Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We determined the proportion of psychiatric treatments for disorders not due to substance use among a cohort of subjects (n = 3,114) seeking treatment for cannabis dependence. Data were retrieved from Danish treatment registers. Cases were compared with a representative sample, which was randomly selected from the general population according to age and gender (n = 15,570). Cannabis users were followed, and reentry into substance abuse treatment was used as an outcome deploying Cox regression analysis. The proportion of treatment for all psychiatric disorders was much higher among cases than among controls: schizophrenia (odds ratio [OR] = 7.9; 95% confidence interval [95% CI] = 6.1-10.2), bipolar disorders (OR = 4.9; 95% CI = 2.8-8.5), other affective disorders (OR = 7.6; 95% CI = 6.1-9.5), and personality disorders (OR = 17.3; 95% CI = 14.5-20.5). All in all, 40.7% of cases, compared with 5.2% of controls, had received psychiatric treatment (OR = 12.5; 95% CI = 11.3-13.8). A history of psychiatric treatment was associated with increased rates of reentry into substance abuse treatment, in general (OR = 1.35; 95% CI = 1.20-1.53), specifically for cannabis (OR = 1.26; 95% CI = 1.07-1.48) and opioid (OR = 1.56; 95% CI = 1.23-1.99) dependence. This is the first study to show that the proportion of psychiatric treatment is much elevated among subjects seeking treatment for cannabis dependence, and that a history of psychiatric problems is associated with higher rates of reentry into substance abuse treatment.
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PMID:Psychopathology among cannabis-dependent treatment seekers and association with later substance abuse treatment. 1730 20

Our previous report [Kedzior, K., Martin-Iverson, M., 2006. Chronic cannabis use is associated with attention-modulated reduction in prepulse inhibition of the startle reflex in healthy humans. J. Psychopharmacol. 20, 471-484.] indicates that chronic cannabis use in healthy humans is associated with deficits in the attentional modulation of prepulse inhibition of the acoustic startle reflex. The aim of the current study was to compare the attentional modulation of prepulse inhibition among healthy controls, otherwise-healthy cannabis users and schizophrenia patients (non-users) utilising the same attentional paradigm. Auditory startle reflex (the eye blink) was recorded from orbicularis oculi muscle while participants were attending to or ignoring 100 dB pulses and 70 dB prepulses separated by 20-200 ms. Cannabis users and schizophrenia patients showed a significant reduction in prepulse inhibition relative to controls while attending to, but not ignoring, auditory stimuli. These results suggest that the reduction in prepulse inhibition observed in cannabis users and in schizophrenia patients appears to be related to attentional dysfunction.
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PMID:Attention-dependent reduction in prepulse inhibition of the startle reflex in cannabis users and schizophrenia patients--a pilot study. 1732 88

Cannabis abuse may precipitate the onset of schizophrenia and a dysfunction of the endocannabinoid system may be involved in the pathology of schizophrenia. Nevertheless, only few studies have addressed the neurobiological consequences of cannabis abuse for the development and course of schizophrenia. We measured the long-term effect of chronic cannabis abuse on the inhibitory function of the brain by the auditory P50 sensory gating in schizophrenic (n=15) and otherwise healthy chronic cannabis abusers (i.e. cannabis controls; n=11) and compared it to that of schizophrenic patients (n=12) and healthy controls (n=18) without cannabis or other drug abuse. All study subjects had to be abstinent from cannabis for at least 28 days. The main finding of our study was a P50 sensory gating deficit in cannabis controls that was correlated with the number of years with daily consumption (r=0.81; p=0.003). In contrast, we found no differences in P50 sensory gating between schizophrenic cannabis-abusers and non-abusers or healthy controls and no correlation with the number of years with daily consumption in those groups. To our knowledge this is the first study comparing the influence of chronic cannabis abuse in schizophrenic and otherwise healthy abusers on the inhibitory function of the brain. Our data provide some evidence that chronic cannabis abuse may affect sensory cortical circuits even after prolonged abstinence and they point to a possible differential effect in schizophrenic and otherwise healthy users.
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PMID:Differential impact of heavy cannabis use on sensory gating in schizophrenic patients and otherwise healthy controls. 1736 20

