Researchers at Stanford Medicine have reported a discovery that could change how doctors think about treating Parkinson’s disease.
Their study, published in the journal Science Signaling, found that blocking an overactive enzyme helped damaged brain cells recover in mice.
Although the work is still in animals, it offers hope that future treatments may slow the disease or even repair some of the early damage.
Parkinson’s disease is a long-term brain disorder that affects millions of people around the world.
The disease mainly damages nerve cells that produce dopamine, a chemical messenger that helps control movement, balance, learning, motivation, and many everyday activities.
As these cells become sick or die, people gradually develop shaking, muscle stiffness, slow movement, and problems with walking.
Many cases of Parkinson’s develop without a clear cause, but some are linked to inherited gene changes. One of the best-known genes is called LRRK2. Changes in this gene make an enzyme become too active, which can interfere with the normal function of brain cells.
The Stanford researchers wanted to understand exactly how this overactive enzyme harms the brain. They focused on tiny structures called primary cilia. These small, hair-like structures sit on the surface of many cells and work like antennas, allowing cells to receive important chemical messages from their neighbors.
When the LRRK2 enzyme became overactive, many brain cells lost these tiny antennas. Without them, the cells could no longer receive an important signal from a protein called sonic hedgehog. This signal normally tells nearby support cells to produce protective substances that help dopamine-producing neurons survive.
The team tested a compound called MLi-2, which blocks the LRRK2 enzyme. At first, the mice received treatment for only two weeks, but the researchers saw little change. They later realized that rebuilding primary cilia takes time, so they extended the treatment to three months.
After the longer treatment, the results were much more encouraging. The primary cilia returned, communication between brain cells improved, and the protective signaling pathway became active again. The scientists also found signs that damaged dopamine neurons were beginning to recover instead of continuing to decline.
Senior author Dr. Suzanne Pfeffer explained that this finding is especially exciting because Parkinson’s disease begins many years before movement problems appear. Early symptoms may include a reduced sense of smell, constipation, and sleep disturbances. Treating people during this early stage could delay or prevent more serious symptoms.
The researchers believe this approach may also help patients who do not carry the LRRK2 mutation, although this still needs to be tested. Several clinical trials of LRRK2 inhibitors are already underway, meaning scientists are actively exploring whether these medicines are safe and effective for people.
This study provides important new clues about why brain cells fail in Parkinson’s disease and how they may be protected. However, the research was performed in mice, so it does not prove the same benefits will occur in humans.
Much more research and carefully designed clinical trials are needed before this treatment can become routine. Even so, the findings are encouraging because they suggest that restoring normal communication between brain cells may become a powerful new strategy for slowing Parkinson’s disease rather than simply treating its symptoms.
If you care about Parkinson’s disease, please read studies that Vitamin B may slow down cognitive decline, and Mediterranean diet could help lower risk of Parkinson’s.
For more health information, please see recent studies about how wheat gluten might be influencing our brain health, and Olive oil: a daily dose for better brain health..
Source: Stanford Medicine.
