December 23, 2024

New Research Reveals Why Diabetes Could Lead to Alzheimer’s Disease

Alzheimer's Disease Dementia ConceptAlzheimer's Disease Dementia Concept
Research from Umeå University shows that type 2 diabetes impedes the elimination of Alzheimer’s-related proteins, suggesting a higher cognitive risk, highlighting the importance of diabetes management.

A study indicates that type 2 diabetes may impair the elimination of Alzheimer’s-related proteins, suggesting potential strategies to mitigate cognitive risks by managing blood sugar levels.

People with type 2 diabetes are at a higher risk of developing Alzheimer’s disease and other cognitive issues. A recent study led by Umeå University in Sweden suggests that this increased risk may be due to the difficulty people with type 2 diabetes have in clearing a protein that is potentially linked to the disease.

“The results may be important for further research into possible treatments to counteract the risk of people with type 2 diabetes being affected by Alzheimer’s,” says Olov Rolandsson, senior professor at the Department of Public Health and Clinical Medicine at Umeå University, research leader and first author of the study.

The substances that the researchers have studied are two so-called beta-amyloids, which are among the most important components of the plaques found in the brains of people with Alzheimer’s disease.

Study Findings on Beta-Amyloids

The researchers measured the concentrations in the blood of the beta-amyloids Aβ1-40 and Aβ1-42 as well as of an enzyme that breaks down the beta-amyloids in a test group with type 2 diabetes and in a healthy control group. The two groups were given infusion of glucose for four hours, which induced acute hyperglycemia, i.e. high blood sugar levels, after which repeated samples were taken from the subjects.

Immediately after the infusion of the sugar solution, the groups had similar values. Soon, the values of beta-amyloids fell sharply in the control group, while the values of the amyloid-degrading enzyme rose. Among the group with type 2 diabetes, there were no changes, i.e. the levels of beta-amyloid did not decrease, nor did there be an increase in the enzyme that breaks down amyloid.

Olov RolandssonOlov Rolandsson
Professor Olov Rolandsson, Department of Public Health and Clinical Medicine, Umeå University. Credit: Mattias Pettersson

The results indicate that the body in people with type 2 diabetes does not have the same ability as in healthy people to take care of beta-amyloid, which could increase the risk that it is then stored in the brain and causes cognitive diseases such as Alzheimer’s.

“More research is needed to confirm the results of this limited study. Hopefully, in the long term, it can also lead to new treatments. But the findings underline the importance of preventing type 2 diabetes as far as possible and that people who do have it should avoid having episodes of high blood sugar,” says Olov Rolandsson.

The study was conducted on ten people with type 2 diabetes and eleven people without diabetes in the control group. The participants were aged 66–72 years.

People with type 2 diabetes are at increased risk of Alzheimer’s disease and other cognitive problems. A new study led by Umeå University, Sweden, shows that the reason may be that people with type 2 diabetes have more difficulty getting rid of a protein that may cause the disease.

“The results may be important for further research into possible treatments to counteract the risk of people with type 2 diabetes being affected by Alzheimer’s,” says Olov Rolandsson, senior professor at the Department of Public Health and Clinical Medicine at Umeå University, research leader and first author of the study.

The substances that the researchers have studied are two so-called beta-amyloids, which are among the most important components of the plaques found in the brains of people with Alzheimer’s disease.

The researchers measured the concentrations in the blood of the beta-amyloids Aβ1-40 and Aβ1-42 as well as of an enzyme that breaks down the beta-amyloids in a test group with type 2 diabetes and in a healthy control group. The two groups were given infusion of glucose for four hours, which induced acute hyperglycemia, i.e. high blood sugar levels, after which repeated samples were taken from the subjects.

Differences in Beta-Amyloid Processing

Immediately after the infusion of the sugar solution, the groups had similar values. Soon, the values of beta-amyloids fell sharply in the control group, while the values of the amyloid-degrading enzyme rose. Among the group with type 2 diabetes, there were no changes, i.e. the levels of beta-amyloid did not decrease, nor did there be an increase in the enzyme that breaks down amyloid.

The results indicate that the body in people with type 2 diabetes does not have the same ability as in healthy people to take care of beta-amyloid, which could increase the risk that it is then stored in the brain and causes cognitive diseases such as Alzheimer’s.

“More research is needed to confirm the results of this limited study. Hopefully, in the long term, it can also lead to new treatments. But the findings underline the importance of preventing type 2 diabetes as far as possible and that people who do have it should avoid having episodes of high blood sugar,” says Olov Rolandsson.

The study was conducted on ten people with type 2 diabetes and eleven people without diabetes in the control group. The participants were aged 66–72 years.

People with type 2 diabetes are at increased risk of Alzheimer’s disease and other cognitive problems. A new study led by Umeå University, Sweden, shows that the reason may be that people with type 2 diabetes have more difficulty getting rid of a protein that may cause the disease.

“The results may be important for further research into possible treatments to counteract the risk of people with type 2 diabetes being affected by Alzheimer’s,” says Olov Rolandsson, senior professor at the Department of Public Health and Clinical Medicine at Umeå University, research leader and first author of the study.

The substances that the researchers have studied are two so-called beta-amyloids, which are among the most important components of the plaques found in the brains of people with Alzheimer’s disease.

The researchers measured the concentrations in the blood of the beta-amyloids Aβ1-40 and Aβ1-42 as well as of an enzyme that breaks down the beta-amyloids in a test group with type 2 diabetes and in a healthy control group. The two groups were given infusion of glucose for four hours, which induced acute hyperglycemia, i.e. high blood sugar levels, after which repeated samples were taken from the subjects.

Immediately after the infusion of the sugar solution, the groups had similar values. Soon, the values of beta-amyloids fell sharply in the control group, while the values of the amyloid-degrading enzyme rose. Among the group with type 2 diabetes, there were no changes, i.e. the levels of beta-amyloid did not decrease, nor did there be an increase in the enzyme that breaks down amyloid.

The results indicate that the body in people with type 2 diabetes does not have the same ability as in healthy people to take care of beta-amyloid, which could increase the risk that it is then stored in the brain and causes cognitive diseases such as Alzheimer’s.

“More research is needed to confirm the results of this limited study. Hopefully, in the long term, it can also lead to new treatments. But the findings underline the importance of preventing type 2 diabetes as far as possible and that people who do have it should avoid having episodes of high blood sugar,” says Olov Rolandsson.

The study was conducted on ten people with type 2 diabetes and eleven people without diabetes in the control group. The participants were aged 66–72 years.

Reference: “Acute Hyperglycemia Induced by Hyperglycemic Clamp Affects Plasma Amyloid-β in Type 2 Diabetes” by Olov Rolandsson, Andreas Tornevi, Pär Steneberg, Helena Edlund, Tommy Olsson, Ulf Andreasson, Henrik Zetterberg and Kaj Blennow, 28 May 2024, Journal of Alzheimer’s Disease.
DOI: 10.3233/JAD-230628