Some interesting articles on the topic:
Good article on the experience of schizophrenia
Article in the journal Nature
New findings support a mathematical model predicting that the slow, steady firing of neurons in the dorsolateral prefrontal cortex that maintains visual representations in working memory relies on a class of NMDA receptors known as NR2B receptors. Blocking these receptors abolished persistent firing among pyramidal Delay cells.
Earlier studies have shown these types of NMDA receptors are often altered in patients with schizophrenia. They also seem to be altered in Alzheimer’s patients. The findings suggest that this may be one cause of cognitive deficits in those with schizophrenia and Alzheimer’s.
Ketamine, an anesthetic often abused as a street drug, also blocked these receptors, explaining at least in part why ketamine abuse can produce schizophrenia-like symptoms.
 Wang, M., Yang Y., Wang C-J., Gamo N. J., Jin L. E., Mazer J. A., et al.
(2013). NMDA Receptors Subserve Persistent Neuronal Firing during Working Memory in Dorsolateral Prefrontal Cortex.
Neuron. 77(4), 736 - 749.
Research into the effects of cannabis on cognition has produced inconsistent results. Much may depend on extent of usage, timing, and perhaps (this is speculation) genetic differences. But marijuana abuse is common among sufferers of schizophrenia and recent studies have shown that the psychoactive ingredient of marijuana can induce some symptoms of schizophrenia in healthy volunteers.
Now new research helps explain why marijuana is linked to schizophrenia, and why it might have detrimental effects on attention and memory.
In this rat study, a drug that mimics the psychoactive ingredient of marijuana (by activating the cannabinoid receptors) produced significant disruption in brain networks, with brain activity becoming uncoordinated and inaccurate.
In recent years it has become increasingly clear that synchronized brainwaves play a crucial role in information processing — especially that between the hippocampus and prefrontal cortex (see, for example, my reports last month on theta waves improving retrieval and the effect of running on theta and gamma rhythms). Interactions between the hippocampus and prefrontal cortex seem to be involved in working memory functions, and may provide the mechanism for bringing together memory and decision-making during goal-directed behaviors.
Consistent with this, during decision-making on a maze task, hippocampal theta waves and prefrontal gamma waves were impaired, and the theta synchronization between the two was disrupted. These effects correlated with impaired performance on the maze task.
These findings are consistent with earlier findings that drugs that activate the cannabinoid receptors disrupt the theta rhythm in the hippocampus and impair spatial working memory. This experiment extends that result to coordinated brainwaves beyond the hippocampus.
Similar neural activity is observed in schizophrenia patients, as well as in healthy carriers of a genetic risk variant.
The findings add to the evidence that working memory processes involve coordination between the prefrontal cortex and the hippocampus through theta rhythm synchronization. The findings are consistent with the idea that items are encoded and indexed along the phase of the theta wave into episodic representations and transferred from the hippocampus to the neocortex as a theta phase code. By disrupting that code, cannabis makes it more difficult to retain and index the information relevant to the task at hand.
 Kucewicz, M. T., Tricklebank M. D., Bogacz R., & Jones M. W.
(2011). Dysfunctional Prefrontal Cortical Network Activity and Interactions following Cannabinoid Receptor Activation.
The Journal of Neuroscience. 31(43), 15560 - 15568.
Commercial use is a long way off, but research with mice offers hope for a ‘smart drug’ that doesn’t have the sort of nasty side-effects that, for example, amphetamines have. The mice, genetically engineered to produce dramatically less (70%) kynurenic acid, had markedly better cognitive abilities. The acid, unusually, is produced not in neurons but in glia, and abnormally high levels are produced in the brains of people with disorders such as schizophrenia, Alzheimer's and Huntington's. More acid is also typically produced as we get older.
The acid is produced in our brains after we’ve eaten food containing the amino acid tryptophan, which helps us produce serotonin (turkey is a food well-known for its high tryptophan levels). But serotonin helps us feel good (low serotonin levels are linked to depression), so the trick is to block the production of kynurenic acid without reducing the levels of serotonin. The next step is therefore to find a chemical that blocks production of the acid in the glia, and can safely be used in humans. Although no human tests have yet been performed, several major pharmaceutical companies are believed to be following up on this research.
 Potter, M. C., Elmer G. I., Bergeron R., Albuquerque E. X., Guidetti P., Wu H-Q., et al.
(2010). Reduction of Endogenous Kynurenic Acid Formation Enhances Extracellular Glutamate, Hippocampal Plasticity, and Cognitive Behavior.
Neuropsychopharmacology. 35(8), 1734 - 1742.
Schizophrenia patients who received 80 hours of computerized training over the course of 16 weeks became better at performing complex tasks that required them to distinguish their internal thoughts from reality.. This improvement coincided with increased activation in a key part of the brain: the medial prefrontal cortex.
Greater activation within the medial prefrontal cortex was also linked with better social functioning six months after training.
31 patients with schizophrenia and 15 healthy controls were involved in the study.
Support for a theory that the overactive firing of dopamine neurons in specific brain regions is involved in converting neutral, external information into personally relevant information among people with schizophrenia, comes from a brain scan study.
The study involved 14 people with a schizophrenia diagnosis and 15 controls.
Those with schizophrenia were significantly more likely to say that generic statements referred to them. Brain activity suggested they had greater difficulty in distinguishing what was self-relevant to what was not.
Once these processes are better understood, approaches such as attentional retraining therapy may be explored as possible treatments of delusions.
