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Researchers Identify New Drug Target for Schizophrenia

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firemonkee57

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Researchers at Mount Sinai School of Medicine may have discovered why certain drugs to treat schizophrenia are ineffective in some patients. Published online in Nature Neuroscience, the research will pave the way for a new class of drugs to help treat this devastating mental illness, which impacts one percent of the world’s population, 30 percent of whom do not respond to currently available treatments.

A team of researchers at Mount Sinai School of Medicine set out to discover what epigenetic factors, or external factors that influence gene expression, are involved in this treatment-resistance to atypical antipsychotic drugs, the standard of care for schizophrenia. They discovered that, over time, an enzyme in the brains of schizophrenic patients analyzed at autopsy begins to compensate for the prolonged chemical changes caused by antipsychotics, resulting in reduced efficacy of the drugs.

“These results are groundbreaking because they show that drug resistance may be caused by the very medications prescribed to treat schizophrenia, when administered chronically,” said Javier Gonzalez-Maeso, PhD, Assistant Professor of Psychiatry and Neurology at Mount Sinai School of Medicine and lead investigator on the study.

They found that an enzyme called HDAC2 was highly expressed in the brain of mice chronically treated with antipsychotic drugs, resulting in lower expression of the receptor called mGlu2, and a recurrence of psychotic symptoms. A similar finding was observed in the postmortem brains of schizophrenic patients. The research team administered a chemical called suberoylanilide hydroxamic acid (SAHA), which inhibits the entire family of HDACs. They found that this treatment prevented the detrimental effect of the antipsychotic called clozapine on mGlu2 expression, and also improved the therapeutic effects of atypical antipsychotics in mouse models.

Previous research conducted by the team showed that chronic treatment with the antipsychotic clozapine causes repression of mGlu2 expression in the frontal cortex of mice, a brain area key to cognition and perception. The researchers hypothesized that this effect of clozapine on mGlu2 may play a crucial role in restraining the therapeutic effects of antipsychotic drugs.

“We had previously found that chronic antipsychotic drug administration causes biochemical changes in the brain that may limit the therapeutic effects of these drugs,”said Dr. Gonzalez-Maeso. “We wanted to identify the molecular mechanism responsible for this biochemical change, and explore it as a new target for new drugs that enhance the therapeutic efficacy of antipsychotic drugs.”


Researchers Identify New Drug Target for Schizophrenia
 
McMurphy's Ghost

McMurphy's Ghost

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They found that this treatment prevented the detrimental effect of the antipsychotic called clozapine on mGlu2 expression, and also improved the therapeutic effects of atypical antipsychotics in mouse models.
So these mice....they all found partners, got good mice jobs, mortgages for houses in mousey suburbia and sent their micey offspring to good local schools for nice middle class mice?

Wow.
 
rasselas.redux

rasselas.redux

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In a breakthrough development scientists have their eye on a new drug that may enable their current drugs to be better tolerated.

"Think of it like Tetris," the Assistant Research Professor of Psychiatry said. "The object of the game is to get a full synaptic saturation without any gaps. This really takes us to the next level of brain gaming."

The science is very hypothetical so this paragraph will drop lots of sciencey terms with a tone of certitude, filling you with a sense of excitement and anticipation for the Research Professor's strapline.

"I think this will ensure the internships of at least two more generations of pseudoscientists not smart enough to get into physics or real medicine," the Assistant Professor explained.
 
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McMurphy's Ghost

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They found that an enzyme called HDAC2 was highly expressed in the brain of mice chronically treated with antipsychotic drugs, resulting in lower expression of the receptor called mGlu2, and a recurrence of psychotic symptoms
?????? So they started with psychotic mice????? Where did they get them and how did they know they were psychotic in the first place?

The whole thing is so teeth grindingly awful. Sometimes the only answer is derision and ridicule.
 
rasselas.redux

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It is ridiculous. On so many levels. Mice, as we all know, are resolutely unaffected by their environment. They are completely immune to any effects of being tortured in laboratory settings.

I read a study some years ago in which rats were induced with psychosis with high levels of THC. They apparently knew these rats were psychotics because they would sit in the corner of their cages, staring into space, and would be unresponsive to sudden, loud noises behind them.

This is one of the reasons that some resist the opening up of the scientific research archives to general public scrutiny.
 
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McMurphy's Ghost

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It is ridiculous. On so many levels. Mice, as we all know, are resolutely unaffected by their environment. They are completely immune to any effects of being tortured in laboratory environments.

I read a study some years ago in which rats were induced with psychosis with high levels of THC. They apparently knew these rats were psychotics because they would sit in the corner of their cages, staring into space, and would be unresponsive to sudden, loud noises behind them.

This is one of the reasons that some resist the opening up of the scientific research archives to general public scrutiny.
The thing that gets me is that on one level these researchers (unless they read the scientific press in a highly selective manner and I suppose many of them do, read selectively that is) they must know just as Bernie Madoff must have done that what they are doing is total b.s.

The one thing that has started to occur to me is this 30% club who are supposedly treatment resistant. It would be interesting to take a closer look at this supposed real group and see what is really going on. I expect one would find many many damaged people but treatment resistant? This number is bandied about unquestioned rather like the 1 in 4 and we know that is b.s.

My hunch is that a really good look would reveal that no such group really exists.
 
rasselas.redux

rasselas.redux

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Aren't there two uses of the term?

1. those persons for whom treatment doesn't work

or

2. those who resist treatment?
 
rasselas.redux

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At the USA's Austen Riggs Centre they specialise in taking in treatment resistant clients and sending them back to their treatment teams with new, treatment compliant outlooks.

