Researchers identify genetic markers linking type 2 diabetes to Alzheimer’s disease.
One of the major long-term complications of type 2 diabetes is an increased risk for developing AD. While previous studies strongly suggested a causative role of diabetes in the onset and progression of AD dementia, the specific mechanistic interactions connecting diabetes and AD had not been previously described. Now, a new study from researchers at the Icahn School of Medicine at Mount Sinai and J.J. Peters Bronx VA Medical Center has found that certain patients with type 2 diabetes may have specific genetic risk factors that put them at higher risk for developing Alzheimer’s disease (AD).
Previous studies show that an estimated 312 million people suffer from type 2 diabetes worldwide, exerting enormous burdens on individuals and on health care systems. Similarly, AD affects nearly 45 million people worldwide and is costly to both individuals and healthcare systems. There is currently no cure for either condition.
Mounting evidence suggests that AD dementia can be traced back to pathological conditions, such as type 2 diabetes, that are initiated several decades before clinical AD onset. The researchers state that since type 2 diabetes is one of the potentially modifiable risk factors for AD, it is critically important for the medical community to uncover the genetics of this complex connection so that new therapeutic interventions may be developed and targeted to at-risk individuals with type 2 diabetes prior to the onset of AD dementia.
to investigate this the current study used recent genome wide association study (GWAS) findings to investigate whether type 2 diabetes and AD share common genetic etiological factors and the potential impact of these genetic factors on the cellular and molecular mechanisms that may contribute to the development of both these diseases.
The genome wide association study look at differences at many points in the genetic code to see if, across a population, one or more variations in the code are found more often in those with a given trait (for example, high risk for a disease). Even the smallest genetic variations, called single nucleotide polymorphisms (SNPs), can have a major impact on a trait by swapping just one of the 3.2 billion letters that make up the human DNA code.
The results identified multiple genetic differences in terms of SNPs that are associated with higher susceptibility to develop type 2 diabetes as well as Alzheimer’s disease. The team explain that many of these SNPs are traced to genes whose anomalies are known to contribute to type 2 diabetes and AD, suggesting that certain diabetic patients with these genetic differences are at high risk for developing Alzheimer’s. The data findings highlight the need for further exploration of genetic susceptibility to Alzheimer’s disease in patients with type 2 diabetes.
The lab surmise that this study will support ongoing research into genetic susceptibility in patients with type 2 diabetes for developing AD and help improve the design of future novel treatments for a sub-population of type 2 diabetes subjects with genetic predisposition to AD. They feel this could benefit patients with type 2 diabetes and reduce the risk for subsequent development of AD. They go on to concluded that outcomes from these studies identifying cellular abnormalities common to both type 2 diabetes and AD can lead to the development of type 2 diabetes therapies that may also help prevent subsequent development of AD in genetically predisposed individuals.