There have been numerous studies on the connection between type 2 diabetes and Alzheimer’s disease and many scientists are focused on discovering if and how they’re connected. One important study revealed that high levels of blood sugar make the protein beta amyloid (connected to Alzheimer’s) significantly more toxic to the brain’s blood vessels cell lining.
The latest study published in the Journal of Clinical Investigation shows this link even clearer. One of the earliest signs of Alzheimer’s is an accumulation of amyloid plaques in the brain. Amyloid beta, which is the main component of the brain plaque in patients suffering from Alzheimer’s, can become increasingly elevated with increased blood sugar levels.
Patients who suffer from diabetes find it difficult to control the glucose levels in their blood which is why they often experience sugar spikes after meals.
The Study in Detail
As we already mentioned, the researches wanted to see exactly what’s the link between blood glucose levels and brain amyloid plaque accumulation. For this purpose, they administered glucose into the system of mice who were bred to develop Alzheimer’s.
According to their findings, if the glucose levels in young mice without amyloid plaque doubled, there was a 20% increase in the brain’s amyloid beta levels. But wait, there’s more. When the scientists redid the same experiment with older mice who already had some amyloid plaque in their brain, the increase was double (40%).
The researchers also noticed that the sugar spikes were causing an increased neuron activity in the brain, which in turn stimulated the production of beta amyloid.
Increased glucose levels make the KATP channels close, exciting our brain cells and leading to excessive firing. This significant increase in neuron firing is more likely to lead to increased amyloid beta production, which in turn leads to the creation of amyloid plaque.
A Potential New Approach
In order to confirm their findings, the mice were given glucose elevating drugs, something most patients take for low blood sugar levels.
These drugs kept the KATP channels open, while their glucose levels increased. However, the amyloid beta production remained unchanged despite it all. The researchers believed that this was proof enough for the KATP channels to be confirmed as the most probably link between amyloid beta levels, glucose and neuronal activity.
They hope that this may inspire other researchers to find a new approach towards the treatment of Alzheimer’s, and maybe even develop a potential cure with these latest findings in mind.