Глицин
#4
Отправлено 15 Январь 2008 - 12:58
Placebo-controlled trial of glycine added to clozapine in schizophrenia.
Evins AE, Fitzgerald SM, Wine L, Rosselli R, Goff DC.
The Psychotic Disorders Unit of the Massachusetts General Hospital, Boston, MA, USA. a_eden_evins@hms.harvard.edu
OBJECTIVE: The purpose of this study was to evaluate the effects of high-dose oral glycine on positive and negative symptoms and cognitive function when added to clozapine in adults with schizophrenia. METHOD: The authors conducted a double-blind, placebo-controlled, parallel-group trial of 60 g/day of glycine added to clozapine for 8 weeks in 30 adults with schizophrenia. Clinical ratings were performed every 2 weeks. RESULTS: Twenty-seven patients completed the trial. Glycine augmentation of clozapine produced no statistically significant change in positive or negative symptoms or cognitive functioning. No subjects showed clinically significant worsening of clinical ratings. CONCLUSIONS: These data, combined with data from previous trials with D-cycloserine and glycine, suggest that agonists at the glycine site may be less effective when combined with clozapine than they are when combined with conventional antipsychotics.
Efficacy of high-dose glycine in the treatment of enduring negative symptoms of schizophrenia.
Heresco-Levy U, Javitt DC, Ermilov M, Mordel C, Silipo G, Lichtenstein M.
Ezrath Nashim-Herzog Memorial Hospital, Department of Psychiatry, Hadassah Medical School-Hebrew University, Jerusalem, Israel. heresco@md2.huji.ac.il
BACKGROUND: Disturbances of N-methyl-D-aspartate (NMDA) receptor-mediated glutamatergic neurotransmission may play an important role in the pathophysiology of negative symptoms of schizophrenia. Glycine, a small nonessential amino acid, functions as an obligatory coagonist at NMDA receptors through its action at a strychnine-insensitive binding site on the NMDA receptor complex. Glycine-induced augmentation of NMDA receptor-mediated neurotransmission may thus offer a potentially safe and feasible approach for ameliorating persistent negative symptoms of schizophrenia. METHODS: Twenty-two treatment-resistant schizophrenic patients participated in a double-blind, placebo-controlled, 6-week, crossover treatment trial with 0.8 g/kg per day of glycine added to their ongoing antipsychotic medication. Clinical assessments, including the Brief Psychiatric Rating Scale (BPRS), the Positive and Negative Syndrome Scale (PANSS), the Simpson-Angus Scale for Extrapyramidal Symptoms, and the Abnormal Involuntary Movement Scale, were performed biweekly throughout the study. Clinical laboratory values and amino acid serum levels were monitored. RESULTS: Glycine treatment was well tolerated and induced increased glycine (P=.001) and serine (P=.001) serum levels. Glycine administration resulted in (1) a significant (P<.001) 30%+/-16% reduction in negative symptoms, as measured by the PANSS, and (2) a significant (P<.001) 30%+/-18% improvement in the BPRS total scores. The improvement in negative symptoms was unrelated to alterations in extrapyramidal effects or symptoms of depression. Low pretreatment glycine serum levels significantly predicted (r= 0.80) clinical response. CONCLUSION: These findings support hypoglutamatergic hypotheses of schizophrenia and suggest a novel approach for the pharmacotherapy of negative symptoms associated with this illness.
High-dose glycine added to olanzapine and risperidone for the treatment of schizophrenia.
Heresco-Levy U, Ermilov M, Lichtenberg P, Bar G, Javitt DC.
Ezrath Nashim-Herzog Memorial Hospital, Department of Psychiatry, Hadassah Medical School-Hebrew University, Jerusalem, Israel.
