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Memory in Schizophrenia.
Kraepelin had an alternative designation for this illness - dementia praecox where the disability was like that in the dementia of old age, but occurring in younger adults, persistent, but not necessarily leading to a similar deterioration
A well functioning patient in a well settled active routine - gardening for others, photography, skilful work with wood, regularly driving forty miles two or three times a week to help out an ex hospital acquaitance, steadily busy during the last ten years, twenty-five years with the illness - I had quite a long discussion with S. re: reading which he has just started,
having always read quite a lot before the onset of illness.
He got a copy of
"The Woodlanders" which he had read as a school project.
He told me that he had
great difficulty in connecting the characters with the descriptions
intervening. He got lost in trying to recall the top of a page with what was going on at the bottom.
He had found the same with other books he had tried to read.
He also
finds that any disturbance affects his ability to retain anything he has started out on. The old belief that the brain was as it was and would stay that way has given way to the surprise of continuing new brain cell creation in the area around the lateral ventricles, and the hippocampal area.
Those in the hippocampal area play a crucial part in managing working memory - that is the updating that has to be done from what is happening now that needs to be attended to, as we move forward in life - current life and prospective possibilities. But, in schizophrenia the hippocampus ability to new cell creation is much reduced
The next five studies take further the work of the hippocampus new cells. Followed by links to three other papers, summarised.
Florian Siebzehnrubl, Ph.D., a postdoctoral researcher in neuroscience in the UF College of Medicine
a need unmet,
The researchers studied how stem cells in a memory-related region of the brain, called the hippocampus, proliferate and change into different types of nerve cells. Scientists have been unsure of the significance of that process in humans.
Over the past two decades, several studies have shown that new nerve cells are generated in the hippocampus.
In animal studies, disrupting nerve cell generation resulted in the loss of memory function, while increasing the production of new nerve cells led to improved memory.
To investigate whether the same is true in humans, the UF researchers, in collaboration with colleagues in Germany, studied 23 patients who had epilepsy and varying degrees of associated memory loss.
They analyzed stem cells from brain tissue removed during epilepsy surgery, and evaluated the patients' pre-surgery memory function.
In patients with low memory test scores, stem cells could not generate new nerve cells in laboratory cultures, but in patients with normal memory scores, stem cells were able to proliferate.
That showed, for the first time, a clear correlation between patient's memory and the ability of their stem cells to generate new nerve cells.
"The findings suggest that if we can increase the regeneration of nerve cells in the hippocampus we can alleviate or prevent memory loss in humans,"
Reif et al 2006 ... the penultimate two paragraphs in Discussion ... quote
" Does the finding of decreased Adult Neurogenesis in Schizophrenia make sense?
Sz is known to go along with several cognitive
deficits, which is stable over time, that is, trait
rather than state dependent.
The prime role of
hippocampus is rather memory formation than affect
regulation.
Thus, diminished Adult neurogenesis, which has been
suggested to result in impaired memory formation,
well contribute to the cognitive impairment
seen in Sz;
improvement of cognitive functioning in
Sz by clozapine might be due to the increase of AN
seen in animal studies.
As learning,46 exercise12 and
enriched environment47 all increase AN as well,
this
directly points toward non-pharmacological treatment
of schizophrenics. The preliminary finding of
reduced AN in Sz provided in the present study is
thus worth being pursued further." In post-mortem examination of the hippocampal area in schizophrenia - a surprise finding as the authors were looking for change in affective llnesses - the area now known to continue producing new cells, neurogenesis was depleted. Depleted hippocampal neurogenesis means reduced working memory. Without enough working memory capacity [ see Gold next ] people with schizophrenia are limited in what they can proceed with on their own - they go astray, they give up: they need help in starting, and maintaining success in getting regularly into activities of interest during the week, a routine that will stabilise the illness. It's an important study. Why no other p.m. reports - there are constant suicides and traffic deaths? Too hard to approach the relatives or to persuade the Coroner at Inquests?<
Gold et al ... demonstrate that in residual schizophrenia there is not enough working memory on hand to cope with life's
difficulties, unless they are limited in scope.There is not enough available working memory to address, hold on to, update and accomodate all the background relevance that are necessary towards achieving a successful conclusion for an intention.
