Alzheimer’s disease is a common neurological illness that hinders brain functions like memory and logic, and it currently has no cure. Scientists have shown Alzheimer’s disease is caused by abnormal protein build-up within and around brain cells. It is also dependent on genetics and aging. People with a family history of Alzheimer’s are more likely to develop it, but the role of specific genes is still unknown.
Scientists have previously found a relationship between Alzheimer’s disease and type 2 diabetes. People diagnosed with type 2 diabetes are 50-150% more likely to develop Alzheimer’s disease. Type 2 diabetes is a health condition that interferes with a person’s pancreas, hindering their ability to regulate their blood sugar levels.
When working properly, the pancreas creates a hormone that regulates blood sugar, called insulin. Type 2 diabetes initially occurs when the pancreas cannot produce enough insulin. This lack of insulin causes our cells to absorb less sugar, resulting in high blood sugar. Type 2 diabetes is generally due to a person’s diet and lack of a functional pancreas, but scientists suggest it could also have an underlying genetic cause.
Researchers from Wuhan University in China wanted to identify the link between type 2 diabetes and Alzheimer’s disease. They hypothesized this link could be caused by a protein that is common in both diseases, called IAPP. IAPP is made when insulin-producing cells in our body, called beta cells, die.
In type 2 diabetes, IAPP aggregates and forms a plaque around brain cells, called an amyloid. Amyloids can be toxic to beta cells and cause more cell death, and thus more IAPP. Scientists have also shown IAPP build-up increases the likelihood of someone developing Alzheimer’s.
Other proteins found in brain cells also form amyloids. For example, proteins responsible for stabilizing brain cell structure, called tau proteins, can cause amyloids. The build-up of IAPP and tau proteins in a person’s brain is like shoving papers into a bag. Initially, the papers go in neatly, but as the bag fills up, the papers start folding and crumpling. The Wuhan scientists wanted to determine how IAPP and tau proteins interact during amyloid formation.
First, the scientists took human tissue samples and spinal fluid from human patients with and without Alzheimer’s that were similar in age and time of death. They performed an enzyme-based procedure to determine the amount of IAPP in each patient’s spinal fluid. The researchers found IAPP was present in large amounts in the brains and spinal fluid of Alzheimer’s patients.
Next, they injected these same human tissue and fluid samples into mice, and then tested the spatial recognition and memory of the mice. To do this, they placed the mice into a dark-bottomed pool of water, and tested their ability to exit without a visible surface. They also put the mice on different ends of a Y maze, and let them explore the maze from memory.
After these tests, the team removed the mice’s brains and stained them to better view the brain cells and to see how IAPP and tau proteins interact. They found these two proteins binded together in the mice’s brains, creating more amyloids and toxicity within the brain and nervous system.
On the other hand, the scientists also found injecting IAPP into the abdomen of the mice decreased the amount of amyloid in the brain, reducing cognitive impairment. Although IAPP is a contributing factor to Alzeimer’s, they suggested it could also be used as a treatment. This is similar to vaccinations because many vaccines contain weakened or dead versions of the viruses they protect against.
Based on their results, these scientists hypothesized drugs designed to remove IAPP could be used interchangeably between patients with type 2 diabetes and Alzheimer’s patients. Given the ability of IAPP to both promote neurotoxicity and reduce cognitive impairment, the researchers suggested future studies should focus on understanding IAPP at a molecular level in order to create preventative treatments for Alzheimer’s.