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Could the Medicine You Take for Your Headaches Also Prevent Alzheimer’s?

While there may be treatments that can reduce the symptoms of Alzheimer’s disease, an all out cure has still managed to elude the medical field. However, BBC News reports that a recent study conducted by Korean scientists and published in Nature Communications has shown promise in reducing the brain cell-killing plaque that accumulates in patients […]

Could the Medicine You Take for Your Headaches Also Prevent Alzheimer’s?

While there may be treatments that can reduce the symptoms of Alzheimer’s disease, an all out cure has still managed to elude the medical field.

However, BBC News reports that a recent study conducted by Korean scientists and published in Nature Communications has shown promise in reducing the brain cell-killing plaque that accumulates in patients with Alzheimer’s disease.

Scientists have reasoned in the past that preventing or removing these plaques could be the key to treating Alzheimer’s. Even though some other drugs have been effective in preventing the formation of this plaque to an extent if taken early on, there are still no methods to remove existing plaque.

While the exact mechanism that eradicates abnormal buildups of this plaque is still unclear, 4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid, also known as the EPPS molecule, used in the study appeared to be effective in mice bred to generate these plaques.

The test group of mice were given water spiked with the EPPS molecule for two weeks, while the control group was given normal water. Both were then monitored for the next three months.

The EPPS mice not only had substantially fewer plaques at the end of the trial than at the beginning, but they also performed better on memory and learning problems such as completing mazes. The control group showed no improvement on either front.

Without human trials, The Alzheimer’s Society and Alzheimer’s Research U.K. said it was important to remain cautious until more funding, likely from Alzheimer’s charities, can provide the resources needed for further testing.

“From a clinician’s point of view, this research is of interest, but we still don’t know if removing amyloid plaques is useful in humans,” said Professor Tom Dening, an expert in dementia research at the University of Nottingham.

Even though the EPPS molecule on its own has only shown some promise, using it in combination with other treatments may enhance its potency. That could even include the use of some medications most people are already familiar with.

According to Tech Times, Researchers from the Boyce Thompson Institute and John Hopkins University discovered that salicylic acid, a component in Aspirin, may enhance neurological disease treatments, including those used for Alzheimer’s, Parkinson’s, and Huntington’s disease.

Salicylic acid (SA) is a natural, widely-used medicine derived directly from plant-life. SA is actually so commonly used that aspirin and acetyl SA medications have a consumption rate of an estimated 80 million tablets every day.

Usually aspirin is prescribed to reduce fever, pain and inflammation, as well as more serious conditions, such as reducing the risks of stroke, heart attacks, and even cancers.

In order to determine if the drug targeted any other factor in human health, they performed tests akin to culturing human cells. Among several other possible targets, they found a particular protein target of interest called Glyceraldehyde 3-Phosphate Dehydrogenase (GAPDH).

GAPDH is known to initiate cell death in both neuronal and non-neuronal cells, leading it to be associated with neuro-degenerative disorders, including Parkinson’s, Alzheimer’s, and Huntington’s disease.

“The enzyme GAPDH, long thought to function solely in glucose metabolism, is now known to participate in intracellular signaling,” said Solomon Snyder, co-author of the study and a professor of neuroscience at Johns Hopkins University.

Their study confirms that GAPDH is a target of salicylates, and has the potential to substantially improve therapeutic mechanisms of drugs used to treat neurological diseases.

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