The brain connections needed, are not assembled, are not there when wanted.
If it is so reduced, you stumble along the way of what you wanted to do and achieve,
often the intention cannot get there: there is just not enough background memory held onto, to keep a focus, to keep out irrelevant distractions. This recent study finds, importantly, limited working memory capacity, in residual schizophrenia. For those left with delivering after-care to people with residual schizophrenia, this requires clinical recognition. With working memory so reduced you cannot rehabilitate yourself. Working memory is what you call upon to keep up with what comes along when carrying forward a decision to do something
Help becomes a clinical need.
Active intervention in schizophrenia is not a social need. It's a medical one. They need somehow to establish themselves in a daily and weekly routine, that they can look forward to, that holds their attention and gives a lead to engagement.
The next three studies explain the disability, They also point to how to deal with it.
The remaining studies paint in the background.
Another study [ this link ...used to work ... Raalten... but if not, link to a journalist summary points to a remedy.
When encouraged and accompanied, given the opportunity to practice, sufferers do store what they have memorised: equally as well as for 'control subjects', by 'chunking'.
.
Automation – chunking – can be done in schizophrenia as normal, requiring less and less working memory with practice.
So routines when met with repeatedly, are stored away, then can be called up to guide an intention into realising activities already rehearsed.
There is an internal framework which points towards outside activities, getting to them already practised, so sparing working memory that would not be able to make the access de novo.
The making of these routines by themselves is beyond their reduced working capacity. .
Sufferers cannot readily rehabilitate by themselves
But routines, helped into by mentors , entering into them made easy until established , then practiced
does give sufferers an internal mapping long-term memory store,
leading to engagement in the programme of activity within a week, that they then can keep up with.
It has been rehearsed, and the working memory capacity, even reduced, allows for this engagement in something that is now not new, but chunked and familiar.
Sufferers need a help over the first steps that they cannot achieve themselves. After that they can do it themselves.
Rehabilitation comes from a recognition of what is, recognisably a clinical abnormality, the limiting consequences from that , which points to a way around that problem.
Mazhari et al :- 2010 Oct 30;179(3):253-8. Epub 2010 May 21.
Abstract
Spatial working memory (SWM) dysfunction is a central finding in schizophrenia; however, more evidence of impaired maintenance over time is required.
Consequently, the present study examined SWM maintenance over short unfilled delays, and with encoding equated. The influence of a vertical reference frame to support maintenance was also investigated. The performance of 58 patients with schizophrenia and 50 healthy controls was assessed using the Visuo-Spatial Working Memory (VSWM) Test across three unfilled delays (0, 2, and 4s). Inaccuracy of direction and distance responses was examined at each delay duration. The results showed that performance was significantly less accurate for both distance and direction responses at 2 and 4s delays in schizophrenia, but was not significantly different from controls at the 0s delay.
Patients showed a particularly marked loss of accuracy between the time interval of 0-2s. Furthermore, schizophrenia participants exhibited significantly greater response variability at the vertical axis of symmetry than controls at the 2 and 4s delays, but not at the 0s delay. These data clearly show both impaired maintenance over time and difficulty using a vertical frame of reference in schizophrenia. The latter findings may reflect, in part, dysfunctional reference-related inhibition[ ??? ed ]
Working memory is the mental ability to hold small amounts of information in an active, readily available state for a short period of time, typically a few seconds.
Conversely, long-term memory involves storing a potentially unlimited amount of information for an indefinite period of time.
Squire and colleagues examined four memory-impaired patients with damage to their medial temporal lobes (MTL), a region of the cerebral cortex containing the hippocampus and linked to long-term memory formation.
The four patients were asked to briefly study an arrangement of objects on a table, then reproduce the objects' relative positions on another table.
