- One of the hallmarks of Alzheimer’s disease are beta-amyloid plaques in the brain.
- Many recent studies have looked for ways to treat and remove beta-amyloid plaques.
- Researchers from the RIKEN Center for Brain Science saythe hormone dopamine may be used as a treatment for Alzheimer’s.
- Using a mouse model, researchers stimulated the production of an enzyme known to break down beta-amyloid plaques.
Clumps or plaques of the protein beta-amyloidTrusted Source in the brain are a hallmark of a type of dementia called Alzheimer’s disease.
When beta-amyloid plaques form, they disrupt communication between nerve cells. They can also stimulate the immune system, causing inflammation that eventually destroys brain cells.
Over the last few years, researchers have been focusing on finding ways to treat beta-amyloid plaques to help slow Alzheimer’s disease progression. For example, two anti-amyloid medications, lecanemab and donanemab, are FDA-approved to help decrease the amount of plaques in people with early Alzheimer’s.
Now, researchers from the RIKEN Center for Brain Science in Japan believe the hormone dopamineTrusted Source may be used to treat Alzheimer’s as it stimulates the production of an enzyme known to break down beta-amyloid plaques in the brain via a mouse model.
The study was recently published in the journal Science Signaling.
For this study, researchers focused on stimulating the production of an enzyme in the body called neprilysinTrusted Source.
Neprilysin is an endopeptidaseTrusted Source, the scientific term for an enzyme that divides peptideTrusted Source bonds.
Past studies have also examined the potential role neprilysin may play in Alzheimer’s disease as it has shown to be effective in degrading beta-amyloidTrusted Source in the brain.
A study published in December 2023 reported that using a neprilysin inhibitorTrusted Source led to increased beta-amyloid.
Research published in December 2022 found injecting a form of neprilysin that can penetrate the blood-brain barrierTrusted Source showed the potential to reduceTrusted Source beta-amyloid plaques in the brain.
To conduct this study, scientists first found when they applied dopamine to brain cells cultured in a dish, neprilysin levels increased and levels of free-floating beta-amyloid decreased.
Next, using a mouse model, researchers used the Designer Receptors Exclusively Activated by Designer Drugs (DREADD) systemTrusted Source to insert minute designer receptors into the dopamine-producing neurons in the ventral tegmental areaTrusted Source of the brain, which is known to stimulate dopamine neurons.
Scientists also fed the mice a matching designer drug. This resulted in an increase in neprilysin production and decreased levels of free-floating beta-amyloid.
Researchers then applied this method to a special mouse model of Alzheimer’s disease where the mice develop beta-amyloid plaques. After eight weeks of treatment, scientists reported the amount of beta-amyloid plaques in the mice decreased.
For the final step of the study, researchers applied their methodology to L-DOPATrusted Source treatment, a dopamine precursor molecule used to treat Parkinson’s disease. Treating the mouse model with L-DOPA led to increased neprilysin and decreased beta-amyloid plaques in the brain.
Scientists also discovered that after three months of L-DOPA treatment, the mice performed better on memory tests than untreated mice.
“We have shown that L-DOPA treatment can help reduce harmful beta-amyloid plaques and improve memory function in a mouse model of Alzheimer’s disease,” said lead study author Naoto Watamura, PhD, from the Laboratory for Proteolytic Neuroscience at the RIKEN Center for Brain Science, in a news release.
“But L-DOPA treatment is known to have serious side effects in patients with Parkinson’s disease. Therefore, our next step is to investigate how dopamine regulates neprilysin in the brain, which should yield a new preventive approach that can be initiated at the preclinical stage of Alzheimer’s disease,” Watamura continued.
David Merrill, MD, PhD, a board certified geriatric psychiatrist at Providence Saint John’s Health Center in Santa Monica, CA, and Singleton Endowed Chair in Integrative Brain Health, told Medical News Today the study shows an underappreciated connection between dopamine and its effects on beta-amyloid plaques in the brain.
“The study goes further in identifying upregulation of neprilysin as (a) possible mechanism for this observed effect,” Merrill continued. “We do see that some Parkinson’s patients also develop Alzheimer’s type amyloid plaques, but interplay between these two neurodegenerative disorders are complex and remain incompletely understood.”
MNT also spoke with Manisha Parulekar, MD, director of the Division of Geriatrics at Hackensack University Medical Center and associate professor at Hackensack Meridian School of Medicine in New Jersey, who expressed excitement about this new research.
“The findings suggest that dopamine treatment could be a potential new way to combat the disease, which is desperately needed,” Parulekar continued.
“I was particularly impressed by the fact that the researchers were able to reduce beta-amyloid plaques in the brains of mice with Alzheimer’s disease using L-DOPA.”
“Beta-amyloid plaques are a hallmark of the disease and are thought to contribute to its progression. If L-DOPA can be shown to be effective in reducing beta-amyloid plaques in humans, it could be a major breakthrough in the treatment of Alzheimer’s disease. We continue to look for effective treatment for Alzheimer’s. Repurposing existing medications may be helpful in expediting the process.”
— Manisha Parulekar, MD, geriatric medicine physician
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