Health

Major Alzheimer’s breakthrough: Surprising Parkinson’s drug hints at new treatment

Scientists have identified a potential new target for treating Alzheimer’s disease that works by restoring the brain’s “self-cleaning” process.

The target is already used in pre-existing drugs against Parkinson’s disease and has demonstrated partial reversal of cognitive deficits in the aged mice studied.

According to the Centers for Disease Control and Prevention (CDC), Alzheimer’s disease affects approximately 5.8 million Americans. This progressive disease is the most common form of dementia and is associated with memory loss and cognitive decline in the brain regions involved in thinking, memory, and language.

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There is no known cure for Alzheimer’s disease, but scientists believe it is caused by an abnormal buildup of proteins in and around brain cells. One of the main components of these abnormal clumps is a protein called beta-amyloid.

Amyloid beta protein is produced when proteins in the brain misfold and clump together. These clumps trigger a series of harmful chemical reactions around our brain cells that damage and eventually destroy them.

Normally, our brain’s cellular cleaning team, which includes an enzyme called neprilysin, removes any excess proteins and cellular debris.

“Neprilysin has been identified as the most potent amyloid-beta degrading enzyme in the brain,” said Naoto Watamura, a researcher at the UK Institute of Dementia Research at University College London and the RIKEN Brain Science Center in Japan. News week.

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Major Alzheimer’s breakthrough: Surprising Parkinson’s drug hints at new treatment
Artist’s rendering of abnormal protein accumulations around neurons in the brains of Alzheimer’s patients. Scientists have identified a potential new target for treating Alzheimer’s disease.

Selvanegra/Getty

However, preliminary data have shown that with age, neprilysin levels in the brain tend to decrease. Studies have also shown that genetically modified mice that do not produce this enzyme develop very high levels of toxic beta-amyloid protein aggregates.

But while these findings suggest that neprilysin plays a key role in the onset of neurodegenerative diseases, methods to target and upregulate its activity have remained elusive – until now.

In a new study published in the journal Scientific signalingWatamura and his colleagues at the RIKEN Brain Sciences Center screened a range of different candidate compounds and found one molecule that could upregulate the activity of this essential enzyme: dopamine.

You may have heard of dopamine as the “pleasure hormone” because of its role in the brain’s reward center. But this neurotransmitter also plays many other roles in our brains. “Dopamine regulates emotion, movement, and motivation,” Watamura said.

And, according to these results, dopamine may also play a role in preventing cognitive decline.

Studying mice, the team found that dopamine release was associated with an increase in the abundance of neprilysin and a subsequent breakdown of beta-amyloid accumulations in the brain’s “personality center,” also known as the prefrontal cortex.

This is not really surprising, as dopamine (or its lack) has already been shown to play a significant role in the development of Parkinson’s disease. Indeed, the majority of existing Parkinson’s medications work by increasing dopamine levels in the brain or mimicking its effects.

One of the main drugs used to treat Parkinson’s disease is levodopa, a precursor to dopamine that is synthesized in the brain’s neurotransmitter. By administering these approved Parkinson’s drugs to aged mice and mice designed to model Alzheimer’s symptoms, Watamura and his colleagues found similar improvements in brain amyloid beta levels and a partial reversal of cognitive deficits.

“I was (surprised) because dopamine, which is likely to be the central role in Parkinson’s disease, might have the potential to treat the Alzheimer’s disease aspect of pathology,” Watamura said.

Their findings may also shed light on established associations between dementia and mental health disorders linked to low dopamine levels.

Further research is needed to confirm these findings in humans, but the researchers hope their results could offer new targets for treating Alzheimer’s disease.

“Based on these results, we want to study another downstream mechanism by which dopamine regulates neprilysin and develop the fundamental therapy for Alzheimer’s disease,” Watamura said.

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