Diabetes Drug Shows Promise in Reducing Alzheimer’s disease

BUSM researchers have found that the diabetic drug, pramlintide, reduces amyloid-beta peptides, a major component of Alzheimer’s disease (AD) in the brain and improves learning and memory in two experimental AD models. These findings, which appear online in Molecular Psychiatry, also found AD patients have a lower level of amylin in blood compared to those without this disease. These results may provide a new avenue for both treatment and diagnosis of AD.

Using AD models, the BUSM researchers investigated the effects of amylin on the pathogenesis of the disease. “Surprisingly, injections of amylin or pramlintide into the AD models reduced the amyloid burden as well as lowered the concentrations of amyloid-beta peptides (Aβ), a major component of AD in the brain,” said senior author Wendy Qiu, MD, PhD, associate professor of psychiatry and pharmacology at BUSM. Pramlintide is an analog of a natural occurring peptide, amylin, produced by the pancreas. “It can easily cross the blood/brain barrier and has shown favorable safety profile for diabetes patients,” she added.

According to the researchers, including lead author Haihao Zhu, MD, PhD, from the department of pharmacology & experimental therapeutics at BUSM, these results argue for a therapeutic application of amylin-class peptides for AD.

“There is broad agreement that more therapeutic avenues need to be explored in addition to targeting Aβ for the treatment of AD,” said Qiu. “Amylin-class drugs not only remove Aβ from the brain, as demonstrated by our study, but also can improve glucose metabolism and cerebrovasculature in the AD brain. Based on their findings the researchers propose that amylin-class peptides have potential to become a new avenue as a challenge test for diagnosis of AD and as well as a therapeutic for the disease. If the clinical trial proves the effect of pramlintide for Alzheimer’s disease, Qiu believes this drug can be applied to Alzheimer’s patients in only three to five years.

This work was supported by grants from the National Institute on Aging, AG-022476, an Ignition Award and a BU ADC pilot grant. Support was also provided through P30 AG13864.

Qiu and her team recently received an investigator –initiated grant from the Alzheimer’s Disease Association to further pursue this study.