Drug already approved for treating Parkinson's could help Alzheimer's patients cleanse their brains: ScienceAlert

Both Parkinson's and Alzheimer's are the result of a continuous loss of neurons. However, both diseases affect different areas of the brain and under completely different conditions.

A new study suggests that a drug already approved to treat Parkinson's disease could serve another purpose: It could improve treatments that help dissolve toxic clots blamed for the most common form of dementia.

As it enters the brain, the drug – called levodopa (or L-DOPA) – converts into the hormone dopamine, a neurotransmitter closely linked to feelings of happiness and motivation that is known to be lacking in brains affected by Parkinson's disease.

This new study, led by researchers at the RIKEN Center for Brain Science in Japan, found that giving dopamine to the brains of mice suffering from an Alzheimer's-like disease was associated with improvements in physical symptoms and memory.

The target of the dopamine-boosting drug is the enzyme neprilysin. Previous studies have shown that this enzyme Dissolve clumps of beta-amyloid protein that clog the brains of Alzheimer's patients, destroying neurons.

Unfortunately, neprilysin cannot pass from the bloodstream into the brain and eliminate the toxic substances there. Therefore, the scientists had to find a way to smuggle the enzyme beyond the body's boundaries.

Through a comprehensive battery of laboratory tests, the team discovered that applying dopamine to neurons in the cortex, hippocampus and basal ganglia increased neprilysin levels and reduced beta-amyloid plaques. Further tests on living mice had the same effect: dopamine increased neprilysin production and reduced the brain damage associated with Alzheimer's.

As a precursor substance that is converted into dopamine in the brain, levodopa was the last link in the chain of experiments. The team also observed a decline in dopamine and neprilysin in older mice, which may be another important clue to the development of Alzheimer's.

“In older mice, dopamine and neprilysin levels in the frontal cortex were lower, a decline that was even more pronounced in Alzheimer's model mice,” the researchers write in their published paper.

“Treatment of Alzheimer model mice with levodopa reduced beta-amyloid deposition and improved cognitive function.”

This is all very promising, but many questions remain. For example, researchers are not sure why dopamine increases neprilysin levels.

Although levodopa is widely approved as a Parkinson's treatment, it is not without side effects, especially with long-term use. Clinical trials will be needed to see if these results can be reproduced in humans and to ensure that the treatment does not do more harm than good.

“It is known that treatment with L-DOPA has severe side effects in patients with Parkinson’s disease,” says RIKEN neuroscientist Watamura Naoto.

“Our next step is therefore to investigate how dopamine regulates neprilysin in the brain. This should lead to a new preventive approach that can be initiated already in the preclinical stage of Alzheimer's disease.”

The study was published in Science signaling.