Mitochondrial DNA Insertions into Nuclei of Brain Cells

 

It has recently been discovered that mitochondria have been inserting bits of mitochondrial DNA into the nuclei of brain cells at unusually high rates. During a study on over 1,200 older adults, it was found that the more mitochondrial insertions an individual had, the younger they died. One of the normal functions of mitochondria is to ship their DNA into the nucleus of the cell to integrate it with the nuclear DNA in a process called numtogenesis. Numtogenesis has been commonly observed in reproductive cells and cancer cells but has never before been observed in brain cells. These insertions were studied on blood cells and brain tissue from the cerebellum and the dorsolateral prefrontal cortex, or DLPFC. What they found is that cells from the DLPFC had an average of 15 times as many insertions as the blood cells and 5 times as many insertions as the cerebellar cells. It was also discovered that mitochondrial insertions increased under certain stressors such as drug treatments or genetic mutations.

 

In my opinion, this is something that definitely needs more attention. I believe this is something necessary to further study. This study seems to suggest that numtogenesis is somehow linked to life span. Since the DLPFC has been known to be affected by many age related and neurodegenerative conditions, the higher rate in mitochondrial insertions in the DLPFC could provide a potential explanation or be linked as a factor. With this knowledge we could potentially develop improved treatments for these conditions.

Mutation Helps Even Carriers of 'Alzheimer's Gene' Avoid Alzheimer's

 

In this article written by Dennis Thompson of HealthDay, published by USNews, the author discusses new research on a cell function-boosting mutation that could help protect even carriers of Alzheimer’s disease from developing it. The mutation causes cells to produce a more powerful version of the protein humanin, which protects against cellular aging. 

Researchers examined over 500 participants, including people 100 years old or nearing 100, and their children. Of these people, they found that 12% of centenarians of Ashkenazi descent carried the P3S variant, which codes for higher levels of humanin. 

They then turned to genetically engineered mice altered to carry the APOE4 gene associated with a higher risk of Alzheimer’s. Researchers treated the mice with PS3 gene-produced humanin. The mice then displayed a marked reduction in amyloid beta, the protein associated with Alzheimer’s that builds up in the brain and impairs cognitive function. This research suggests that the P3S variant may be a reason why carriers of the APOE4 gene avoid Alzheimer’s.  

I found this research to be both fascinating and incredibly relevant to me. My grandmother died of Alzheimer’s, as have many of my other family members. Her caretakers were always giving her medications and I never understood how they helped. This research could lead to future treatments, and as there is a likelihood that I personally carry the APOE4 gene, I find it important to be well informed on the subject. Additionally, I believe it is important for all people to be educated on the disease. It is important to know the signs and symptoms, as dementia can be a common misdiagnosis before motor functions become impaired.   

Article: Mutation Helps Even Carriers of 'Alzheimer's Gene' Avoid Alzheimer's

Additional Info: A rare mutation protects against Alzheimer's disease, Stanford-led research finds