Protein ‘behind Alzheimer’s fits’

March 19, 2009

Scientists in Scotland say they may have found what causes some Alzheimer’s patients to develop epilepsy.

The amyloid protein, which forms in clumps in patients’ brains, makes nerve cells too sensitive and prone to seizures, tests in mice suggest.

The cells short-circuit and fire too many electrical signals, the Journal of Neuroscience reports.

If true in humans too, which the experts say is likely, it may mean some patients will need different drugs.

A mainstay of treatment for Alzheimer’s is a class of drugs called the cholinesterase inhibitors.

They work by stopping the breakdown of acetylcholine, an important neurotransmitter associated with memory.

But an unwanted effect is that this can also increase a person’s susceptibility to seizures.

However, medication to control seizures can also make Alzheimer’s symptoms worse.

A third of Alzheimer’s patients have some degree of epilepsy, posing a treatment dilemma for doctors.


Stem cell study enters new era

March 10, 2009
At a White House ceremony attended by scientific leaders, President Obama on Monday ordered the National Institutes of Health to issue guidelines removing the Bush administration’s limits on human embryonic stem cell research funding within 120 days.

Obama also ordered the White House Office of Science and Technology Policy — in a “Scientific Integrity” memorandum — to create a plan to fill federal science positions solely based on merit and to insulate them from political interference. “Political officials should not suppress or alter scientific or technological findings,” says the memorandum.

“The two (orders) are a nice pairing: One is a very concrete step on stem cells, and the other sets a much wider tone on how science will be conducted,” says attorney Robert Kenney of Hogan & Hartson in Washington, D.C., who specializes in federal research funds.


Gene could allow lab-grown teeth

February 24, 2009

Scientists believe they have found a way to grow teeth in the laboratory, a discovery that could put an end to fillings and dentures.

The team from Oregon have located the gene responsible for the growth of enamel, the hard outer layer of teeth which cannot grow back naturally.

Other scientists are already growing the inner parts of teeth in animals – but they have no hard enamel coatings.

The Proceedings of the National Academy of Sciences work may plug this gap.

Experiments in mice have shown that the gene, a “transcription factor” called Ctip2, has several functions involving immune responses and the development of skin and nerves.

The work at Oregon State University made the link with enamel by studying mice bred to lack Ctip2.

Lead researcher Dr Chrissa Kioussi said: “It’s not unusual for a gene to have multiple functions, but before this we didn’t know what regulated the production of tooth enamel.”

The scientists found that Ctip2 was crucial for the enamel-producing cells, called ameloblasts, to form and work properly.

Dr Kioussi said: “This is the first transcription factor ever found to control the formation and maturation of ameloblasts, which are the cells that secrete enamel.”

Controlling the gene in conjunction with stem-cell technology could make the artificial creation of functional teeth a real possibility.


Vitamin D helps control MS genes

February 5, 2009

The first evidence of how vitamin D deficiency and genetics interact to increase the risk of multiple sclerosis has been reported by researchers.

A UK and Canadian team found that vitamin D helps to control a gene known to increase MS risk, the PLoS Genetics journal reports.

It suggests that vitamin D supplements taken during pregnancy and early in life could prevent the disease.

The condition results from the loss of nerve fibres and their protective myelin sheath in the brain and spinal cord, causing neurological damage.

It is not entirely clear what causes MS but other research has suggested vitamin D, produced in the body through exposure to sunlight, plays a part.

Specifically there is evidence that populations from Northern Europe have an increased risk of developing MS if they live in areas receiving less sunshine.

The researchers found that proteins activated by vitamin D in the body bind to a particular DNA sequence next to the gene, altering its function.

They believe that vitamin D deficiency in mothers or even in a previous generation may lead to altered expression of the gene in their offspring.


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