Individuals with type 2 diabetes face a higher likelihood of developing Alzheimer’s disease and other cognitive issues. Recent research from Umeå University in Sweden suggests this increased risk may stem from the struggle these individuals have in eliminating a protein that could contribute to the disease.
“These findings could significantly influence ongoing research aimed at discovering potential treatments to reduce the risk of Alzheimer’s in those with type 2 diabetes,” remarks Olov Rolandsson, a senior professor at Umeå University’s Department of Public Health and Clinical Medicine, who led the research and is the study’s primary author.
The scientists focused on two types of beta-amyloids, which are crucial components of the plaques commonly associated with Alzheimer’s disease.
They analyzed the levels of beta-amyloids Aβ1-40 and Aβ1-42, along with an enzyme that helps break down these beta-amyloids in both a group of individuals with type 2 diabetes and a healthy control group. Both groups were given a glucose infusion lasting four hours, which prompted a condition known as acute hyperglycemia (high blood sugar levels), after which blood samples were repeatedly collected.
At first, both groups showed comparable levels right after the sugar infusion. However, the beta-amyloid levels in the control group quickly decreased, while the levels of the enzyme that degrades amyloid increased. Conversely, the group with type 2 diabetes did not display any changes; their beta-amyloid levels remained elevated, and there was no increase in the amyloid-degrading enzyme.
These results suggest that individuals with type 2 diabetes have a reduced capacity compared to healthy individuals to manage beta-amyloid, potentially leading to its accumulation in the brain and raising the risk of cognitive disorders like Alzheimer’s.
“Additional research is essential to validate the findings of this preliminary study. Ideally, this could pave the way for new treatment options in the future. Nonetheless, this emphasizes the crucial need to prevent type 2 diabetes as much as possible, and for those who have it, to minimize instances of high blood sugar,” states Olov Rolandsson.
The study involved ten participants with type 2 diabetes and eleven healthy individuals in the control group, all aged between 66 and 72 years.
Individuals with type 2 diabetes face a higher likelihood of developing Alzheimer’s disease and other cognitive issues. Recent research from Umeå University in Sweden suggests this increased risk may stem from the struggle these individuals have in eliminating a protein that could contribute to the disease.
“These findings could significantly influence ongoing research aimed at discovering potential treatments to reduce the risk of Alzheimer’s in those with type 2 diabetes,” remarks Olov Rolandsson, a senior professor at Umeå University’s Department of Public Health and Clinical Medicine, who led the research and is the study’s primary author.
The scientists focused on two types of beta-amyloids, which are crucial components of the plaques commonly associated with Alzheimer’s disease.
They analyzed the levels of beta-amyloids Aβ1-40 and Aβ1-42, along with an enzyme that helps break down these beta-amyloids in both a group of individuals with type 2 diabetes and a healthy control group. Both groups were given a glucose infusion lasting four hours, which prompted a condition known as acute hyperglycemia (high blood sugar levels), after which blood samples were repeatedly collected.
At first, both groups showed comparable levels right after the sugar infusion. However, the beta-amyloid levels in the control group quickly decreased, while the levels of the enzyme that degrades amyloid increased. Conversely, the group with type 2 diabetes did not display any changes; their beta-amyloid levels remained elevated, and there was no increase in the amyloid-degrading enzyme.
These results suggest that individuals with type 2 diabetes have a reduced capacity compared to healthy individuals to manage beta-amyloid, potentially leading to its accumulation in the brain and raising the risk of cognitive disorders like Alzheimer’s.
“Additional research is essential to validate the findings of this preliminary study. Ideally, this could pave the way for new treatment options in the future. Nonetheless, this emphasizes the crucial need to prevent type 2 diabetes as much as possible, and for those who have it, to minimize instances of high blood sugar,” states Olov Rolandsson.
The study involved ten participants with type 2 diabetes and eleven healthy individuals in the control group, all aged between 66 and 72 years.
There is a heightened challenge in eliminating a protein that could contribute to the disease.
“These findings could be significant for future studies exploring potential treatments that might reduce the risk of Alzheimer’s in individuals with type 2 diabetes,” explains Olov Rolandsson, a senior professor in the Department of Public Health and Clinical Medicine at Umeå University, and the leading researcher of the study.
The focus of the research was on two specific beta-amyloids, which are key components of the plaques that accumulate in the brains of Alzheimer’s patients.
The scientists assessed blood levels of the beta-amyloids Aβ1-40 and Aβ1-42, along with an enzyme responsible for breaking down these beta-amyloids, in a group of individuals with type 2 diabetes as well as in a healthy control group. Both groups underwent a four-hour glucose infusion, which temporarily raised their blood sugar levels, after which multiple blood samples were collected.
Initially, both groups registered similar values right after the glucose infusion. But soon after, the beta-amyloid levels in the control group dropped significantly, while the levels of the enzyme that degrades amyloid increased. In contrast, there were no noticeable changes in the type 2 diabetes group; the beta-amyloid levels did not decrease, nor did the enzyme levels rise.
This suggests that individuals with type 2 diabetes may lack the capability that healthy individuals have to process beta-amyloid, possibly leading to its accumulation in the brain and increasing the likelihood of cognitive issues like Alzheimer’s disease.
“We need more research to validate these findings from this small-scale study. In the long run, this could potentially result in new treatment options. However, these results emphasize how critical it is to prevent type 2 diabetes when possible, and for those who have it, to steer clear of high blood sugar spikes,” remarks Olov Rolandsson.
The study involved ten participants with type 2 diabetes and eleven healthy controls, all aged between 66 and 72 years.
Individuals diagnosed with type 2 diabetes face a greater risk of developing Alzheimer’s disease and other cognitive impairments. A recent study led by Umeå University in Sweden suggests that this increased risk may stem from the difficulty these individuals have in eliminating a harmful protein linked to the disease.
“These findings could be significant for future studies exploring potential treatments that might reduce the risk of Alzheimer’s in individuals with type 2 diabetes,” explains Olov Rolandsson, a senior professor in the Department of Public Health and Clinical Medicine at Umeå University, and the leading researcher of the study.
The focus of the research was on two specific beta-amyloids, which are key components of the plaques that accumulate in the brains of Alzheimer’s patients.
The scientists assessed blood levels of the beta-amyloids Aβ1-40 and Aβ1-42, along with an enzyme responsible for breaking down these beta-amyloids, in a group of individuals with type 2 diabetes as well as in a healthy control group. Both groups underwent a four-hour glucose infusion, which temporarily raised their blood sugar levels, after which multiple blood samples were collected.
Initially, both groups registered similar values right after the glucose infusion. But soon after, the beta-amyloid levels in the control group dropped significantly, while the levels of the enzyme that degrades amyloid increased. In contrast, there were no noticeable changes in the type 2 diabetes group; the beta-amyloid levels did not decrease, nor did the enzyme levels rise.
This suggests that individuals with type 2 diabetes may lack the capability that healthy individuals have to process beta-amyloid, possibly leading to its accumulation in the brain and increasing the likelihood of cognitive issues like Alzheimer’s disease.
“We need more research to validate these findings from this small-scale study. In the long run, this could potentially result in new treatment options. However, these results emphasize how critical it is to prevent type 2 diabetes when possible, and for those who have it, to steer clear of high blood sugar spikes,” remarks Olov Rolandsson.
The study involved ten participants with type 2 diabetes and eleven healthy controls, all aged between 66 and 72 years.
