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MAY MAY MAY

funny this comes out the woodwork about the time the patents run out

on Lustral/Zoloft

& soon to run out on Venlafaxine.

So they are going to invent a class of new drugs that MAY work.

they'l find out eventually in phase4 trials when the people hurl

themselves to their deaths ........arround about the time that they

discover they got it wrong AGAIN

and they re-invent the wheel AGAIN

still there is always E.C.T. to wipe the minds of the people like us

that were the victims of the ssri expeiment

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Protein may regulate depression

January 7 2006 at 12:38 PM

http://news.bbc.co.uk/1/hi/health/4584866.stm

Depression is linked to the chemical serotonin

Scientists say they have pinpointed a protein which they believe may

play a pivotal role in depression.

A team from Rockefeller University in New York found mice deficient

in the protein - p11 - showed signs of depression-like behaviour.

In contrast, raising levels was shown to have an anti-depressant

effect on the animals.

Writing in the journal Science, they say p11 appears to help

regulate a brain chemical linked to mood.

However, a UK expert said the biochemical regulation of depression

was likely to be complex.

The chemical, serotonin, is a key target of anti-depressants, and

has been implicated not only in depression, but also in anxiety

disorders.

Brain cells use serotonin, and other chemicals, to communicate with

each other.

The chemicals bind to receptors on the surface of the receiving

cells. However, exactly how these receptors work remains a mystery.

Drawn to surface

The Rockefeller team found that p11 seems to play a role in drawing

one particular type of serotonin receptor to the surface of cells.

This suggested that a lack of p11 might result in a deficiency of

receptors - and thus increase the likelihood of depression.

The researchers examined the brains of depressed people and mice

showing signs of depressed behaviour - and found p11 levels were

substantially lower in both.

Next, they showed that treating mice with two types of anti-

depressants and electroconvulsive therapy (ECT) all boosted p11

levels in the animals' brains.

Lead researcher Dr Greengard said: " They all work in totally

different ways, but in all cases they caused the same biochemical

change.

" So, it's pretty convincing that p11 is associated with the main

therapeutic action of anti-depressant drugs. "

The researchers were able to trigger symptoms of depression in mice

by lowering their p11 levels, and produce the opposite effect by

raising levels of the protein.

Further analysis showed that this seemed to be related to the number

and responsiveness of serotonin receptors on the surface of the

animals' brain cells.

Treatment hope

Professor Nutt, head of psychopharmacology at Bristol

University, told the BBC News website the research held out hope of

new drugs which would work in different ways to those currently

available for depression.

He said currently drugs helped about 60% of people to get well, had

some effect on another 20%, but were of little help for the

remaining 20%.

The hope would be that a new drug would boost success rates

and " improve the efficacy of those that we already have, " he said.

Professor Dave Kendall, of the University of Nottingham, said the

research was interesting, but questioned whether depression was

likely to be controlled by just one protein.

He said: " There are a number of proteins that increase in various

parts of the brain following anti-depressant treatments of various

sorts. "

Professor Kendall said drugs that directly activated the receptor

studied by the Rockefeller team had been shown to increase, not

decrease anxiety in studies on animals.

" Maybe p11 has other functions in addition to controlling receptor

expression that are important in depression, " he said.

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" Professor Kendall said drugs that directly activated the receptor

studied by the Rockefeller team had been shown to increase, not

decrease anxiety in studies on animals. "

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