In today's edition:
- Enzyme takes us a step closer to eternal youth
- Has universal ageing mechanism been found?
- Memories may be stored on your DNA
- Tiny 'paddleboat' could ship drugs around the body
Enzyme takes us a step closer to eternal youth
- 19 November 2008 by Linda Geddes
Telomerase is present naturally in some mammalian cells and maintains the protective caps called telomeres at the ends of our chromosomes, which unravel with each cell division as we get older.
One of the latest studies confirms that at least one type of human cell can be restored to a youthful state by boosting telomerase levels. The other suggests that boosting telomerase can result in longer life in animals.
Effros's experiment used a drug called TAT2 that boosts telomerase production without altering anyone's DNA. When killer T-cells from people with HIV were exposed to TAT2, it enhanced the cells' ability to fight the virus.
A previous study indicated that some people with HIV that don't develop AIDS have killer T-cells with high telomerase activity and longer telomeres. Since T-cells fight many viruses, TAT2 might eventually be deployed to boost resistance to a whole range of diseases.
TAT2 also increased the cells' ability to divide and stopped their telomeres from shortening, which raises the possibility that it might provide more general treatments for ageing.
Some safety concerns remain, however, not least because cancer cells produce telomerase at higher than normal rates. However, when TAT2 was added to tumour cells it did not affect the amount of telomerase they produced, nor their growth characteristics. Also, telomerase is extracted from the Astragalus plant, which is used in Chinese medicine without any obvious adverse effects.
Blasco's team bred mice engineered to be resistant to cancer with mice engineered to produce 10 times the normal levels of telomerase in epithelial tissue. These animals lived up to 50 per cent longer than normal mice. source
My comment: Ok, breeding cancer resistant humans is kind of demanding task, but the first part of the article is extremely interesting! First that this drug had such a magnificent result on HIV. I wonder what the side effects are, because obviously, there are always some side effects. But what's even more interesting is that thre is a herb that is wildly used that produce telomerase. Isn't this weird? Sure, it's not wise to take the herb in big quantities, but the very fact that we're using it is very significant.
Has universal ageing mechanism been found?
- 17:00 26 November 2008 by Linda Geddes
An overworked protein that causes yeast to age when it neglects one of its functions may trigger ageing in mice too. If the same effect is found in people, it may suggest new ways to halt or reverse age-related disease.
As we get older, genes can start to be expressed in the wrong body tissues - a process that is thought to contribute to diseases like diabetes and Alzheimer's. But while sunlight or chemicals are known to cause limited DNA damage, it's still unclear why genes expressions change.
To investigate, David Sinclair and colleagues at Harvard Medical School turned to yeast cells. These produce a dual-function protein called Sir2 that, while being involved in DNA repair, also helps keep certain genes switched off.
As yeast cells age, the protein can't do both jobs and neglects its role as a gene suppressor.
Now Sinclair's team has shown that SIRT1, the mammalian version of Sir2, also begins to neglect its gene-suppressor role in mice whose DNA is damaged, and that this may contribute to ageing.
This raises the hope that, if gene-suppressing proteins become similarly overworked in ageing people, they could become prime targets for drugs to keep us young. source
My comment: Hope is hope, but what's more interesting is why the protein starts neglecting its role. Is it because it spends too much time in gene repairs? If so, imagine the drug from the previous article that keeps the telomere long and healthy, combined with thes little warrior-SIRT1. Many people that we're probably the last generation to die or the first to live forever. It's not that hard to believe that.
Memories may be stored on your DNA
- 02 December 2008 by Devin Powell, Washington DC
REMEMBER your first kiss? Experiments in mice suggest that patterns of chemical "caps" on our DNA may be responsible for preserving such memories.
To remember a particular event, a specific sequence of neurons must fire at just the right time. For this to happen, neurons must be connected in a certain way by chemical junctions called synapses. But how they last over decades, given that proteins in the brain, including those that form synapses, are destroyed and replaced constantly, is a mystery.
Now Courtney Miller and David Sweatt of the University of Alabama in Birmingham say that long-term memories may be preserved by a process called DNA methylation - the addition of chemical caps called methyl groups onto our DNA.
Many genes are already coated with methyl groups. When a cell divides, this "cellular memory" is passed on and tells the new cell what type it is - a kidney cell, for example. Miller and Sweatt argue that in neurons, methyl groups also help to control the exact pattern of protein expression needed to maintain the synapses that make up memories.
They started by looking at short-term memories. When caged mice are given a small electric shock, they normally freeze in fear when returned to the cage. However, then injecting them with a drug to inhibit methylation seemed to erase any memory of the shock. The researchers also showed that in untreated mice, gene methylation changed rapidly in the hippocampus region of the brain for an hour following the shock. But a day later, it had returned to normal, suggesting that methylation was involved in creating short-term memories in the hippocampus.
To see whether methylation plays a part in the formation of long-term memories, Miller and Sweatt repeated the experiment, this time looking at the uppermost layers of the brain, called the cortex.
They found that a day after the shock, methyl groups were being removed from a gene called calcineurin and added to another gene. The exact pattern of methylation eventually stabilised and then stayed constant for seven days, when the experiment ended. source
My comment: Fascinating. Why? Because we know so little about our brain and this study give a good idea what the process might be on cellular level. I'm very interested in this, because this could in the least be useful in memory degenerating diseases.
Tiny 'paddleboat' could ship drugs around the body
- 04 December 2008 by Paul Marks
A MICROSCOPIC swimming machine that works like a paddle steamer could help deliver drugs inside the body and move chemicals around inside miniaturised labs. The device is the first artificial microswimmer to move without using chemical propulsion or bending itself into different shapes.
For microscale swimmers, the viscosity of water presents a much bigger barrier to motion than we are used to on everyday scales. It is like swimming through honey for a human.
That's why bacteria like Escherichia coli use a rotating corkscrew-like tail called a flagellum to propel themselves forward. With a continuously rotating propeller rather than a backwards-forwards swimming motion, the bacteria barrel along.
Now Golestanian and Pietro Tierno at the University of Barcelona in Spain have been able to achieve a similar goal with a micromachine that swims by mimicking a paddle wheel. The researchers built their microswimmer from two beads, 1 and 3 micrometres in diameter. They coated the beads in a protein called streptavidin that binds strongly to DNA and then fastened them together with two 8-nanometre strands of DNA.
The beads are made of a magnetic material and so align themselves with any applied magnetic field. By rotating this magnetic field, the researchers set the beads spinning, and were delighted to find that the beads moved through water at about 1 micrometre per second.
The movement occurs only when the micromachine is close to the bottom of a vessel. This is because there is a less mobile boundary layer that "sticks" to the bottom surface of the fluid container and so exerts a larger force on the rotating bead than the rest of the water. This makes the whole thing move, just as a paddle wheel can propel a boat because water resists the paddles more than air does.
The team believes its technology can easily be shrunk to the nanoscale - the level at which it would be useful as a drug carrier. "Microscale and nanoscale hydrodynamics are not all that different," says Golestanian. source
My comment: Fun again! Let's see how long until it hit the pharmacy companies.