Researchers at UCSD School of Medicine and an international team of scientists discovered genetic overlap between Alzheimer’s disease and two high-risk factors of cardiovascular disease. The study was published on April 10, 2015, via the scientific journal, Circulation.
The two risk factors are C-reactive protein and plasma lipids. CRP is a type of substance that increases with inflammatory reaction in a body, and plasma lipids are types of fat, mostly composed of fatty acids and cholesterol.
Scott LaFee, a scientific journalist from UCSD Health System, explained the significance of the work of the researchers.
“The key here was that they identified that the genes, [CRP and plasma lipids], have some connection with those risk factors of Alzheimer’s disease,” LaFee told the UCSD Guardian. “So the idea being that if you can control those risk factors, you can ideally slow the progression of Alzheimer’s disease.”
In the past, scientists were aware that a correlation exists between Alzheimer’s disease and cardiovascular disease. However, the relationship between the two diseases was and still is unclear. To extract further knowledge of the link between the two diseases, the researchers dug into minor details of examining specific genetic signals.
According to the article published in Circulation, the researchers engaged in a statistical investigation and found out that the overlap associated with Alzheimer’s disease, CRP and the three components of total cholesterol in single nucleotide polymorphisms enriches AD SNPs, which increases the risk of developing Alzheimer’s disease. SNPs refer to the most common genetic variations in human body.
“Using summary statistics from genome-wide association studies of over 200,000 individuals, we investigated overlap in single nucleotide polymorphisms associated with clinically diagnosed Alzheimer’s disease and C-reactive protein, triglycerides, high- and low-density lipoprotein levels,” the researchers reported. “We found up to 50-fold enrichment of Alzheimer’s disease SNPs for different levels of association with CRP, LDL, HDL and TG-SNPs.”
The contemporary treatments for Alzheimer’s disease are not capable of fully controlling the symptoms of the disease. On the other hand, the treatments for cardiovascular disease are relatively much more effective, and the link between the two diseases may open a new pathway to Alzheimer’s disease’s effective treatment.
“This finding suggests that here you have two risk factors for cardiovascular disease, which are more controllable; you can lower cholesterol, you can lower blood lipids and inflammatory protein,” LaFee said. “And that may have an impact on prospects of people getting Alzheimer’s disease.”
Ole A. Andreassen, senior co-author of the research, spoke about the importance of potential success in finding an effective treatment.
“Currently, there are no disease-modifying therapies, and much attention has been focused upon prevention and early diagnosis,” Andreassen said to UCSD Health System. “Delaying dementia onset by even just two years could potentially lower the worldwide prevalence of Alzheimer’s disease by more than 22 million cases over the next four decades, resulting in significant societal savings.”
Alzheimer’s disease is a neurological disorder that degenerates memory and cognition. Some of its symptoms include loss of memory, impaired speaking and writing and change in personality and behavior. In the U.S., more than 5 million people suffer from the disease, most of the patients being over the age of 65.