When the number of objects was three or less, the patients' ability to recall was similar to that of control subjects without brain damage.
The impaired patients easily remembered where the objects had been placed in relation to each other.
But "their performance abruptly collapsed when the limit of working memory was reached," said Squire. The patients could not remember the locations of four or more objects because doing so involved tapping into long-term memory functions in the medial temporal lobe.
Link to the original article protogenic repair Every day of our lives, in the hippocampus, we make thousands of cells," Pieper said.
Yet most of these new neurons die within four weeks of being born, for unknown reasons.
McKnight and colleagues divided their 1,000 potential drugs into 100 pools of 10 and treated mice with the cocktails. They injected the mice with BrdU
[ thymidine analog bromodeoxyuridine
(BrdU, 50 mg/kg) to score birth and survival of proliferating
hippocampal neural precursor cells. ]
to label newly divided cells, and looked for growth in this population in the hippocampus. After separating the effective pools into individual components, the researchers discovered eight chemicals that boosted new neuron numbers. Pieper and colleagues then focused on one particular molecule—dubbed P7C3 for pool 7 compound3
— because it was orally bioavailable, crossed the blood-brain barrier, and appeared to be non-toxic to the animals.
How does P7C3 rescue newborn neurons?
Normally, many of these cells undergo apoptosis, a process regulated by mitochondria.
They focused on the model lacking NPAS3, a transcription factor that controls adult neurogenesis
The neurogenesis deficit in mice without NPAS3 is not due to a lack of proliferation. Rather, animals lacking the transcription factor are able to form neural precursor cells, but the cells do not survive the maturation process. "
The mutant mice also have other deficits, Pieper and colleagues report, including reduced dendritic branching and dendritic spine density, as well as "aberrant hyperexcitability of synaptic transmission both in the outer molecular layer of the dentate gyrus and in the CA1 region of the hippocampus." Researchers wondered if P7C3 could also assist new neuron formation in mutant mice with impaired neurogenesis.
Promisingly, P7C3 administered continuously to NPAS3 knockout mice after prenatal day 14 (either via the mother or, after weaning, directly) helped rescue many of the structural and functional abnormalities in the dentate gyrus in these animals.
read.
The old belief that the brain was as it was and would stay that way has given way to the surprise of continuing new brain cell creation in the area around the lateral ventricles, and the hippocampal area.
Those in the hippocampal area play a crucial part in managing working memory - that is the updating that has to be done from what is happening now that needs to be attended to, as we move forward in life - current life and prospective possibilities. But, in schizophrenia the hippocampus ability to new cell creation is much reduced Three Studies of memory in schizophrenia explain what is in the way of recovery and rehabilitation.
Memory is faulty. 1. prospective memory This type of memory, prospective memory, which appears to be impaired by schizophrenia, enables you to remember that you have to do something in the future, without being prompted by something else or somebody else The authors hypothesized that patients with schizophrenia would have problems with tasks requiring prospective memory. They might mistake remembering they have to do something with remembering they've actually done it. Their hypothesis stemmed from the theory that people with schizophrenia confuse real ( 'outside' ) concrete acts, things, which they are impelled to notice, [ passivity - can't keep out intrusive thoughts or outside connections that seem to force in ] with 'internal thinking'... 'constructive day dreaming ' ) thought 'events'.
To test their hypothesis the researchers, based at NIMH and at the University of Warwick, compared the prospective memory of people with and without the disease.
In each test participants manoeuvred a ball around an obstacle course for 90 seconds. The ongoing activity was a commercial battery-powered game ("Kongman"; TOMY Toy Corporation, 1982) in which a steel ball was to be moved around an obstacle course by pressing a button at the appropriate time points in order to open or close certain routes through which the ball could travel. Each game lasted 90 seconds, and participants were instructed to accumulate as many points as possible during each game until the time was up. The game commenced by each participant winding a timer at the base of the game. During the course of the game the timer moved from the start to the finish position (taking 90 seconds).