The goal of the present study was to examine the rate of cannabis use among participants in the Cognitive Assessment and Risk Evaluation (CARE) Program, a longitudinal program for individuals who are "at risk" for developing a psychotic disorder. Cannabis abuse was assessed in 48 individuals identified as at risk for psychosis based on subsyndromal psychotic symptoms and/or family history. At 1 year follow-up, 6 of the 48 (12.5%) at risk subjects had made the transition to psychosis. Of the 32 subjects who had no use or minimal cannabis use, one subject (3.1%) converted to psychosis. Of the 16 subjects who met criteria for cannabis abuse/dependence, five (31.3%) converted to psychosis. The results show a significant association between cannabis abuse and conversion to psychosis in this sample. Nicotine use was also found to be significantly associated with later conversion. The significant associations between cannabis and nicotine abuse and conversion to psychosis in individuals at risk for schizophrenia suggest that early identification and intervention programs should screen for and provide education about the deleterious effects of these substances.
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PMID:Cannabis abuse and risk for psychosis in a prodromal sample. 1738 38

Substance abuse is the most prevalent comorbid psychiatric condition associated with schizophrenia. Cannabis is a drug frequently used for schizophrenic patients. In the last decades the endocannabinoid system and their endogenous ligands have been discovered. Endogenous cannabinoids act in the brain on cannabinoid CB1 receptor. On the other hand this system may be involved in several brain functions through neuromodulation dopaminergic and other neurotransmitter system involved in schizophrenic and substance abuse disorders. Advances of genetic research have addressed the focus on the search of candidate genes for both disorders. In this review we have summarized the studies published about the CNR1 gene on schizophrenia and substance abuse disorders.
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PMID:[Endocannabinoid system and CNR1 gene polymorphisms in schizophrenia and addictive disorders]. 1740 83

Cannabis is the most widely used illegal drug in Spain. Currently, its use is on the rise as risk perception is decreasing, primarily among young people. It is well known that cannabis negatively influences course and prognosis in schizophrenic patients. However, the relationship between cannabis use and development of a psychotic or schizophrenic disorder remains controversial. The study of this topic has been approached using longitudinal cohort studies, which study cannabis use and psychotic or schizophrenic disorders. In addition to the classic Swedish conscript study published by Andreasson et al. 1987, during the past years, six more longitudinal cohort studies have been published. The data demonstrate that there are both temporal and dose-response relationships, and that early initiation of cannabis use is highly correlated with the development of psychotic symptoms. Cannabis consumption can increase the risk of developing schizophrenia in a vulnerable population twofold, to the extent that some studies suggest a causal relationship. The current knowledge base makes it necessary to warn the population about the relationship between cannabis use and the development of psychosis.
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PMID:[Cannabis consumption and development of psychosis: state of the art]. 1750 95

Cannabis use is extremely prevalent in young people and there is controversy over the psychosocial harm of this use. One risk stands out--that of the possibility of cannabis being a risk factor of an illness as serious and incapacitating as schizophrenia. An avalanche of information has emerged recently on this subject, which it is essential to review. There are a number of cohort studies that support the idea of cannabis use as inducing psychotic symptoms and a precipitating factor of schizophrenia. These studies haves some methodological limitations, which we subject to critical analysis, such as the different outcome evaluations, heterogeneity in the measurements of vulnerability to the psychosis, the difficulty in controlling the possible confusion factors and the inadequate interpretation of the results obtained. In conclusion, we consider that the use of cannabis is clearly associated with the inducement of psychotic symptoms and is, possibly, a risk factor of schizophrenia in people with a genetic or psychosocial vulnerability, preventive methods being necessary in high-risk groups. These are fundamentally those of users of large quantities of cannabis and those who initiate use in adolescence.
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PMID:[A review about cannabis use like as risk factor of schizophrenia]. 1769 20

