Alzheimer's Disease Cause & Cure: Blood Pressure Drug Can Help Lower Condition's Progression: Study

A new study, published in Alzheimer's Research and Therapy, finds a potential link between a blood pressure drug and Alzheimer's disease.

Alz.org revealed that someone in the United States develops Alzheimer's disease every 67 seconds. One in three seniors dies with the condition or another dementia and it's the only cause of death in the country that cannot be prevented, cured or slowed. But, this notion might change with the results of this new study.

The FDA-approved drug for blood pressure known as candesartan, which is sold as Atacand, can potentially reduce the progression of Alzheimer's disease, Science World Report has learned.

Per UPI, Atacand, an angiotensin receptor blocker, is used to control blood pressure. Previous studies reported that patients with high blood pressure treated with several drugs were at lower risk of developing Alzheimer's disease or will develop it at a slower pace.

"Our findings make sense in many ways," said Dr. Juan Saavedra, a researcher at Georgetown University. "Hypertension reduces blood flow throughout the body and brain and is a risk factor of Alzheimer's disease. Previous epidemiological studies found that Alzheimer's progression is delayed in hypertensive patients treated with ARBs."

The researchers exposed neuronal cultures excessive glutamate, an injury that causes neurons to die and treated them with candesartan. They observed that the drug prevented the glutamate from killing the neurons.

The scientists also learned that the drug prevented the inflammation and other processes that contribute to the neuronal death. Aside from this, it also keeps the changes from amyloid metabolism, which is an essential factor for the condition. When amyloid plaques build up, it plays a role in the progress of Alzheimer's disease.

The team also compared their results with autopsy sample from individuals with Alzheimer's disease. They found out that the expression of genes altered by excess glutamate matched the damage in the patients' brains.

"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 first study author Abdel G. Elkahloun, Ph.D., from the Comparative Genomics and Cancer Genetics Branch of the National Human Genome Research Institute.

The researchers concluded that the blood pressure drug might be a potential prevention from the condition. "We hypothesize that candesartan, or other members of the ARB group, may not only slow progression of Alzheimer's but also prevent or delay its development," Saavedra said.