14 DAY TRIAL // A team of scientists believes it has found an explanation for why people who suffer from diabetes are more likely to develop a neurodegenerative form of dementia known as Alzheimer's disease. Apparently, a chemical pathway involved in insulin transport is to blame.
The anomaly stems from a single malfunctioning gene, which is capable of disrupting this insulin pathway. Such an effect is characteristic of diabetes, and the genetic mutation that causes it is commonplace in Alzheimer's patients.
Scientists from The City College of New York say that the new discovery could potentially be used to develop a therapy against both conditions, an integrated approach that would target them simultaneously. The research group was led by biologist Dr. Chris Li.
Interestingly, the root cause of Alzheimer's has eluded researchers for decades. While some of the mechanisms the disease uses to grab a foothold in the human brain are known, and some theories explaining them exist, the real reasons behind why the condition appears are still unknown.
One of its hallmarks is represented by neural plaques formed by excessive accumulations of the beta-amyloid protein, which occurs naturally in nerve cells. When the molecules responsible for breaking it down malfunction, the protein accumulates and starts damaging neurons.
Previous studies have demonstrated that mutations in the human amyloid precursor protein (APP) gene may be responsible for this effect. These mutations are visible in cases where Alzheimer's is transmitted through the family line.
“People with type 2 diabetes have an increased risk of dementia. The insulin pathways are involved in many metabolic processes, including helping to keep the nervous system healthy,” Li explains. He adds that the study he and his team conducted was carried out on C. elegans worms.
“What we found was that mutations in the worm equivalent of the APP gene slowed their development, which suggested that some metabolic pathway was disrupted. We began to examine how the worm equivalent of APP modulated different metabolic pathways and found that the APP equivalent inhibited the insulin pathway,” he says.
The group now plans to study humans, in order to determine whether or not our version of the gene plays a similar role in underlying both type II diabetes and Alzheimer's disease, PsychCentral reports.