This article is particularly interesting: Psychodynamic Psychopharmacology: Addressing the Underlying Causes of Treatment Resistance | Austen Riggs

Apparently it is expectancy effects based on poor relationships with prescribers that lead to nocebo effects; conversely good prescribing practices create good placebo effects.

They also seem to have applied the cycle of change model to treatment resistance.

Clearly, anyone that resists anti-emotionals isn't thinking straight.

This is abundantly clear I would imagine to anyone that has never taken them themselves. ;)
 
rasselas.redux

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The concept of treatment resistance in bipolar disorder is clinically familiar but lacks a standard definition. Whether the term refers to nonresponse to 1 or more standard treatments, at what dosages, and for what phases of bipolar disorder is unclear. Treatment resistance in bipolar disorder should always be based on a specific phase of treatment: mania or depression and acute or maintenance.

Treatment resistance is extremely common. Even under optimal maintenance conditions, almost half of bipolar patients with symptom remission will have a recurrence in 2 years under standard care (including medication combinations)
from here: Treatment-Resistant Bipolar Disorder - Psychiatric Times
 
rasselas.redux

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They used to call it non-compliance but now it's adherence and concordance.


Depression and antidepressants

The adherence habits of those prescribed anti-depressants have recently been summarised elsewhere (Mitchell, 2006b). Roughly 10% of patients prescribed antidepressants fail to pick up their first prescription and about a third collect only the initial (typically 4-week) prescription. Of those who start medication, non-adherence rates increase with time (Bultman & Svarstad, 2002). In a study of 200 patients attending 14 family doctors in five different practices, non-adherence rates were 16% at week one, 41% at week two, 59% at week three and 68% at week four (Johnson, 1981). In those on long-term maintenance treatment, discontinuation rates for selective serotonin reuptake inhibitors (SSRIs) are above 70% (Mullins et al, 2005). Of all those who discontinue medication, 60% have not informed their doctor by 3 months and a quarter have not done so by 6 months (Maddox et al, 1994; Demyttenaere et al, 2001). This is sometimes referred to as covert non-adherence.
Mania and mood stabilisers

Studies appear to support the observation that one-quarter to one-third of patients maintained on lithium are poorly adherent (Cochran, 1986). About a third of those prescribed lithium report that their adherence behaviour is poor and in a similar number sub-optimal serum levels indicate poor adherence (Scott & Pope, 2002). Johnson & McFarland (1996) performed a 6-year longitudinal cohort study to determine patterns of lithium use in a large US ‘health maintenance organisation’. Lithium users took the drug on an average of 34% of the days. As in other areas, more patients are partially adherent than entirely non-adherent (Colom et al, 2000).
Schizophrenia and antipsychotics

Perhaps the most striking data come from studies of full discontinuation by people with schizophrenia. Even in highly monitored randomised controlled trials, discontinuation rates can be greater than 50%. At least five large-scale studies have shown that adherence with both old and new antipsychotics is poor in the long term. For example, Rosenheck et al(1997) found that 68% of patients treated with haloperidol and 43% of those treated with clozapine had discontinued medication before the end of a 1-year trial. In the 18-month Clinical Antipsychotic Trials for Intervention Effectiveness (CATIE) study (Lieberman et al, 2005) a remarkable 74% of patients discontinued medication prematurely. The most common reasons for discontinuation were patient choice, lack of effect or intolerability of side-effects.
snipped from Why don’t patients take their medicine? Reasons and solutions in psychiatry

Why don
 
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rasselas.redux

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For long-term therapies, the studies show that

- over 70% do not adhere to treatments for depression
- about 66% of the time bipolar treatment wasn't adhered to
- over 70% of schizophrenia diagnosed did not adhere

So in drug maintenance therapy, adherence is a minority pursuit.


Lack of insight or the result of insight?
 
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firemonkee57

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This number is bandied about unquestioned rather like the 1 in 4 and we know that is b.s.
1 in 4 is a figure quoted for the full spectrum of mental illness,from mild to severe. If one is only counting the most severe cases as mental illness then that number indeed would be bs.
 
McMurphy's Ghost

McMurphy's Ghost

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At the USA's Austen Riggs Centre they specialise in taking in treatment resistant clients and sending them back to their treatment teams with new, treatment compliant outlooks.

This article is particularly interesting: Psychodynamic Psychopharmacology: Addressing the Underlying Causes of Treatment Resistance | Austen Riggs

Apparently it is expectancy effects based on poor relationships with prescribers that lead to nocebo effects; conversely good prescribing practices create good placebo effects.

They also seem to have applied the cycle of change model to treatment resistance.

Clearly, anyone that resists anti-emotionals isn't thinking straight.

This is abundantly clear I would imagine to anyone that has never taken them themselves. ;)
I dread to think what an oppressive place the Austin Riggs Centre must be.
"Psychiatry has benefited from an increasingly evidence-based perspective and a proliferation of safer, more tolerable, and perhaps more effective treatments during the last two years. "

An odd perspective because it is the rise of evidence based medicine that is tearing the backside out of the idea that the benefit of taking antipsychotics outweights the risks.
 
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McMurphy's Ghost

McMurphy's Ghost

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They used to call it non-compliance but now it's adherence and concordance.








snipped from Why don’t patients take their medicine? Reasons and solutions in psychiatry

Why don
Reading that made me feel quite sick. Especially as not taking medication seems to have been the right decision all along after all. From the Editor's desk

quotation below.

but an increasing body of evidence that the adverse effects of treatment are, to put it simply, not worth the candle. The combination of extrapyramidal symptoms, dangers of tardive dyskinesia and the neuromalignant syndrome,4 weight gain and the metabolic syndrome, sedation, postural hypotension, and interference in sexual function would need to be offset by massive symptomatic and social functioning improvement to make the benefit/risk ratio positive. "

effing idiots.
 
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