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Mitochondria are dynamic. They are constantly changing in size, number and location, traveling between many different parts of the cell to meet different demands. Photo used for representational purposes only | Photo credit: Getty Images/iStockphoto
In 1817, a British physician named James Parkinson published An essay on tremor paralysisFirst describing cases of the neurodegenerative disorder now known as Parkinson’s disease. Today, Parkinson’s disease is the most common disease. Second most common neurodegenerative disease It affects approximately 1 million Americans in the U.S. and more than 10 million worldwide.
The characteristic tremor that occurs in patients suffering from this disease is the result of Dying brain cells that control movementTo date, there is no treatment available that can stop or slow the death of those cells.
we are Researchers conducting the studyParkinson’s diseaseFor more than a decade, Our Laboratory The role of mitochondria — the powerhouses that fuel cells — in Parkinson’s disease is being investigated.
Our research proves that A key protein was identified This could raise the possibility of new treatments for Parkinson’s disease and other neurological conditions.
Mitochondrial dynamics and neurodegeneration
Unlike true power plants, which are fixed in size and location, mitochondria are quite dynamic. They constantly change in size, number, and location, traveling between many different parts of the cell to meet different demands. Mitochondrial dynamics These are important not only for the function of mitochondria, but also for the health of cells as a whole.
A cell is like a factory. Many departments must work together for smooth operation. Since many key processes are interconnected, a decrease in mitochondrial mobility can cause a domino effect across departments and vice versa. Collective malfunction The inflammation that occurs in various parts of the cell ultimately leads to cell death.
Emerging studies have linked imbalances in mitochondrial processes Different Neurodegenerative DiseasesInvolved Parkinson’s diseaseIn many neurodegenerative disorders, certain disease-associated factors, such as toxic proteins and environmental neurotoxins, disrupt the harmony of mitochondrial fusion and division.
Impaired mitochondrial dynamics also destroys the cell Cleaning and waste recycling processesThis leads to the accumulation of toxic proteins that form harmful aggregates inside the cell. In Parkinson’s, the presence of these toxic protein aggregates is a Diagnosis of the disease,
Targeting mitochondria to treat Parkinson’s
Our team hypothesized that restoring mitochondrial function by altering its dynamics could provide protection against neuronal dysfunction and cell death.
In an attempt to restore mitochondrial function in Parkinson’s, we targeted a key protein that regulates mitochondrial dynamics Dynamin-related protein 1, or Drp1This protein, naturally found in abundance in cells, is transported to mitochondria when they divide into smaller sizes for greater mobility and quality control. However, too much Drp1 activity causes excessive division, leaving mitochondria fragmented and impairing function.
Using various laboratory models of Parkinson’s, including neuronalcell cultures and the mouse and mice In the model, we found that the presence of environmental toxins and toxic proteins associated with Parkinson’s causes mitochondria to become fragmented and dysfunctional. Their presence coincides with the build-up of those same toxic proteins, leading to poor health and eventual death of neuronal cells.
We also observed behavioral changes in the mice that affected their movements. However, by reducing the activity of Drp1, we were able to restore mitochondria Their general movement and functioning improved. Their neurons were protected from the disease and they were able to continue their work.
In our 2024 study, we found Additional benefits To target Drp1.
we exposed neuronal cells to manganese, a heavy metal is associated with an increased risk of neurodegeneration and parkinsonism. Surprisingly, we found that manganese was higher Harmful to the cell’s waste recycling system Compared to its mitochondria, toxic proteins build up before the mitochondria become inactive. However, inhibiting Drp1 reactivated the waste recycling system, allowing toxic proteins to be cleared despite the presence of manganese.
Our findings indicate that blocking Drp1 through more than one pathway could protect cells from decay. Now, we have identified a few FDA-approved compounds that target Drp1 and are testing them as potential treatments for Parkinson’s.
Rebecca Zhangqiuzhi Fan is a Post-Doctoral Research Associate in Environmental Health Sciences at Florida International University
Kim Tieu is a professor of environmental health sciences at Florida International University
This article is republished from The Conversation under a Creative Commons license. Read the original article Here
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