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Driving out malaria (date 1/12/01)

Malaria is a big killer. Next to TB it is the most destructive of all human diseases, infecting 500 million people every year. It is well nigh impossible to eradicate the Anopheles mosquitos that carry the parasite because they are simply too numerous. One theory is to swamp a population of flies with sterile males to halt reproduction. However, the practicalities of such a programme are restrictive - the females that lay sterile male eggs need constant blood meals. But even wiping out a population in one area would only lead to neighbouring populations colonising the area rapidly afterwards. A team of scientists at the Commonwealth Science and Industry Research Organisation in Australia have found a way to safely "infect" entire populations with detrimental genes that harm the chances of survival. The team, led by Stephen Davis, modelled a scenario whereby they would release genetically-engineered male flies that each had two copies of an "A" type gene and two copies of a "B" type gene. Individuals that inherit "A" and "B" together will be fine, but those who inherit only an "A" or "B" will die. Modifying 3% of the population is enough to spread the genes throughout the entire population. The hybrid offspring of engineered males and wild females are O.K. as they will have one "A" and one "B", but when the hybrids mate, although hybrid/engineered crosses are fine, some hybrid/wild crosses die because they only have an "A" or "B" in isolation. The tendency is for a positive selection pressure which favours "driving" the "A" and "B" genes through the population, since the offspring of wild flies die more often than those of engineered flies. In theory, genes that kill the malaria parasite or make the flies susceptible to insecticides could be tagged to these "A" and "B" genes which would then also spread through the population. The hypothesis remains to be tested.



Source: New Scientist (01/12/01)


Curing the headache of Alzheimers? (date 01/12/01)

A product that can be bought across the counter in pharmacies may prove to be a simple way of helping Alzheimer's sufferers. A study from the Erasmus Medical Centre in Rotterdam has demonstrated that taking an average of just two anti-inflammatory pills in a week may be enough to reduce the risk of developing the condition by 80%. The drug is ibuprofen, the first aid to many a headache sufferer. The drawback is that regularly dosing up on non-steroidal anti-inflammatories such as ibuprofen can cause serious gut disorders, and others, known as Cox-1 inhibitors, can lead to intestinal bleeding. A new generation of such anti-inflammatories, called Cox-2 inhibitors, have no such reaction with the gut. The team of scientists working on the project estimate that the number of people suffering from Alzheimer's worldwide in 2025 could be reduced from 9 million to 2 million. It is not known exactly how the drugs work. They may break up the amyloid plaques that accummulate in the brain's of Alzheimer's patients or they may help prevent immune-cells called macrophages from attacking healthy brain cells. It is likely that these new drugs will act as preventatives rather than cures. A large scale trial of the drugs is currently being undertaken through the US National Institute of Ageing.

Source: New Scientist (01/12/01)


Blocking immune responses in MS (date 25/10/01)

Multiple Sclerosis is an auto-immune disease in which myelin, the protein sheath that protects nerves in the spinal cord and brain, is attacked by the body's own immune system. It appears that the cerebro-spinal fluid of MS sufferers contains abnormally high levels of chemical messengers called chemokines. These chemokines normally act by attracting immune cells, such as monocytes and T cells, to the central nervous system (CNS), where they then attack the myelin sheaths. Theory therefore suggests that targeting the chemokines or the receptors that the chemokines bind to might prevent or at least attenuate the influx of immune cells to the CNS and give the damaged myelin a chance to repair. A team of scientists at the University of California created antibodies to one of these chemokines and showed a reduced rate of demyelination in mice injected with the antibodies. Crippled mice were able to walk again, though the improvements were only temporary. Trials have begun on a small molecule that binds to a chemokine receptor. Drugs based on small molecules, such as molecules that bind to these chemokines, would be much more desirable than drugs based on larger proteins such as antibodies because these smaller molecules are much less likely to provoke an immune reaction and they would also be available in an easily-administered pill form.

