Experimental drug shows promise to treat Alzheimer

An experimental drug has been found to protect Alzheimer's-inflicted mice from memory deterioration, despite a high-glycemic-index (GI) diet meant to boost blood sugar levels.

The experimental drug from the US-based Eli Lilly and Company mimics the hunger-signalling hormone ghrelin.

"The present results suggest that ghrelin might improve cognition in Alzheimer's disease via a central nervous system mechanism involving insulin signalling," authors of the study published in the journal Scientific Reports wrote.

"With chronic diseases like diabetes and Alzheimer's, you need to do a long-term study," said examiner Inga Kadish, assistant professor at University of Alabama School of Medicine at Birmingham.

"So we did an experiment with the worst-case scenario, a high-GI diet. Alzheimer's disease has 10 or 20 risk factors and some of the strongest risk factors are diabetes or metabolic syndrome."

In contrast to short-term administration of the "ghrelin agonista drug -- which impairs insulin sensitivity and glucose tolerance, which are signs of metabolic syndrome and diabetes -- the researchers found that the long-term ghrelin agonist treatment did not impair insulin signalling and glucose tolerance in Alzheimer's disease mice fed with a high GI diet.

In the study, the Alzheimer's disease-model mice showed a deterioration in spatial learning as they turned older -- in other words, they got lost when trying to swim to a platform hidden just beneath the water surface that they previously were trained to find in a four-foot-wide pool.

The test mice fed with the ghrelin agonist and the high-GI diet showed long-term cognitive enhancement in this water maze test as compared to the mice fed with a normal diet or high-GI diet only.

The test mice also showed more activity, reduced body weight and fat mass. They also showed a beneficial impact of the long-term ghrelin agonist treatment on insulin signalling pathways in hippocampal brain tissue.

Alzheimer's patients show significant shrinkage of the hippocampus, a part of the brain cortex that has a key role in forming new memories.