About these topic collections

I’ve been reporting on memory research for over ten years and these topic pages are simply collections of all the news items I have made on a particular topic. They do not pretend to be in any way exhaustive! I cover far too many areas within memory to come anywhere approaching that. What I aim to do is provide breadth, rather than depth. Outside my own area of cognitive psychology, it is difficult to know how much weight to give to any study (I urge you to read my blog post on what constitutes scientific evidence). That (among other reasons) is why my approach in my news reporting is based predominantly on replication and consistency. It's about the aggregate. So here is the aggregate of those reports I have at one point considered of sufficient interest to discuss. If you know of any research you would like to add to the collection, feel free to write about it in a comment (please provide a reference).

Some interesting articles on the topic:

Crux of Schizophrenia’s Emotional and Social Deficits May Be Cognitive

Good article on the experience of schizophrenia

Our understanding of schizophrenia

Article in the journal Nature

Latest news

News in brief

Schizophrenia patients' ability to monitor reality may be helped by computerized training

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.

Brain activity linked to delusion-like experience

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.

More clues in the genetics of schizophrenia

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.

Mutations not inherited from parents cause more than half the cases of schizophrenia

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.

Brain development goes off track as vulnerable individuals develop schizophrenia

Two new research studies point to progressive abnormalities in brain development that emerge during adolescence as at-risk individuals develop schizophrenia.

Role of DISC1 gene in schizophrenia clarified

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.

Communication Breakdown in Brain Caused by a Gene Defect May Contribute to Schizophrenia

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.

Cognition already seriously impaired in first episode of schizophrenia

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.

Schizophrenia and Manic-depressive Disorder: Genetic Variant Impairs Communication Within Brain

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.

Autism and schizophrenia may reflect different variations in the same genes

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.

Is schizophrenia our price for having a large brain?

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.

Schizophrenia candidate genes affect even healthy individuals

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.

Brain function in schizophrenia can improve with support, holds promise for cognitive rehabilitation

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.

Scans link 2 key pieces of schizophrenia puzzle

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.