Going back to the neuro articles the thing that really stands out to me is how fibrin is concsidered the new target for Alzheimer’s disease. Fibrin correlates to beta-amyloid protein build-up in Alzheimer’s. As the beta-amyloid protein accumulates so does fibrin. According to Justin Paul, a graduate student, and Sidney Strickland, head of the Laboratory of Neurobiology and Genetics, fibrin could be an important fighting tool against Alzheimer’s. Sidney and Paul have discovered “that brains of Alzheimer’s patients have increased fibrin levels,” a finding that had previously been unexplored.
The function of Alzheimer’s is damage to the barrier that blocks blood from percolating into the brain. This damage allows fibrin and other blood proteins to seep through.
The Experiment
The researchers performed various experiments, either decreasing or increasing the deposition of fibrin in the brain’s of mice. An enzyme from snake venom called ancrod, which causes the liver to clear fibrin from the bloodstream, was used to decrease fibrin. To increase it, they used tranexamic acid, which prevents the breakdown of fibrin clots.
The Results
The effects of the experiment were as predicted. The only knew information gained from it was the fact that beta-amyloid protein plaques in the mice’s brain did not change with fluctuating levels of fibrin. However, the inflammatory cells surrounding them did. “The number of microglia associated with each plaque - the number of the little inflammatory cells that get excited by fibrin deposition - are reduced when there’s less fibrin around, and increased when you can’t degrade the fibrin,” Paul says. Also, a decrease in fibrin using ancrod decreased the blood-vessel deterioration in the brain. “So reducing inflammation might be the link to preventing blood-brain damage, as well,” says Paul.
Final Quote
“Fibrin is a critical component for increased inflammation in Alzheimer’s disease. And fibrin and fibrinogen, based on our study, should be considered a new therapeutic target. Although, beta-amyloid may be the cause of Alzheimer’s, alternative approaches need to be considered,” according to Paul.
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2 comments:
That was a very interesting experiment. After reading your post, I surfed the web to see if there were any anti-coagulants treatments (that inhibits the activity of Factor XIIIa and/or fibrin aggregation) that were being investigated for the possible treatment of delay of Alzheimer’s disease.
I did find that in the case of dementia associated with Alzheimer’s disease, aspirin and in some cases, warfarin (Coumadin) can be prescribed to an AD patient in order to delay and/or cease the progression of senile plague growths. Unfortunately, due side effects, warfarin is not ideal for long term therapy and is indicated in patients with atrial fibrillation.
http://www.aafp.org/afp/981101ap/sloane.html
Interestingly, I did find that cigarette smoke contains chemicals that causes delayed fibrin self-assembly and prevent fibrin cross-linking by inactivation of factor XIIIa. Unfortunately smoking itself carries great health risks and I’m guessing there isn’t any research investigating the benefits of cigarette smoke on Alzheimer’s patients.
http://www.sciencemag.org/cgi/content/abstract/217/4560/642
Unfortunately, anticoagulants will never be a primary anti-amyloid plaque therapy in AD patients simply because of the dangers of inhibiting essential clotting pathways and long term side effects associated with such treatment.
That is very interesting about smoking and its affects on fibrin assembly. I wonder if it's nicotine that plays the role in the delay of fibrin self assembly. If smoking does help AD hopefully the researchers can find a way around the possiblity of lung cancer.
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