TFAM Protein: Investigational Treatment for Neurodegenerative Diseases?

In summary: Code=annphamIn summary, the TFAM protein successfully entered and energized the DNA of the mice's mitochondria, enabling them to run two times longer on their rotating rods than a control group cohort. The study also describes a scalable method of producing the protein in needed quantities.
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Does using the TFAM protein like this solve the problem of oxidative DNA to the mitchondrial DNA? thanks why/why not? can anyone shed some light on this? thanks

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An investigational protein that transformed normal laboratory mice into super-jocks holds great promise in developing new treatments for neurodegenerative diseases like Parkinson's, Alzheimer's and ALS (Lou Gehrig's Disease), say researchers at the University of Virginia Health System.

A study published in the February 17, 2009 online edition of Mitochondrion reports that the protein, rhTFAM (an abbreviation for recombinant-human mitochondrial transcription factor A), succeeded in entering and energizing the DNA of the mice's mitochondria, enabling them to run two times longer on their rotating rods than a control group cohort.

Because many neurodegenerative diseases cause mitochondria to malfunction, medical researchers have been focusing on developing methods for repairing and restoring them. The new UVA study represents an important step toward achieving that goal. It shows that a naturally occurring protein, TFAM, can be engineered to rapidly pass through cell membranes and target mitochondria. Study findings show that rhTFAM acts on cultured cells carrying a mitochondrial DNA disease as well as lab mice.

Conducted in conjunction with Gencia Corporation, a Charlottesville-based biotechnology firm that owns rhTFAM, the study also describes a scalable method of producing the protein in needed quantities.

Mitochondria are the cellular engines that transform food into fuel in our bodies and perform their work in the energy-intensive tissue of our brains, retinas, hearts and skeletal muscles. When damaged, mitochondria slow down, stop generating energy effectively and begin to over-produce oxygen free radicals. If produced in excess, oxygen free radicals chemically attack all cell components, including proteins, DNA and lipids in cell membranes.

"In simple terms, an overabundance of these free radicals cause cells to start rusting," notes lead study author James P. Bennett, Jr., M.D., PhD, a professor of neurology and psychiatric research at the UVA School of Medicine and director of its Center for the Study of Neurodegenerative Diseases.

While the UVA findings are preliminary, Bennett considers them encouraging. "We've shown that the human mitochondrial genome can be manipulated from outside the cell to change expression and increase mitochondrial energy production," he notes. "This is arguably the most essential physiological role of the mitochondria."

Although important questions remain about the technology, mechanisms and therapeutic potential of rhTFAM, Bennett believes his team's findings could contribute to the development of treatments that repair and restore damaged mitochondria in cells. "We're looking toward the day when we can reverse or delay the progression of various neurodegenerative diseases and other conditions where cell energy production is deficient, including cancer, diabetes and aging," he says.

Gencia made rhTFAM available to UVA under a material transfer agreement. One study author, Francisco R. Portell, has an affiliation with the company.

Study authors also include Shilpa Iyer, Ravindar R. Thomas, Lisa D. Dunham and Caitlin K. Quigley. All work at the Center for the Study of Neurodegenerative Diseases and the Morris K. Udall Parkinson's Disease Research Center of Excellence at UVA.
 
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  • #2

Related to TFAM Protein: Investigational Treatment for Neurodegenerative Diseases?

1. What is TFAM protein and how does it work?

TFAM (mitochondrial transcription factor A) is a protein that plays a crucial role in the maintenance and regulation of mitochondrial DNA. It helps to initiate transcription of mitochondrial genes, which are responsible for producing proteins essential for mitochondrial function. In neurodegenerative diseases, TFAM protein levels are often decreased, leading to mitochondrial dysfunction and cell death.

2. What are the potential benefits of using TFAM protein as an investigational treatment for neurodegenerative diseases?

Studies have shown that increasing TFAM protein levels can improve mitochondrial function and reduce cell death in neurodegenerative diseases such as Alzheimer's and Parkinson's. This could potentially slow down or even reverse the progression of these diseases, providing significant benefits for patients.

3. What stage is the research on TFAM protein currently at?

TFAM protein is still in the preclinical stage of research, meaning it has not yet been tested on humans. However, promising results from animal studies have led to further investigation and potential clinical trials in the near future.

4. Are there any potential risks or side effects associated with TFAM protein treatment?

As with any new treatment, there are potential risks and side effects that need to be carefully evaluated. However, since TFAM protein is a naturally occurring protein in the body, it is expected to have minimal side effects. Further research will be needed to determine any potential risks.

5. When can we expect TFAM protein to be available as a treatment for neurodegenerative diseases?

It is difficult to predict an exact timeline for when TFAM protein may become available as a treatment for neurodegenerative diseases. The research is still in the early stages and will require further testing and clinical trials before it can be approved for use in patients. It is important to continue to support and fund research in this area to potentially bring TFAM protein treatment to patients in the future.

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