Recent work in mice suggested that the immune system is involved in
removing beta-amyloid, the main Alzheimer's-causing substance in the
brain. Researchers have now shown for the first time that this may apply
in humans.
Researchers at the Peninsula College of Medicine and Dentistry,
University of Exeter with colleagues in the National Institute on Aging
in the USA and in Italy screened the expression levels of thousands of
genes in blood samples from nearly 700 people. The telltale marker of
immune system activity against beta-amyloid, a gene called CCR2, emerged
as the top marker associated with memory in people.
The team used a common clinical measure called the Mini Mental State
Examination to measure memory and other cognitive functions.
The previous work in mice showed that augmenting the CCR2-activated
part of the immune system in the blood stream resulted in improved
memory and functioning in mice susceptible to Alzheimer's disease.
Professor David Melzer, who led the work, commented: "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, co-author, commented: "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."
Alzheimer's disease is the most common form of dementia and affects around 496,000 people in the UK.
Journal Reference:
- Lorna W. Harries, Rachel M. Bradley-Smith, David J. Llewellyn, Luke C. Pilling, Alexander Fellows, William Henley, Dena Hernandez, Jack M. Guralnik, Stefania Bandinelli, Andrew Singleton, Luigi Ferrucci, David Melzer. LeukocyteCCR2Expression Is Associated with Mini-Mental State Examination Score in Older Adults. Rejuvenation Research, 2012; : 120518094735004 DOI: 10.1089/rej.2011.1302
Courtesy: ScienceDaily
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