Reduced amplitudes of auditory evoked mismatch negativity (MMN) have often been found in schizophrenic patients, indicating deficient auditory information processing and working memory. Cannabis-induced psychotic states may resemble schizophrenia. Currently, there are discussions focusing on the close relationship between cannabis, the endocannabinoid and dopaminergic system, and the onset of schizophrenic psychosis. This study investigated the effects of cannabis on MMN amplitude in 22 healthy volunteers (age 28+/-6 years, 11 male) by comparing Delta(9)-tetrahydrocannabinol (Delta(9)-THC) and standardized cannabis extract containing Delta(9)-THC and cannabidiol (CBD) in a prospective, double-blind, placebo-controlled cross-over design. The MMNs resulting from 1000 auditory stimuli were recorded by 32 channel EEG. The standard stimuli were 1000 Hz, 80 dB SPL, and 100 ms duration. The deviant stimuli differed in frequency (1500 Hz). Significantly greater MMN amplitude values at central electrodes were found under cannabis extract, but not under Delta(9)-THC. There were no significant differences between MMN amplitudes at frontal electrodes. MMN amplitudes at central electrodes were significantly correlated with 11-OH-THC concentration, the most important psychoactive metabolite of Delta(9)-THC. Since the main difference between Delta(9)-THC and standardized cannabis extract is CBD, which seems to have neuroprotective and anti-psychotic properties, it can be speculated whether the greater MMN amplitude that may imply higher cortical activation and cognitive performance is related to the positive effects of CBD. This effect may be relevant for auditory cortex activity in particular because only MMN amplitudes at the central, but not at the frontal electrodes were enhanced under cannabis.
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PMID:Acute effects of Delta9-tetrahydrocannabinol and standardized cannabis extract on the auditory evoked mismatch negativity. 1788 51

While cannabis is associated with positive syndrome schizophrenia (SZ), it is unclear whether cannabinoids are also related to negative symptoms such as affective blunting. We examined whether cannabis use is associated with schizotypy and utilized event-related potentials (ERPs) to assess affect processing. Cannabis users demonstrated increased P300 amplitudes for unpleasant trait words, and demonstrated higher positive syndrome schizotypy which correlated with levels of cannabis use. The cannabis group also exhibited lower negative syndrome schizotypy. The lack of blunted responses during the affect ERP and decreased negative subscale schizotypy scores provide evidence that the endocannabinoid theory of schizophrenia may be primarily relevant in relation to positive syndrome SZ.
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PMID:Affect processing and positive syndrome schizotypy in cannabis users. 1789 20

Cannabis use may increase the risk of developing schizophrenia by precipitating the disorder in genetically vulnerable individuals. Neuregulin 1 (NRG1) is a schizophrenia susceptibility gene and mutant mice heterozygous for the transmembrane domain of this gene (Nrg1 HET mice) exhibit a schizophrenia-related phenotype. We have recently shown that Nrg1 HET mice are more sensitive to the behavioral effects of the main psychoactive constituent of cannabis, Delta(9)-tetrahydrocannabinol (THC). In the present study, we examined the effects of THC (10 mg/kg i.p.) on neuronal activity in Nrg1 HET mice and wild type-like (WT) mice using c-Fos immunohistochemistry. In the lateral septum, THC selectively increased c-Fos expression in Nrg1 HET mice with no corresponding effect being observed in WT mice. In addition, THC promoted a greater increase in c-Fos expression in Nrg1 HET mice than WT mice in the central nucleus of the amygdala, the bed nucleus of the stria terminalis and the paraventricular nucleus of the hypothalamus. Consistent with Nrg1 HET mice exhibiting a schizophrenia-related phenotype, these mice expressed greater drug-free levels of c-Fos in two regions thought to be involved in schizophrenia, the shell of the nucleus accumbens and the lateral septum. Interestingly, the effects of genotype on c-Fos expression, drug-free or following THC exposure, were only observed when animals experienced behavioral testing prior to perfusion. This suggests an interaction with stress was necessary for the promotion of these effects. These data provide neurobiological correlates for the enhanced behavioral sensitivity of Nrg1 HET mice to THC and reinforce the existence of cannabinoid-neuregulin 1 interactions in the CNS. This research may enhance our understanding of how genetic factors increase individual vulnerability to schizophrenia and cannabis-induced psychosis.
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PMID:Heterozygous neuregulin 1 mice display greater baseline and Delta(9)-tetrahydrocannabinol-induced c-Fos expression. 1790 22


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