Two of the largest studies yet carried out on the genetics of schizophrenia in Chinese populations have turned up three genetic loci, or chromosomal regions, previously not known to be related to the disease.
Following on from earlier studies showing that a rare de novo mutation accounts for 1-2% of sporadic (non-hereditary) cases of schizophrenia, study of the human genome has found 40 new (not inherited) mutations, all from different genes and most of them protein-altering, involved in more than half the cases of sporadic schizophrenia.
The potentially large number of mutations makes a gene-therapy approach to treating schizophrenia unlikely. Researchers suspect, however, that all of the mutations affect the same neural circuitry mechanisms.
The study's results also help to explain two puzzles: the persistence of schizophrenia, despite the fact that those with the disease do not tend to pass down their mutations through children; and the high global incidence of the disease, despite large environmental variations.
Two new research studies point to progressive abnormalities in brain development that emerge during adolescence as at-risk individuals develop schizophrenia.
The Disrupted In Schizophrenia gene (DISC1) and its protein product plays many distinct roles in the development and functioning of the brain, including regulation of new neuron production in the cerebral cortex, and the programmed migration of these neurons.
New research has found a molecular switch that regulates this protein. If it malfunctions, the brain may not develop properly.
It’s suggested that perhaps 10% of psychiatric illness is primarily driven by defects in this switch system.
Nearly a third (30%) of those with a specific deletion on chromosome 22 develop schizophrenia, making it one of the largest genetic risk factors for the disorder. Mouse research now suggests that the gene defect produces a faulty connection between the hippocampus and the prefrontal cortex.
A meta-analysis of 47 studies of first-episode schizophrenia suggest that significant and widespread cognitive problems appear to exist in schizophrenia in its earliest phase, making it very hard for people with the disorder to work, study or be social.
Patients struggled the most with processing speed and with verbal learning and memory, especially when encoding information. Measured IQ and other cognitive abilities dropped the most between the high-risk period just before symptoms appear and the first acute phases.
A genetic variant that increases risk of schizophrenia, and also manic-depressive disorder, has been found to be associated with impaired communication between the two hemispheres of the dorsolateral prefrontal cortex.
In contrast, the link between the DLPFC and the hippocampus was improved, as were the connections between the amygdala and a number of other regions.
Copy number variations in the same genes may determine whether individuals suffer from autism or schizophrenia, according to a review. The review identified seven genetic regions linked to both disorders, of which five were deleted in one disease and duplicated in the other.
Comparison of the brains of healthy and schizophrenic humans with chimpanzee and rhesus macaque brains indicates that expression levels of many genes and metabolites that are altered in schizophrenia, especially those related to energy metabolism, also changed rapidly during evolution.
It’s suggested that the human brain, which uses 20% of the body's total energy supply compared with about 13% for nonhuman primates, runs so close to the limit of its metabolic capabilities, that small changes in energy-related genes can cause mental problems.
The finding also confirms previous evidence that brain metabolism is substantially altered in schizophrenia.
New research indicates that schizophrenics’ memory problems may be related to differences in how their brains process information. While both schizophrenic patients and healthy individuals used their frontal cortex while remembering and forgetting, healthy subjects used the right side when asked to remember spatial locations and schizophrenics used a wider network in both hemispheres. When healthy people were correct in their remembering, there was an increased activation of the right frontal cortex, an increase that didn’t occur when they couldn’t remember, and this was associated with a lack of confidence in their memory. However, schizophrenic patients showed an activation pattern on error trials indicating that they were remembering something, albeit incorrect. This was associated with a feeling of confidence about their memory.
Lee, J. et al. 2008. Origins of Spatial Working Memory Deficits in Schizophrenia: An Event-Related fMRI and Near-Infrared Spectroscopy Study. PLoS ONE, 3(3), e1760.
Full text at http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0001760
A study of over 2000 healthy young men has found that those with several of the genetic variants linked to schizophrenia had small reductions in cognitive ability such as decreased attentional capacity and worse performance on memory tasks, as well as atypical experiences that might be associated with schizophrenia.
A study shows how people with schizophrenia can be helped to remember information just as well as their healthy counterparts, as long as they are given proper cues and memory aids.
The study involved 17 schizophrenia patients and 26 healthy controls. Participants performed incidental encoding tasks of words and faces in response to instructions to make either deep (abstract/concrete) or shallow (alphabetization) judgments for words and deep (gender) judgments for faces, followed by subsequent recognition tests.
Both groups recognized significantly more words encoded deeply than shallowly, activated regions in the inferior frontal cortex, and showed greater left frontal activation for the processing of words compared with faces. However, during deep encoding and material-specific processing (words vs. faces), participants with schizophrenia activated regions not activated by controls, including several in prefrontal cortex.
The findings suggest that an important reason for cognitive deficits in those with schizophrenia is their failure to use everyday memory strategies.
Bonner-Jackson, A., Haut, K., Csernansky, J.G. & Barch, D.M. 2005. The Influence of Encoding Strategy on Episodic Memory and Cortical Activity in Schizophrenia. Biological Psychiatry, 58 (1), 47-55.
Brain scans have linked two key, but until now unconnected, brain abnormalities in schizophrenia. They have shown that the less patients' frontal lobes activate during a working memory task, the more the chemical messenger dopamine, thought to underlie the delusions and hallucinations of schizophrenia, rises abnormally in the striatum. Given that dopamine activity in the striatum is under the control of the prefrontal cortex, this suggests that the excess dopamine activity that antipsychotic drugs quell may be driven by a defect in the prefrontal cortex.
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