Health
Dopamine treatment eases Alzheimer's symptoms
A new way to fight Alzheimer's disease has been discovered by Takaomi Nishido and his team at the RIKEN Center for Brain Science (CBS). Using mice with Alzheimer's disease, the researchers found that treatment with dopamine can alleviate physical symptoms in the brain and improve memory. The study was published in the journal Science. Science Signaling The study, published August 6, examines the role of dopamine in promoting the production of neprilysin, an enzyme that breaks down harmful plaques in the brain that are a hallmark of Alzheimer's. If similar results are obtained in human clinical trials, they could lead to fundamentally new treatments for Alzheimer's.
The formation of hardened plaques around neurons is one of the earliest signs of Alzheimer's disease, often starting decades before behavioral symptoms such as memory loss are noticeable. These plaques form from fragments of the peptide beta-amyloid that builds up over time. In the new study, Saido's team at RIKEN CBS focused on the enzyme neprilysin, because previous experiments showed that genetic engineering to produce excess neprilysin in the brain (a process called upregulation) reduced beta-amyloid plaques and improved memory in mice.
While genetically engineering mice to produce neprilysin is useful ly, treating patients with the disease requires drug therapy. Taking pills or injecting neprilysin is not practical because it cannot enter the brain through the bloodstream. So the first step in the new study was to painstakingly screen many molecules to determine which ones could naturally upregulate neprilysin in the right parts of the brain. Building on previous work, the team narrowed their search to a hormone produced in the hypothalamus, and found that administering dopamine to brain cells grown in a culture dish increased neprilysin levels and reduced levels of free beta-amyloid.
Now the real experiments began. Using the DREADD system, the researchers inserted tiny designer receptors into dopamine-producing neurons in the ventral tegmental area of mice. By adding a matching designer drug to the mice's food, the researchers could continuously activate only those neurons in the mice's brains. Just like in the dish, the activation increased neprilysin and reduced levels of free-floating beta-amyloid, but only in the front of the mice's brains. But can treatment remove plaques? Yes, it can. The researchers repeated the experiment using a special mouse model of Alzheimer's disease, in which mice form beta-amyloid plaques. Eight weeks of chronic treatment resulted in a significant reduction in plaques in the prefrontal cortex of these mice.
The DREADD system is a great system for precisely manipulating specific neurons. However, it is not very useful in a human clinical setting. In the last experiment, we tested the effect of L-DOPA treatment. L-DOPA is a dopamine precursor molecule that is often used to treat Parkinson's disease because it enters the brain from the blood and is converted to dopamine there. Treating model mice with L-DOPA increased neprilysin and reduced beta-amyloid plaques in both the frontal and posterior parts of the brain. Model mice treated with L-DOPA for three months performed better on memory tests than untreated model mice.
The results showed that in normal mice, neprilysin levels naturally decrease with age, especially in the frontal regions of the brain. This makes neprilysin a potential biomarker for diagnosing pre- or at-risk stages of Alzheimer's disease. How dopamine increases neprilysin levels remains unclear, and this is the next research topic for Dr. Said's group.
“We have shown that L-DOPA treatment helps reduce harmful beta-amyloid plaques and improves memory function in a mouse model of Alzheimer's disease,” explains Naoto Watamura, first author of the study. “However, L-DOPA treatment is known to have serious side effects in Parkinson's disease patients. Therefore, our next step is to investigate how dopamine regulates neprilysin in the brain. This should lead to new preventive approaches that can be initiated at the preclinical stage of Alzheimer's disease.”
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Sources 2/ https://www.sciencedaily.com/releases/2024/08/240806163735.htm The mention sources can contact us to remove/changing this article |
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