What do Alzheimer’s disease (AD) and Type 2 diabetes have in common? For one thing, they are both linked to oxidative brain damage and accelerated aging.
One of the hormones controlling metabolism of insulin* and glucose, Glucagon**-like peptide-1 (GLP-1), is also a potent neuroprotector. Its presence in neurons of the hippocampus is linked to better learning. A synthetic analog of GLP-1, Exenatide, a drug used to treat Type 2 diabetes, accelerated neurogenesis, improved synaptic plasticity and cognitive performancee in animal models. These effects make Exenatide very attractive candidate to treat AD. But how exactly does it work in this case?
Interestingly, Exenatide worked very well in the mice mutants imitating familial AD, but not so well in the mice mutant reproducing synaptic dysfunction in age-dependent AD. This might meat that unlike the age-dependent and familial forms of AD differs in the mechanisms of energy deficits. Previously, insulin has been shown to improve cognitive performance in humans suffering from age-related AD.
Source: Cell Death and Disease (2013) 4, e612; doi:10.1038/cddis.2013.139
* Insulin: hormone decreasing concentration of glucose in the blood
** Glucagon: hormone increasing concentration of glucose in the blood