Online Now
.
Work in the late 1990s showed fragments of beta amyloid could actually attack red blood cell membranes and cause them to destruct, says Dr. Hill, neuroscientist at the Medical College of Georgia and Veterans Affairs Medical Center in Augusta. "And, there is some evidence that red blood cells of Alzheimer's patients have been damaged so we think red blood cells are more fragile in some Alzheimer's patients allowing them to be more likely to break open.
Although the XmnI polymorphism's (which can significantly increase fetal hemoglobin expression in adults) protection mechanism is not clear, the researchers found in certain circumstances, adult hemoglobin bound better to beta amyloid, so if there are higher levels of fetal hemoglobin, there may not be as much interaction and subsequent injury, Dr. Hill says.
To determine the impact of the genetic mutation on Alzheimer's risk, studies need to be done on more Alzheimer's patients and their families, including taking blood levels of fetal hemoglobin, says Dr. Rodney T. Perry, UAB molecular geneticist and a study corresponding author. "More studies are needed to confirm the physiologic basis of the interaction," says Dr. Perry who already is working with Dr. Hill to submit a grant to pursue more answers. If they document higher fetal hemoglobin levels in healthy family members with the XmnI polymorphism, the hypothesis that it is providing some sort of protective measure is more likely, says Dr. Perry. Also the amount of disease protection has yet to be determined, he notes. "It may be a small protection."
Either way, the role needs pursuing, Dr. Perry says. "It helps in trying to fill in the pieces of the puzzle of what is going on in the pathogenesis and different etiologies of the disease, how it may come about." If they are right, the findings could open the doors to treatment approaches that increase fetal hemoglobin levels, Dr. Hill says. One such drug, hydroxyurea, already is used to treat sickle cells patients because fetal hemoglobin will not sickle.
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