BACKGROUND: Clinical trials indicate that glycine site agonists of the N-methyl-D-aspartate (NMDA) receptors may reduce negative and cognitive symptoms in treatment-resistant schizophrenia when used as adjuvants to conventional antipsychotics but possibly not to clozapine. In this study, we assessed whether high-dose glycine may also be therapeutically beneficial when added to olanzapine and risperidone treatment. METHODS: Seventeen olanzapine- or risperidone-treated schizophrenia patients participated in a double-blind, placebo-controlled, 6-week crossover treatment trial with.8 g/kg/day glycine added to their ongoing antipsychotic medication. Clinical assessments were performed biweekly throughout the study. Clinical laboratory parameters and amino acid serum levels were monitored. RESULTS: Glycine treatment was well tolerated and resulted in a significant (p <.0001) 23% +/- 8% reduction in negative symptoms. Significant improvements were also registered in cognitive and positive symptoms. The negative symptoms improvement remained significant even following covariation for changes in other symptom clusters and extrapyramidal side effects. High posttreatment glycine serum levels significantly predicted (r =.60) clinical response. CONCLUSIONS: These findings indicate that the efficacy of olanzapine and risperidone may be augmented using high-dose adjuvant glycine treatment and suggest that these atypical antipsychotics may affect NMDA receptor-mediated neurotransmission differently than clozapine.
#5
Отправлено 15 Январь 2008 - 01:18
Palmer C, Ellis KA, O'Neill BV, Croft RJ, Leung S, Oliver C, Wesnes KA, Nathan PJ.
Behavioural Neuroscience Laboratory, School of Psychology, Psychiatry and Psychological Medicine, Monash University, Victoria, Australia.
N-methyl-D-aspartate (NMDA) receptors play an important role in learning and memory. Targeting the glycine modulatory site of the NMDA receptor has been suggested as a therapeutic strategy to improve cognition, although findings have not been convincing. We used the Cognitive Drug Research computerised assessment system to examine the effects of high-dose glycine on a number of cognitive processes in healthy young subjects. The study was a randomised placebo controlled repeated measures design in which each subject received acute placebo or glycine (0.8 g/kg) orally, with treatment conditions separated by a 5-day washout period. No significant effects of glycine were found on measures of working memory, declarative memory, attention or perceptual processing. These findings, together with those of previous studies, cast doubt over the ability of acute high-dose glycine to improve cognitive function in healthy subjects and suggest that the optimum dose of glycine for improving cognition may vary between different populations, possibly due to differences in endogenous glycine levels and the functional status of NMDA receptors. Copyright © 2007 John Wiley & Sons, Ltd.
Если Вы здоровы надо есть фрукты и овощи, а не таблетки.
Таблетки - для больных.
#6
Отправлено 15 Январь 2008 - 09:06
]]>Модуляция рецептора NMDA и применение глицина: новое направление в терапии шизофрении?]]>
]]>Интервью с Дэном Джавитом (Javitt) относительно глицина и исследований шизофрении]]>
Но результаты исследований оказались неубедительны, и сейчас, насколько я понимаю, на роль модуляторов глицинового сайта NMDA подбирают другие молекулы.
Что касается назначения глицина направо и налево по 1-3 таблетки "от нервов", то это наверняка плацебо-терапия. 8)
#7
Отправлено 15 Январь 2008 - 06:24
++++Были надежды относительно больших доз глицина в терапии шизофрении:
]]>Модуляция рецептора NMDA и применение глицина: новое направление в терапии шизофрении?]]>
]]>Интервью с Дэном Джавитом (Javitt) относительно глицина и исследований шизофрении]]>
Но результаты исследований оказались неубедительны, и сейчас, насколько я понимаю, на роль модуляторов глицинового сайта NMDA подбирают другие молекулы.
Что касается назначения глицина направо и налево по 1-3 таблетки "от нервов", то это наверняка плацебо-терапия. 8)
Спасибо за ссылки.
#10
Отправлено 17 Январь 2008 - 04:00
А ммм... можно спросить на что действовал препарат?Может и плацебо, но у женщин-алкоголичек истероидного типа,при хорошей подаче препарата, действует отлично.