The rim surround of the timer was covered and colored with red and green colored paper, such that the first 25 seconds were red and the remaining 65 seconds green. The Prospective Memory task was to turn a counter (a poker chip that was similar on both sides) over once during each game.
However, participants were instructed to turn the counter over only when the timer reached the green zone (i.e., they could not respond prospectively immediately, but had to wait for some proportion of time into the game before responding). Participants were to play the game a total of 10 times (i.e., 10 trials). After each of the ten games, participants were asked if they had remembered to turn the counter over during the game. The experimenter employed a stopwatch to note the time at which the counter was turned over, and whether it was in the green or red zone. The participants' response to the question concerning whether they remembered to turn over the counter was also noted.
The game was sufficiently easy and enjoyable that participants engaged in the game and all participants performed extremely well.
They were then asked [ the holding injunction ] to turn over a counter when they were at least 25 seconds into the test. The time delay ensured that prospective [ i.e. recall for a future event ] memory had to be used. Participants with schizophrenia were more likely to forget to turn over the counter. At the end of the test the participants were asked if they had remembered to turn over the counter. Approximately a third of the time participants with schizophrenia reported they had done so when they had not.
2. a study published in the British Journal of Psychiatry 2000
Cognitive function in a catchment-area-based population of patients with schizophrenia
C KELLY et al:
Academic Department, Gartnavel Royal Hospital, Glasgow, Scotland.
All patients with schizophrenia in a catchment area were identified (n=182). Measures of assessment were: National Adult Reading Test (NART), Mini-Mental State Examination (MMSE), go to ( see below ) Rivermead Behavioural Memory Test (RBMT), Executive Interview (EXIT), FAS Verbal Fluency and Health of the Nation Outcome Scales (HoNOS).
Results We assessed 138 patients, mean age 48 years (standard deviation (s.d.) 15). Only 14% were in-patients. The mean premorbid IQ as assessed by NART was 98 (s.d. 14); 15% of patients had significant global cognitive impairment (MMSE); 81% had impaired memory (RBMT see below ); 25% had executive dyscontrol (EXIT); and 49% had impaired verbal fluency (FAS). Scores on the functional impairment sub-scale of HoNOS correlated with all measures of cognitive impairment.
Conclusions Cognitive dysfunction is pervasive in a community-based population of patients with schizophrenia.
3,
Measuring memory impairment in community-based patients with schizophrenia B J PSYCHIATRY 2006 189 132-136 a
Case-control study
Correspondence: Dr Mohammed Al-Uzri, Neuropsychopharmacology Unit, Department of Health Sciences, Leicester General Hospital,
Leicester LE5 4PW, UK. Tel(0) 116 225 7924; fax: +44(0) 116 225 7925; email: mmaul@le.ac.uk
Department of Health Sciences, University of Leicester and Leicestershire Partnership NHS Trust
J. Bruce, MBChB, MRCPsych, S. Frost, MBBS, MRCPsych and D. Mackintosh, MBChB, MRCPsych
Leicestershire Partnership NHS Trust
We identified every patient with a possible diagnosis of schizophrenia, from psychiatric records, in one catchment area of approximately 100 000 people in south Leicestershire. This included examining old records of all psychiatric patients in the catchment area to make sure no potential patient was missed. The diagnoses were confirmed using ICD-10 criteria (World Health Organization, 1992). The area can be described as a suburban British residential area with a predominantly middle-class working population. The two consultants responsible for the area have a policy of not discharging patients with schizophrenia from their care even if the patients need minimal psychiatric input. The only exceptions were cases of severe and incapacitating schizophrenia that necessitated a referral to rehabilitation psychiatry. Such patients usually move out of the area into long-term care units or sheltered accommodation.
