Diabetes drug could treat Alzheimer’s disease

Ross Vincent
The Gateway (University of Alberta)
EDMONTON (CUP) – Researchers at the University of Alberta have discovered that a drug originally developed to treat diabetes shows great promise in the treatment and prevention of Alzheimer’s disease.
Jack Jhamandas, a researcher in the faculty of medicine and dentistry’s neurology division, discovered that AC253 – a drug developed to treat diabetes but that never made it to market – can block the toxic effects of amyloid, a protein found in large quantities in the brains of Alzheimer’s patients.
Amyloid kills brain cells by activating specific target receptors on the cells, which Jhamandas compares to a key fitting in a keyhole. The drug blocks these receptors from being activated, thereby preventing cell death.
“[This discovery] identifies an avenue for treating Alzheimer’s in a definitive manner, rather than just providing symptomatic relief,” Jhamandas said.
Alzheimer’s afflicts approximately 400,000 Canadians and will likely increase with an aging population. There is currently only symptomatic treatment, meaning doctors treat the symptoms, not the cause.
The drug AC253 was designed to prevent the effects of a protein similar to amyloid found in the pancreas of diabetic patients, but it proved ineffective during human testing. The similarity between the proteins involved in both diseases inspired Jhamandas and his team to apply the drug to Alzheimer’s treatment.
The next step is to test the drug on lab mice that are genetically engineered to develop Alzheimer’s. If tests are successful, Jhamandas is confident they will have a strong case to begin human clinical trials.
Jhamandas’ team also found a second way to prevent neuronal death. Using a relatively new technique, they managed to block or “silence” the genes that produce the cell receptors that amyloid acts upon, diminishing the protein’s harmful effects.
The team also discovered that large amyloid deposits are only found in parts of the brain responsible for cognition and memory, the same parts affected by Alzheimer’s. They also found that the frequency of amyloid receptors increases in parallel to the quantity of amyloid. This link suggests a direct correlation between the concentration of the protein and increased susceptibility to its toxic effects.
“We don’t really know why that is the case, but it’s a potentially important observation because it tells us that we might be able to interfere with the disease process itself with this drug as opposed to treating symptoms,” Jhamandas said.