A drug used to treat high blood pressure could be the answer to treating and preventing Alzheimer’s disease.
Alzheimer’s disease is a progressive degenerative brain disease. It causes cognitive decline and memory loss. In Alzheimer’s disease, damaged cells release too much glutamate, an important neurotransmitter involved in most aspects of brain function. The excess glutamate leads to chronic overexposure to calcium, which in turn speeds up brain cell damage.
Using neuronal cultures, the researchers studied the effects of the high blood pressure medication on the toxic effects of excessive glutamate. The medication, candesartan, is an angiotensin receptor blocker sold under the brand name Atacand.
The researchers found that candesartan prevented neuronal death caused by glutamate. The drug also prevented neuronal inflammation and changes in amyloid metabolism. The latter change is especially important since the buildup of amyloid plaques are a hallmark of the disease. The researchers then compared the gene expression in the cultures to autopsy samples from Alzheimer’s
patients that were published in gene databases.
"The correlations were impressive. The expression of 471 genes that were altered by excess glutamate in our cultures were also altered in brain autopsy samples from patients who suffered from Alzheimer's disease. Candesartan normalized expression of these genes in our cultures," said study author Abdel G. Elkahloun, from the Comparative Genomics and Cancer Genetics Branch of the National Human Genome Research Institute.
The researchers hypothesize that candesartan and/or other angiotensin receptor blockers have the potential to slow down the progression of Alzheimer’s and prevent or delay its development.
They say their findings support testing candesartan and other angiotensin receptor blockers in controlled clinical studies on patients at early stages of Alzheimer’s.
The research was published online on January 28, 2016, in the journal Alzheimer’s Research and Therapy
Sources: Journal study Alzheimer’s Research and Therap
y, Georgetown University Medical Center press release