We excluded patients with organic brain disease, head injuries or comorbidity, and those whose first language was not English. None of the participants had had electroconvulsive therapy in the year prior to taking part in the study. Patients older than 60 years were also excluded, because Kelly et al (2000) suggested that people above this age with schizophrenia have a poorer cognitive performance than younger patients. The patients' performance on the memory test was compared with that of controls (n=71). Members of the control group live in the same city and were recruited by advertisements in the local hospital, university and supermarkets. They had no history of mental illness, and were subjected to the same exclusion criteria as the patient group. Measures
Rivermead Behavioural Memory Test
Participants were assessed with the Rivermead Behavioural Memory Test (RBMT; Wilson et al, 1985). This test of everyday memory has good ecological validity, and is made up of 12 measures, each aimed at testing one aspect of everyday memory:-
a. remembering a name;
b. remembering a hidden belonging;
c. remembering an appointment;
d. picture recognition;
e. immediate recall of a newspaper article;
f. delayed recall of a newspaper article;
g. face recognition;
h. remembering a new route (immediate);
i. remembering a new route (delayed);
j. delivering a message;
k. orientation questions;
l. knowing the date.
The RBMT has a screening score ( 0-12 simply pass or fail ), and is not very demanding in terms of effort or time (it takes 25-30 min to administer). It has been used before in schizophrenia studies, for example by McKenna et al (1990) and Kelly et al (2000)..... back to top
National Adult Reading Test
The National Adult Reading Test (NART; Nelson, 1982) is an estimate measure of premorbid intelligence. It has been widely used in psychiatric research and in particular in studies of schizophrenia (Gilvarry et al, 2001).
Positive and Negative Syndrome Scale
The Positive and Negative Syndrome Scale (PANSS; Kay et al, 1987) was given to patients only. It is a widely used scale for symptom ratings in schizophrenia.
Health of the Nation Outcome Scales
The Health of the Nation Outcome Scales (HoNOS; Wing et
We report a high prevalence of memory impairment (over 80%) in a population-based study of patients with schizophrenia.
This is based on the screening score of the RBMT, where a score of less than 10 is considered to represent impaired memory. This is, to the best of our knowledge, the second population-based study of cognitive impairment in schizophrenia after that by Kelly et al (2000). Significantly, we were able to replicate their findings regarding memory impairment using the same test, but in a demographically different population.
The patients who took part in our study were relatively young and free from psychotic symptoms, living in the community and with no documented comorbidity. The exclusion criteria were also designed to avoid the participation of any patients disadvantaged in terms of age and language. Except for years in education, there was no significant demographic or clinical difference between the patients who took part in the study and those who declined. This suggests that participants might have better memory functioning than those who declined to take part in the study. Therefore, the prevalence of memory impairment reported would be a conservative estimate of its overall prevalence in schizophrenia when taking other confounding factors (clinical or demographic) into consideration. This is supported by the findings of Tamlyn et al (1992) who used the same test (RBMT) to examine their cohort; they reported a much higher prevalence of memory impairment in their subgroup of chronically ill and hospitalised patients, 27 out of 28 of whom scored in the impaired range.
The prevalence of schizophrenia in our study population (1.9 per 1000) is at the lower end of that expected (1.4-4.6 per 1000 population; Jablensky, 2000).
This could be explained by the demographic characteristics of the catchment area. As a suburban district, it is more likely to have a lower prevalence of psychotic disorders compared with city centres, which are associated with higher morbidity in general (Mortensen et al, 1999). In addition, patients who develop schizophrenia might well migrate towards the city centre, especially when they need supported or hostel accommodation, which is most likely to be available in urban areas.
This was particularly true for our study because patients who needed rehabilitation services and supported accommodation were moved outside the catchment area.
RBMTand schizophrenia
Our study suggests that the RBMT is a good clinical marker for memory impairment in schizophrenia. This is supported by previous use of the RBMT in studies of schizophrenia, which consistently showed that people with this disorder underperform on this test (McKenna et al, 1990; Kelly et al, 2000).
Our study had the advantage, compared with previous studies, of the inclusion of a control group. This made it possible to examine the ability of the RBMT in discriminating between patients and controls. It is not common in psychiatric research to have an instrument with such a good ability (76%) to predict patient or control status.
