A recent study suggests that a drug formerly used to treat depression may be the key towards battling brain shrinkage including diseases such as dementia and Alzheimer's. Trazodone, a drug discovered in the sixties was once used for patients suffering from depression, however, in the dawn of modern drugs, its use was made less frequent.
Fortunately, a study reveals that Trazodone may have another purpose; slowing down brain shrinkage. According to Daily Mail, Trazadone has already been proven to be safe for human use and has shown results proving that it can reduce brain shrinkage as per the early tests.
Moreover, researchers discovered that Trazodone is capable of preventing brain damage in mice that suffered from dementia. However, the effectiveness of Trazodone for humans with dementia has yet to be proven.
"We know that trazodone is safe to use in humans," says Professor Giovanna Mallucci, team leader from the Medical Research Council's Toxicology Unit in Leicester, along with Cambridge University. "So a clinical trial is now possible to test whether the protective effects of the drug we see on brain cells in mice with neurodegeneration also applies to people in the early stages of Alzheimer's disease and other dementias."According to Mallucci, trazodone has already been used on patients who suffer from advanced dementia. However, further steps need to be taken still, in order to see if the drug can effectively slow dementia down at an early stage.
Furthermore, trazodone is not alone in the battle against brain shrinkage. Apparently, an anti-cancer drug known as dibenzoylmethane was also used on mice and rendered promising results. Studies prove that dibenzoylmethane is capable of blocking the natural defense mechanism in cells which result in overactivity of the patients' brains with such degenerative conditions.The approach researchers hope to take, now equipped with the knowledge on trazodone and dibenzoylmethane, is to alter the natural defense mechanism of brain cells. In the event that a virus infects a brain cell, viral proteins tend to build up. As a response, cells shut down in order to prevent further spread which leads to prolonged inactivity of brain cells which will eventually kill the cells of starvation.
Many neurodegenerative diseases produce faulty proteins that cause these defense mechanisms to activate, matched with the disease's actual effects, the end results are definitely devastating.Looking back, in 2013 a UK medical research council team was able to stop brain cells from dying in an animal as reported by BBC. This feat was a first of its nature to be accomplished, thus making global headlines and sparking enthusiastic hopes for people suffering from degenerative illnesses such as Alzheimer's, Parkinson's, multiple sclerosis, and Huntington's. Preventing brain cells from dying is a remarkable accomplishment, given that brain cells do not have the ability to regenerate easily.
Unfortunately, the compound used in 2013 was found to be unsuitable for humans as it had had side effects that caused organ damage. Despite the negative effect the compound had on the pancreas, the findings were still noted as a turning point for the field. Four years later, two drugs have been found to have the same protective effect on the brain and have already been proven to be safe for human use. "It's really exciting," says Mallucci.Several experts are optimistic about these two drugs in the fight against brain shrinking diseases including Dr. Doug Brown, from the Alzheimer's Society. "We're excited by the potential of these findings, from this well-conducted and robust study," Brown claims. "As one of the drugs is already available as a treatment for depression, the time taken to get from the lab to the pharmacy could be dramatically reduced."
Along with Brown, other doctors including Dr. David Dexter from Parkinson's UK finds the study to be "a very robust and important study." He later added that "If these studies were replicated in human clinical trials, both trazodone and DBM could represent a major step forward."
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