Source: New Scientist (25/10/01)


Low libido (date 04/10/01)

Many people who have suffered from depression are well aware that taking drugs, such as Prozac, to combat depression can lead to an unwanted loss in their libido and/or problems in reaching orgasm. Drugs like Viagra work by increasing bloodflow but crucially don't directly affect desire or arousal. A group of scientists at Varnalis, a Berkshire-based company are co-developing a new drug with the makers of Prozac, Eli Lilly, to try to combat these effects. This new drug, enticingly named VML 670, activates a receptor in the brain called 5-HT(1A) which is linked to arousal. Tests on willing rats indicated increase in sex drive. Drugs such as Prozac (known as selective serotonin re-uptake inhibitors, SSRI) work by increasing the amount of serotonin, a neurotransmitter in the brain which results in an overall improvement in mood. These drugs also appear to block the 5-HT(1A) receptor. Ecstasy has a similar effect. The hope is that 5-HT(1A) drugs will out-compete the serotonin to increase arousal in patients taking SSRIs. The new drug is not expected to be used in non-depressed individuals!

Source: New Scientist (6/10/01)


Addicted to pleasure (date 15/09/01)

The idea of gene therapy to treat alcoholism might seem like something out of a science fiction novel, but scientists at the Brookhaven National Laboratory in New York State have been evaluating the effectiveness of this technique in the treatment of addiction. Admittedly, their subjects were lab rats but the results of their studies may eventually be applied to humans. Previous studies have shown that alcoholics have reduced levels of a receptor, D2, which binds to dopamine. Dopamine is linked to feelings of pleasure and is released through the action of alcohol or certain drugs. This could mean that people with fewer D2 receptors take more dopamine-releasing substances to get the same increased pleasure effect.The researchers injected a virus containing the gene for D2 receptors into the brains of two groups of rats, one addicted to alcohol and the other non-addicted. They discovered that this increased the number of D2 receptors and also reduced the alcohol intake of the addicted and non-addicted rats. Since it has also been shown that when dopamine is released as a reward for certain behaviour patterns it also physically reinforces the connections between neurons responsible for that behaviour it would seem that any treatment capable of reducing levels of alcohol-induced dopamine release might be one way of tackling addiction.

Source: New Scientist


BSE (date 15/09/01)

Protecting humans against vCJD, the human form of mad cow disease (BSE), has proved a difficult task because it was believed that any vaccine effective against the culprit mutant prion would also attack the normal prion that is found naturally in human tissues. However, researchers at the University of Zurich have produced a vaccine that makes mice immune to the vCJD prion. When a vaccine containing genes that code for antibodies against the mutant prion was injected into fertilised mouse eggs, these genes enabled the mice to make antibodies against vCJD from birth. When these mice were later injected with the disease-causing prion the animals remained healthy, whereas unvaccinated animals developed the disease. A team of scientists at Cleveland Clinic Foundation in Ohio demonstrated that the vaccine works by blocking the point at which rogue prions try to pair with normal prions, a process that would normally convert the normal prion into the mutant form.

Source: New Scientist


Diabetes (date 15/09/01)

In a similar vein it seems that some cases of diabetes might be caused by a rogue prion-like protein as well. Conventional theories of diabetes state that diabetes develops when muscle and adipose (connective fatty) tissue become resistant to insulin, raising blood fatty acid levels and thus leading to the death of insulin-releasing beta cells. A controversial study by Garth Cooper, a molecular biologist at the University of Auckland, demonstrates that a build-up of the mis-folding form of the protein amylin, which is produced in the insulin-producing cells of the pancreas, is related to an increased rate of beta cell death. Amylin aggregates are also seen in the beta cells of 90% of patients with type II diabetes. In addition, mice given the human gene for amylin develop diabetes and die. In contrast, mice engineered to produce a non-misfolding version of amylin do not develop diabetes It appears that, as with vCJD and BSE, amylin aggregates are associated with the misfolding form of amylin. However, there is no evidence that misfolding amylin is infectious.

Source: New Scientist





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