Genetic Variants May Increase One’s Risk of Developing Alzheimer’s Disease (AD)
Two teams, led by Dr. Phillippe Amouyel of the Institut Pasteur de Lille in France and Julie Williams, a professor of psychological medicine at Cardiff University School of Medicine in Wales, have found 3 genetic variants that appear to increase the likelihood that one will develop AD in his or her lifetime. Prior to this study, four genetic variants had been definitively associated with the disease–APP, PS1, PS2, and APOE. This study concluded that defects in the CLU, CR1, and PICALM genes as well as 13 other potential candidate variants, that will need further studies to confirm conclusion.
It is unknown what function these genes play, although prior studies have shown that two of the genes, CLU and CR1, may play a role in the elmination of one of the major components of amyloid plaques. “This is the most important finding in the genetic [component] of Alzheimer’s in more than 10 years,” said study co-author Alison Goate, a professor of genetics in psychiatry at Washington University School of Medicine and a member of the Alzheimer’s Association Medical & Scientific Advisory Council.
Although it remains unknown how the genes play a role in the development of AD, increased levels of CLU in the brains of CSF of AD patients have been found. PICALM may play a role in nerve cell synapses and affect beta-amyloid deposits in the brain.
Common Infections May Speed Up Memory Loss in Alzheimer’s Patients
Researchers out of Southampton University have studied 222 elderly persons with Alzheimer’s Disease (AD) and believe that common infections in the chest or urinary tract could actually double memory loss. The study, published in the September 7 issue of the Journal of Neurology (Story from BBC NEWS: http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/8241833.stm) surmises that such infections lead to higher levels of an inflammatory protein called tumour necrosis factor (TNF) in the blood. Better care for such infections is of utmost importance.
The researchers followed the participants for 6 months. Of the 222 participants, 110 developed a total of 150 infections in areas such as the chest, stomach, intestines, and urinary tract, which led to the production of TNF proteins. These are collectively known as acute systemic inflammation events (SIEs).
“The worse the infection, the worse the affect on the memory,” stated Professor Clive Holmes of the University of Southampton, who led the study. Subjects with more than one SIE during the 6-month period had 2-times the rate of cognitive decline from baseline at the start of the study compared with those who had no SIEs.
Patients who entered the study with high baseline levels of TNF and then suffered an SIE over the 6-month study had a 10-fold increase in cognitive decline over those who were SIE-free.
The study looked at patients with mild, moderate and severe AD. “One might guess that people with with a more rapid rate of cognitive decline are more susceptible to infections or injury, but we found no evidence to suggest that people with more severe dementia were more likely to have infections or injuries at the beginning of the study,” stated Holmes.
“If further work proves that TNF is causing more brain inflammation, it may be possible to use drugs that block TNF to help dementia receptors.”
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