Diabetes in youth may increase risk for neurodegenerative disease, like Alzheimer's disease later in life: Study

Young people with diabetes may have a significantly higher risk of developing Alzheimer's disease later in life, according to a new study by researchers in the Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center at the University of Colorado Anschutz Medical Campus.

In the study, published this week in the journal Endocrines, scientists showed the presence of specific blood biomarkers indicating early signs of neurodegeneration and Alzheimer’s disease (AD) in young people with youth-onset diabetes.

“Preliminary evidence shows that preclinical AD neuropathology is present in young people with youth-onset diabetes,” said the study’s lead author Allison Shapiro, PhD, MPH, assistant professor of pediatrics and endocrinology at the University of Colorado School of Medicine. “These preliminary data suggest the potential for an early-onset AD risk trajectory in people diagnosed with diabetes in childhood or adolescence.”

That includes both type 1 and type 2 diabetes.

Most studies investigating the connection between AD and diabetes have focused on people over age 40 who have a 60-80% greater likelihood of developing dementia, and possibly AD, compared to the same age group without diabetes.

But this study examined the same association in a much younger age group.

The study looked at about 80 people, focusing on blood biomarkers and PET scans to search for evidence of neurodegenerative disease in young adults with diabetes. Some had type 1 diabetes, some had type 2 and others had no diabetes. Study participants with youth-onset diabetes came from the SEARCH for Diabetes in Youth Study, a multi-center population-based registry and cohort.

In addition to the higher blood biomarkers of AD observed in the young people with youth-onset diabetes, “Those with youth-onset diabetes showed elevated accumulation of amyloid proteins in areas of the brain where AD occurs,” Shapiro said.

These new data have researchers concerned given the rising burden of obesity among the nation’s youth and the younger ages at which people are developing diabetes. Shapiro said about 20% of young people in the U.S. have obesity. Obesity contributes to diabetes and inflammation which drive numerous other diseases including AD.

“We are about to enter into a different world of health care because of the obesity epidemic in young people,” Shapiro said. “Young people are catching up with adults. We are now seeing more aging-related diseases in young people.”

“We are not saying these people have AD or have cognitive impairment,” she said. “We are saying that this trajectory is concerning.”

Alzheimer’s disease is often seen as a late-life disease, but this study shows that early life factors may play a significant role in developing the neurodegenerative disease, Shapiro said.

She and her fellow researchers in the LEAD Center, a research and training center at the Colorado School of Public Health, and the University of Colorado Alzheimer's and Cognition Center are hoping to obtain additional funding for future testing of this same group of people as they get older. Follow-up of these participants is critical, Shapiro said, to better understand the risk and its driving factors as well as providing clinical insights for doctors caring for people with youth-onset diabetes.

She said that cognitive testing, which is considered for older adults with diabetes, might benefit younger people too.

“The field of diabetes care is beginning to recognize the importance of cognitive testing as a part of clinical follow-up,” said Shapiro. “And it should be something we consider in youth-onset diabetes as well.”

Reference:

Shapiro, A.L.B.; Coughlan, C.; Bettcher, B.M.; Pauley, M.E.; Kim, J.; Bjornstad, P.; Rajic, B.; Truong, J.; Bell, C.; Choi, Y.J.; et al. Biomarkers of Neurodegeneration and Alzheimer’s Disease Neuropathology in Adolescents and Young Adults with Youth-Onset Type 1 or Type 2 Diabetes: A Proof-of-Concept Study. Endocrines 2024, 5, 197-213. https://doi.org/10.3390/endocrines5020014