How to engineer negligible senescence in humans – part II LysoSENS

Have you ever seen these kinds of people?

• mid-life
• obese
• smokers
• addicted to junk food, grills and lacking the daily salad

Did you notice they look too old for their chronological age? Why is that?

As a species which does age, we develop housekeeping issues as we age:

• our cells accumulate many types of intracellular junk that they can’t recycle

and this besides the difficulties of cleaning our bodies and our homes as we become frailer.

Our cells literally become crowded with junk – at a faster rate in people who already introduce too much junk in their bodies – yet it happens in all of us nevertheless. There are several substances which accumulate in our bodies – the best known is lipofuscin, also called the pigment of aging. Macroscopically we can see it in people with age spots – familiar, isn’t it?

Can’t our cells simply recycle this mess like they do during our youth?

The responsible organelle for intracellular recycling is the lysosome.

Its tools of the trade are:

1. specific enzymes

2. a specific acid pH

As time goes by, our lysosomes either become dysfunctional or they are not adaptable enough to deal with this kind of junk. Let’s not forget that nature doesn’t invest foolishly – by mid-life, most people were already dead by predators, starvation, accidents, so we didn’t develop better lysosomes during evolution.

What is the LysoSENS solution all about then?

The solution per se contains two main steps:

1. identify the enzymes that are able to break down this intracellular junk
2. insert such enzymes into our dysfunctional aged lysosomes

Step 1 was started when Dr. Aubrey de Grey had the idea of searching for soil bacteria which may already contain the necessary enzymes to break down lipofuscin – the current state of affairs is that a couple of such species were identified and the specific enzymes must now be identified. Caveat: lipofuscin is not the only substance we accumulate as we age, so several other enzymes may be necessary once we identify the lipofuscin-breaking ones!

Step 2 could be achieved through Enzyme Replacement Therapy (ERT) by periodically inserting such enzymes to break down the newly formed intracellular junk.

How can we test it in humans?

As previously mentioned in part I, since aging is not officially a disease, accomplishing this task will first be accomplished in diseases which share a common mechanism to one or several types of aging damage.

Enzyme Replacement Therapy may change the fate of Lysosomal Storage Diseases (LSDs) patients. Several types of intracellular junk accumulates at a faster rate and at a younger age because these patients lack certain enzymes or have dysfunctional variants of them, while healthy, normal people are able to deal with it and don’t develop their symptoms and signs.

As regards senescence, there are three types of diseases where cells become choked with intracellular junk and they all increase in incidence and prevalence as we count more years:

1. Atherosclerosis

2. Neurodegenerative brain diseases

3. Age-related macular degeneration

All these diseases may be slowed down by lifestyle, some of them can be “managed” with drugs, but none of them can be cured. Until we bring such therapies into practice – and even afterwards – it still pays to avoid putting more junk than necessary into your body – by not smoking, by avoiding working in toxic environments and of course, by eating less in the first place!

So this is the plan for LysoSENS, but that’s not all that needs to be done. As we age we accumulate extracellular junk too – more about it in the next part!

Bibliography:

“Ending aging” by Aubrey de Grey (link)

Anca Ioviţă is the author of Eat Less Live Longer: Your Practical Guide to Calorie Restriction with Optimal Nutrition available on Amazon and several other places. If you enjoyed this article, don’t forget to sign up to receive updates on her second book regarding a comparative biography of aging from the simplest to the most complex organisms known.