A similar ability (76%) was reported in previous work (Palmer et al, 1997); however, this involved a more demanding neuropsychological battery which is difficult to incorporate into everyday clinical practice, and furthermore lacked the specificity of everyday memory. Therefore, the RBMT has the potential to become an important tool in our clinical practice for the identification of memory impairment in schizophrenia, which may help predict functional outcome.
Specificity of memory impairment
The premorbid IQ reported for the patients in this study was much higher than that reported in previous studies. This is another indication that our sample can be considered among the less ill of patients with schizophrenia, making the memory impairment reported even more significant. The difference in premorbid IQ between patients and controls was small in clinical terms, but statistically significant. However, even after correcting for this difference in premorbid IQ, patients' performance on the RBMT was worse than that of controls. Therefore, the underperformance of patients on the RBMT, as a measure of working memory, cannot be explained as a symptom of generalised reduction of intellectual ability, but is rather a specific cognitive deficit. Furthermore, this deficit was not related to symptom rating, except for negative symptoms, or medication in clinically stable patients. This supports the view that memory impairment is a core element of the clinical presentation of schizophrenia.
The association between memory impairment and the negative symptoms sub-scale of the PANSS is an important replication of previous findings (Berman et al, 1997). Conceptually, both denote the lack of a normally existing function. More importantly, this is further evidence that they may have a common underlying substrate (Rossi et al, 1997). This is an important contribution of neuropsychology towards better understanding of the underlying pathophysiology of schizophrenia.
Memory impairment and level of functioning
The association of memory impairment with occupational group provides further evidence for the importance of such impairment in schizophrenia. This echoes previous findings (Green, 1996), which suggested an association between memory impairment and functional outcome. This would have important implications for the development of any intervention that involves the use of memory. First, it suggests that patients with such impairment might not benefit from interventions that require intact memory. Second, it might be necessary to include memory remediation programmes in rehabilitation services to improve level of functioning. Further validity for the RBMT comes from the significant correlation with the functional impairment sub-scale of the HoNOS. This finding echoes that previously reported by Kelly et al (2000), which reinforces the importance of memory impairment in influencing level of functioning in patients with mental illness.
Age and memory impairment
An interesting finding emerged when we divided the patient and control groups, separately, into three different age categories. The average RBMT scores for the controls were not significantly different across age-groups and remained within the normal memory category.
In contrast, the patients' average RBMT scores remained within the impaired memory range across age-groups.
In addition, there was a significant reduction in the average score for the oldest group of patients, which suggests that memory impairment as a subset of cognitive performance is compromised before the age of 60 years (cf. Kelly et al, 2000). We can conclude that memory decline might have a different course in schizophrenia compared with that in the general population and that older people with schizophrenia (aged 46-60 years) are significantly disadvantaged compared with younger people with this disorder.
The significance of the association between illness duration and memory impairment reported in this study raises important issues. Ostensibly, one can conclude that memory function in schizophrenia has a deteriorating course. However, it is important to examine the impact of potential mediating factors, such as the course of the illness, before such a conclusion can be drawn definitively.
This is particularly important in the absence of clear neuropathological evidence to support a degenerative nature of the illness (Woods, 1998). Therefore, what can be concluded from the result of this study is that longer illness duration might carry a higher risk of worsening functional memory impairment. extracted from the original article
A try at Repair ?
Semantic hyperpriming in schizophrenia:-
Laurent Lecardeur
Centre de Recherche Fernand-Seguin, Montréal, Québec H1N 3V2, Canada.
Email:lecardeur@cyceron.fr
Sonia Dollfus
Centre Esquirol, CHU de Caen Centre d’Imagerie, Neurosciences et d’Application aux Pathologies,
UMR 6232 14074 Caen, France
Emmanuel Stip
Centre de Recherche Fernand-Seguin Hôpital, Louis-H. Lafontaine, Montréal, Québec, Canada
Impairment of memory is one of the principal cognitive symptoms of schizophrenia. Pomarol-Clotet et al1 reported on a meta-analysis in which they evaluated the results of studies on semantic priming in schizophrenia.
