Jake Bugg at Brighton Dome
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Jake Bugg at Brighton Dome

Matthew Nicholls - April 19, 2018

Young blood promotes brain regeneration

On the “growing old is natural” vs “it should be medically reversed” debate, vampires have crossed the picket line from the get-go and scientists have just proven they may have been onto something.

THeir solution to the problem of ageing is clear; vampires suck juvenile blood to stay alive and regain their own youth. Stealing children to use as blood banks would probably scare off your friends and family but do vampires know something we don’t?

Recent scientific research suggests that we could reverse the ageing process using a newly identified biological molecule found in young blood that restores the regenerative capacity of old brains.

A signpost of getting old is a decline in our cognitive ability, mainly noticed by the worsening of our memory and a difficulty when trying to learn new things.

Our brains undergo this due to a reduction in neurogenesis, the process by which neural progenitor cells produce fresh neurons. Evidence suggests that when we age the number of these cells drop but epigenetic mediators are also thought to play a role in age-related regenerative decline.

Epigenetic mediators are molecules which cause the structure of DNA to change, resulting in altered gene expression. Within the last few years, research using heterochronic parabiosis studies (anatomically linking two animals) have shown that exposing aged individuals to young blood can lead to the rejuvenation of many functions in an ageing brain. In these studies, a young mouse’s vascular system is joined to an older mouse, exposing the older mouse to the younger blood.

A new study published in Cell Reports, identified Tet2 as an epigenetic enzyme, a chemical that can alter how genes are expressed and the proteins they produce. Tet2 can undergo regenerative decline and enhance certain cognitive functions in the adult mouse brain.

The infusion of young blood into adult mice caused Tet2 levels to increase in the hippocampus, the area of the brain involved in memory and learning. Tet2 is evolutionarily conserved between mice and humans and catalysed the oxidation of 5-methylcytosine to 5-hydroxy-methylcytosine, associated with age-related disorders such as stroke, cardiovascular diseases, and cancer.

The tag that Tet2 leaves on DNA has been shown to decline in the hippocampus with age, confirming that the DNA of young mice is regulated differently than older ones. Interestingly, the genes which are affected by this epigenetic change are the ones which have been previously associated with the process of neurogenesis.

Tet2 is clearly a key player in cognitive decline as young mice with inhibited Tet2 lost their ability to birth new neurons and perform simple memory tasks but mice with over-expressed Tet2 showed a significant improvement in memory tasks.

These findings show that Tet2 can rescue regenerate decline and enhance some cognitive functions in the adult mouse brain. Although ageing is something we will all go through, it can be rather ambiguous.If our brains remain healthy and able to continue neurogenesis, we would stay young forever even if your bodies wrinkle and ache, at least in theory.

What is of more scientific interest, however, is that targetting Tet2 could also lead to better therapies for treating neurological disorders such as Alzheimer’s and Parkinson’s disease.

It remains to be confirmed whether these findings are translatable to human systems but they do provide an exciting approach to targeting adult stem cell functions to rejuvenate regenerative capacity. So you can put your fangs away, for now.

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