Scientists have now discovered a gene that accelerates aging in elders of the age of 65 years or older, and contributes to neurodegenerative diseases. This revelation can shape future policies and course of treatment for neurodegenerative diseases such as dementia.
The study was carried out by scientists from Columbia University Medical Center (CUMC) and was published in the journal Cell Systems.
Professor of pathology at CUMC and study’s co-author, Asa Abeliovich said,” If you look at a group of seniors, some will look older than their peers and some will look younger. The same differences in aging can be seen in the frontal cortex, the brain region responsible for higher mental processes.”
Asa further went on to say, “Our findings show that many of these differences are tied to variants of a gene called TMEM106B. People who have two ‘bad’ copies of this gene have a frontal cortex that, by various biological measures, appears 12 years older that those who have two normal copies.”
The researchers admitted that previously man studies have managed to identify single genes that contribute to diseases such as Alzheimer’s, but they only cause small changes that affect the neurobiology of nerve cells, hence their contribution is not that significant.
One such gene is apolipoprotein E (APOE) which increases risk for Alzheimer’s, but damage caused by individual genes is quite insignificant considering the major risk factor for neurodegenerative disease, aging.
The researchers pointed out that according to their research, the biomarkers are more accurate and present themselves in the frontal vortex part of the brain, the part which is responsible for higher mental processes.
The gene in question is a variant of the TMEM106B gene. If a person has two ‘bad’ copies of this gene, their frontal cortex appears to be 12 years older than normal. To reach this conclusion, the scientists had to analyse brain samples of 1906 carcasses.
Firstly, they assessed the gene expression levels, also known as transcriptome levels of the autopsied bodies, which helped paint a picture of the brain’s chemistry at different ages of an individual’s life.
After which, the scientists compared the transcriptome data with the mean transcriptome levels of individuals at that age. Luckily the scientists managed to narrow down their investigation to 100 genes that they know expressed themselves differently with age.
Then they compared the difference with the individual’s actual bioligcal and their perceived age, this helped to assess how badly the genes affected the aging process. This comparison helped to assess the state of the frontal cortex, that is whether it was younger or older than its actual age.
The scientists then looked for the genome of each person, looking for specific genetic copies that were linked with an increase in differential age. They also found other variants beside the TMEM106B gene, inside the progranulin gene, but its contribution in aging was much less significant than TMEM106B.
Although both genes are located on different chromosomes, their involvement is in the same signaling pathway, and both are responsible for a rare neurodegenerative condition known as frontotemporal dementia.
Frontotemporal dementia collectively defines a set of rare conditions that mostly affect the frontal and temporal lobes of the brain. The study however did not show how the genes increase risk of neurodegenerative diseases.
The scientists also mentioned that aging and neurodegenerative diseases are deeply connected and go hand in hand with each other, since aging increases risk of neurodegenerative diseases, while neurodegenerative diseases accelerate aging and cause early death.
Luckily for us, as time passes on and technology improves we might be able to clearly see why and how these genetic factors contribute to neurodegenerative diseases such as alzheimers, parkinsons etc, hence better inform patients how to better take care of themselves, how to reverse aging and possibly even cheat death.