Scientists have long known that controlling blood pressure reduces the risk of Alzheimer's disease.
But the latest news really surprised both doctors and pharmacologists: a well-known drug to reduce pressure candesartan (Atakand, Candesar) limits the damage to neurons in this disease.
The results of the experiments, published in a recent issue of the journal Alzheimer's Research and Therapy, suggest the use of candesartan and other angiotensin II receptor blockers for the treatment of Alzheimer's disease in the early stages.
"Our discovery has a lot of possible explanations. For example, hypertension is accompanied by a violation of the blood supply to the nervous system and is a risk factor for Alzheimer's, "explains Dr. Juan Saavedra, a researcher at the Medical Center at Georgetown University (USA).
High blood pressure can cause irreparable damage to small blood vessels in the brain, including those that nourish our memory and mental activity. Therefore, scientists have long insisted on the need to combat hypertension as one of the ways to prevent dementia.
By the way, earlier it was already reported about slowing the progression of Alzheimer's disease in patients with hypertension, who were treated with blockers of angiotensin II receptors (candesartan, valsartan).
In 2013, neurologists at Johns Hopkins University (USA) stated that regular intake of this group of drugs reduces the risk of developing Alzheimer's disease by at least 50% in people after 75 years with normal cognitive performance. A similar effect is observed in the treatment of beta-blockers, calcium channel blockers and other drugs, but to a lesser extent.
Recently, the University of Georgetown decided to test how candesartan affects the culture of nerve cells. They were interested in whether this medicine is able to directly affect their function. For this, the cells were treated with a large amount of glutamic acid, which accelerates the death of neurons in the early stages of Alzheimer's disease, and then scientists introduced candesartan.
The result surpassed expectations:
candesartan prevented glutamate-induced death of neurons. It also became clear that candesartan not only saved life for nerve cells, but also helped to reduce the level of inflammation and slowed the accumulation of beta-amyloid protein, a marker of Alzheimer's disease.
"We believe that candesartan and other members of this group of drugs can not only prevent or delay Alzheimer's disease, but also slow its progression," commented Dr. Saavedra.
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