About 496,000 people in the UK suffer from dementia, with Alzheimer’s disease being the most common. According to a recent study in mice, the immune system plays a role in removing beta-amyloid, which is main substance that causes Alzheimer’s in the brain. For the first time, researchers have now demonstrated that this may also be the case in humans.
Researchers from the Peninsula College of Medicine and Dentistry at Exeter’s University collaborated with a team from the National Institute on Aging in the USA and in Italy to screen expression levels of thousands of genes in blood samples from nearly 700 people. They discovered that the best marker associated with memory in people was a gene called CCR2, which showed immune system activity against beta-amyloid. Using the Mini mental State Examination, the team measured memory and other cognitive functions.
Earlier animal studies demonstrated that memory and function in mice susceptible to Alzheimer’s improved when researchers augmented the CCR2-activated part of the immune system in the animals’ blood.
Study leader, Professor David Melzer, declared:
“This is a very exciting result. It may be that CCR2-associated immunity could be strengthened in humans to slow Alzheimer’s disease, but much more work will be needed to ensure that this approach is safe and effective”.
Dr Lorna Harries, who co-authored the study, concluded:
“Identification of a key player in the interface between immune function and cognitive ability may help us to gain a better understanding of the disease processes involved in Alzheimer’s disease and related disorders.”
Written By Petra Rattue