Producing stem cells from other persons would be a major step forward.
Usually, stem cells are made from cells from your own body. Taking a cell from your body, like a skin cell, and converting it into a stem cell is a time-consuming and very expensive process.
However, if you could use ready-made stem cells derived from other people, this would hasten the process considerably. You can pick prepared stem cells from the shelf and immediately implant them.
Also, these stem cells could be acquired from young people, so that these stem cells are also younger and less damaged. This is very interesting, because mostly elderly people would need stem cell treatments and creating stem cells from their already aged cells yields stem cells of lower quality compared to stem cells extracted from young people.
The Nobel prize winner Shinya Yamanaka is setting up a stem cell bank with stem cells of other people, tweaking specific receptors on the stem cells (HLA receptors), so that these stem cells won’t be rejected by a considerable part of the population.
Such stem cells could be produced in large quantities, can be of better quality when derived from a young person and would be immediately available, which would all entail huge advantages.
In the future, new technologies like CRISPR-cas 9 will allow scientist to tweak stem cells even more, giving them all kinds of new qualities, like evading rejection by the host, being more powerful, specific or versatile, among other things.
Source: Scientific American
CRISPR-cas9 is one of the most promising new developments in medicine, and in science in general.
For decades, editing genes was a laborious, difficult and expensive process. It could take many months to years to change just one gene, and it would cost hundreds of thousands of dollars, while requiring a state of the art lab. Presently, with CRISPR-cas9 you can change a gene in less than a day at a cost of around 50 dollars.
However, CRISPR-cas9, how revolutionary it may be, is being superseded by even better versions.
In other words, CRISPR 2.0 has arrived.
This is technology like CRISPR–cpf1, which is a smaller, less complex version of the original CRISPR-cas9 protein. Because of its smaller size, CRISPR-cpf1 is easier to insert into viruses, which can carry it into cells. Another advantage is that CRISPR-cpf1 cuts the DNA in a better way (it creates “sticky ends” instead of “blunt ends”).
Another example is DNA base editors. The team of professor David Liu at Harvard University developed an adenine base editor (ABE), which is a hybrid of a cas9 protein and a protein that can edit specific pieces of DNA, called adenines.
Base editors are much more accurate than CRISPR-cas9, and this by a long margin. Contrary to CRISPR-cas9, they create much less double-strand breaks and other (off-target) mutations.
The adenine base editor can change an adenine base into a guanine base, which could fix about half of the 32 000 point mutations that cause disease (point mutations account for about two third of the mutations in the human genome associated with disease – about 32000 out of the 50000 disease-causing mutations).
Besides CRISPR-cas9, also CRISPR–cas13 has been developed, which can modify RNA instead of DNA, opening up a whole new world of possibilities to modify the transcriptome, enabling more fine-tuned control of cells compared to editing the genome (DNA).
The toolbox to manipulate the genome, transcriptome, and epigenome is being extended on a continuous basis, paving the way for the manipulation of cells, and life, in ways never seen before.
We are often being told – especially by sellers of food supplements and skin cremes- that antioxidants slow down the aging process. Antioxidants would delay aging by mopping up reactive free radicals that otherwise damage our DNA. These dreadful free radicals are produced as a side effect by our metabolism.
But mounting evidence shows that antioxidants don’t slow down aging. And the free radicals aren’t always the bad guys. Free radicals can even function as a benign warning sign, revving up the cell’s defense mechanisms, like detoxification enzymes and repair proteins, protecting our cells against age-related damage.
Studies have shown that genetically modified worms that produce more free radicals, live 32% longer. Giving worms a weed-controlling herbicide that creates a surge in free radical production makes these worms even live 58% longer.
While free radicals aren’t always bad, antioxidants can be damaging. A large meta-analysis of 230 000 patients has shown that people who take antioxidants have an increased rate of death.
In conclusion, taking antioxidants isn’t always a good thing. Of course, when you are deficient of certain antioxidants, you do have to take them to replenish the ranks. But taking extra antioxidants to slow down the aging process doesn’t seem to work unfortunately. Meanwhile, aging seems much more complex than just free radicals damaging our cellular machinery.