Semantic priming is a component of long-term implicit memory. They argued that hyperpriming (i.e. greater semantic priming in patients than healthy controls) could be an artefact of a general slowing in schizophrenia. As a consequence, these authors aimed to consider general slowing as a moderator variable in their statistical analysis. The measure of general slowing that they chose corresponded to the difference in response time between controls and patients, when prime and target were unrelated. In our opinion, this measure is not the most suitable as it reflects other cognitive processes. Individuals need to inhibit the prime so as to be able to process the target, since prime and target do not share any semantic relationship. Consequently, response time in an unrelated condition could be the expression of an accurate inhibitory process rather than of a general slowing as proposed by the authors. Some arguments support this view. First, we evaluated slowing in a simple reaction task in two different studies.2,3
Values were included as covariates in the analyses of covariance of priming effects. Despite confirming general slowing, there was evidence of significant increased priming in patients with schizophrenia compared with controls. Consequently, hyperpriming can be demonstrated even if general slowing is taken into account and controlled.
Second, we demonstrated that the time required to inhibit an unrelated prime was significantly enhanced in patients with schizophrenia compared with healthy controls.
General slowing was also controlled.
Consequently, we demonstrated that the increased priming effect in patients compared with controls was mainly induced by increased time required to inhibit the unrelated prime. Our results support impairment of the inhibition of semantically unrelated information in patients with schizophrenia. Pomarol-Clotet et al suggested that ‘the greater the slowing, the greater the amount of priming’. Given our results, an alternative explanation has to be considered. We suggest that hyperpriming in patients with schizophrenia could reflect decreased abilities to inhibit irrelevant information such as semantically unrelated information.
REFERENCES
1 Pomarol-Clotet E, Oh TMSS, Laws KR, McKenna PJ. Semantic priming in schizophrenia: systematic review and meta-analysis. Br J Psychiatry 2008; 192: 92 –7.[Abstract/Free Full Text]
2 Lecardeur L, Giffard B, Laisney M, Brazo P, Delamillieure P, Eustache F, Dollfus S. Semantic hyperpriming in schizophrenic patients. Increased facilitation or impaired inhibition in semantic association processing? Schizophr Res 2007; 89: 243 –50.[CrossRef] [Medline]
3 Lecardeur L, Brazo P, Dollfus S, Giffard B, Laisney M, Eustache F, Stip E. Does hyperpriming reveal impaired spreading of activation in schizophrenia? Schizophr Res 2007; 97: 289 –91.[CrossRef] [Medline]
In the largest UK study of twins with schizophrenia two hundred sixty seven twins were invited to complete a comprehensive series of intelligence and memory tests. Both identical and non-identical twins took part, in some pairs both twins were affected by the illness and in others only one twin. Sophisticated genetic modelling statistical analyses were then used to determine to what extent the intelligence deficits were related to the genetic risk for the illness.
The researchers found a significant correlation between intelligence and schizophrenia with 92% of the covariance between the two accounted for by shared genetic variance. Genetic influences also explained most of the covariance between working memory and schizophrenia.
Environmental effects, though separately linked to neurocognition and schizophrenia did not in general contribute to their correlation. These results imply that to some extent the genes that influence schizophrenia are the same as those responsible for intelligence and working memory Identifying those genes would effectively allow us to identify some of the genes contributing to schizophrenia.
Substantial Genetic Overlap between Neurocognition and Schizophrenia: Genetic Modelling in Twin Samples authored by Timothea Toulopoworking memory.ulou; Marco Picchioni; Fruhling Rijsdijk; Mei Hua-Hall; Ulrich Ettinger; Pak Sham; Robin Murray Arch Gen Psychiatry 2007;64 1348-1355
prospective memory at fault: an experimental study
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