Author: Kris Verburgh, MD
A Mitochondrial Superoxide Signal Triggers Increased Longevity in Caenorhabditis elegans. Wen Yang, Siegfried Hekimi. PLoS Biology, 2013.
Is the oxidative stress theory of ageing dead? Pérez VI et al. Biochim Biophys Acta, 2009. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. Bjelakovic, G. et al. JAMA, 2007. Picture: cc Wikicommons
Progeria is often called a disease of accelerated aging. Patients mostly die of a heart attack at age 13, looking frail and old with bald heads, a wrinkled skin, a beaked nose, tin lips and tired looking eyes. It’s a very rare disease, afflicting about 1 in 8 million people. The official medical name is Hutchinson-Gilford syndrome.
However, some scientists believe that progeria isn’t in fact a disease of accelerated aging. They consider progeria a disease that resembles aging, but that isn’t really like the aging process itself.
After all, progeria doesn’t exhibit all the symptoms of the classic aging process. Patients with progeria don’t seem to have an increased risk of other typical age-related diseases, like dementia, cancer, cataract, diabetes, a declining immune system, increased cholesterol and triglycerides (fats), deteriorating eyesight or hearing loss.
Why then does progeria looks so similar to the aging process itself? This is probably because the final result of progeria is in some way the same as the aging process: massive loss of cells. As well as in progeria as in aging, cells everywhere in the body die and the final result of this massive cell die off is that the body looks old and frail.
In progeria, cells massively die because of extensive DNA damage. A malfunctioning protein in the nucleus of the cell makes the nucleus (that stores the DNA) unstable. This contorted and twisted nucleus damages the DNA inside it and causes the cell to die.
In aging, cells everywhere in the body also die, but this because of other ways of damage than only DNA damage. As we age, cells get damaged by protein agglomeration, advanced glycation end products, continuous growth signals, clogged up lysosomes and malfunctioning mitochondria, inevitably resulting in cells succumbing everywhere in our body, making our tissues and organs frail and weak.
So it’s possible that progeria isn’t really an aging disease, but a syndrome that only bears resemblance with the aging process. The same goes for other seemingly ‘accelerated aging diseases’, like Werners syndrome or Cockayne syndrome, which also mainly involve DNA damage.
While many people look at progeria and other progeria-like diseases as evidence that aging mainly involves DNA damage, those diseases in fact show that the aging process involves much more than only DNA damage.
Author: Kris Verburgh, MD
Picture: The Cell Nucleus and Aging: Tantalizing Clues and Hopeful Promises. PLoS Biology Vol. 3/11/2005. Creative Commons Attribution 2.5 Generic license.
The older we get, the more our brains are susceptible to brain shrinkage. This shrinkage is accompanied by a steady cognitive decline, meaning difficulty to concentrate, forgetfulness or difficulty in retrieving words.
However, research has shown that this brain shrinkage can be substantially reduced by taking B vitamins.
Researchers from the University of Oxford gave old people vitamin B6, B9 (folic acid) and B12 during 2 years.
They found that the brains of people taking B vitamins shrunk seven times less compared to the placebo group.
The researchers concluded that B vitamins ‘may substantially slow down, or even potentially arrest the disease process in those with early stage cognitive decline’ and that ‘this is the first treatment that has been shown to potentially arrest Alzheimer’s related brain shrinkage’.
B vitamins play an important role in metabolism. These vitamins are the oil that greases the wheels of our metabolism. The brain is metabolically very active and therefore needs a lot of B vitamins.
One can simply buy B vitamins in the supermarket or pharmacist and preferably a supplement that contains as much different B vitamins as possible (like vitamin B1, B2, B3, B5, B6, B9 and B12).
Author: Kris Verburgh, MD
– Preventing Alzheimer’s disease-related gray matter atrophy by B vitamin treatment. Proceedings of the National Academy of Sciences, 2013
– Vitamin B12 status and rate of brain volume loss in community-dwelling elderly. Neurology, 2008.