The Psychological & Neuroscientific musings of sandygautam
Posts tagged psychosis
Am happy, will seek novelty; am sad, will stick with familiar
Feb 25th
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I have earlier written about the entrepreneurial roller-coaster and how when entrepreneurs are in a happy mood, they focus on long-term vision related creativity; while when they are in negative mood they focus on the task at hand. I had also tried to relate this to prevention and promotion focus and weave it in the narrative of preventive focus as depressive and promotion focus as being manic in nature.
Another bit of research extends the thesis and adds to our knowledge base. This new article by Winkielman et al suggest that people in sad mood tend to value familiarity whereas those in a happy mood are more open and welcoming of novelty.
Here is the abstract of the study:
People often prefer familiar stimuli, presumably because familiarity signals safety. This preference can occur with merely repeated old stimuli, but it is most robust with new but highly familiar rototypes of a known category (beauty-in-averageness effect). However, is familiarity always warm? Tuning accounts of mood hold that positive mood signals a safe environment, whereas negative mood signals an unsafe environment. Thus, the value of familiarity should depend on mood. We show that compared with a sad mood, a happy mood eliminates the preference for familiar stimuli, as shown in measures of self-reported liking and physiological measures of affect (electromyographic indicator of spontaneous smiling). The basic effect of exposure on preference and its modulation by mood were most robust for prototypes (category averages). All this occurs even though prototypes might be more familiar in a happy mood. We conclude that mood changes the hedonic implications of familiarity cues.
The authors reasoning is as follows:
Happy or sad mood signal the safety of the environment.
Much psychological research points out that one signal of environmental safety or danger is an individual’s mood (e.g., Clore, Schwarz, & Conway, 1994; Schwarz, 2002). Bad mood signals a problem, tuning individuals toward safety concerns, whereas good mood signals that an environment is benign. Tuning accounts assume that mood adjusts cognitive and affective reactions so that they best serve the individual in the specific context.
In a safe environment, one can experiment or value novelty. In an unsafe environmental it makes sense to stick to tried and proven things.
After all, familiarity is only a heuristic cue to safety. Thus, as with any heuristic cue, its validity and hedonic meaning vary by context (Hertwig, Herzog, Schooler, & Reimer, 2008). Specifically, the familiarity-positivity link should depend on whether individuals are tuned toward safety concerns. Familiarity should be valued in an unsafe environment, but less so in a benign environment (e.g., Bornstein, 1989). Analogously, in a strange city a familiar face elicits a warm glow, whereas locally the same face prompts a yawn. Numerous studies (and parents) have observed that in unsafe environments infants are neophobic, but in safe settings, they are less so (Shore, 1994). Similarly, in multiple species, stress increases neophobia, whereas comfort reduces it.
Thus they hypothesize that sad mood should lead to mare liking for familiarity while happy mood should lead to novelty preference. They do some clever experimentation and get exactly the same result.
To me this is extension of promotion focus is expansive, is happy, is creative and long-term, and is novelty preferring versus prevention focus is restrictive, is sad, is focused on the task at hand, and is familiarity preferring. In other words people in safe environments having promotion focus are manic while those in unsafe environments and having prevention focus are depressive.
Another finding that struck out from the current paper was that the (false) memory for prototype was increased in positive mood condition. This is congruent with the fact that the promotion focus / mania condition has a more narrative focus that tries to weave a narrative around things and remembers a gist rather than is accuracy based and tries to recall the exact events. thus, I believe the risk of delusions and hallucinations magnifies as one goes deep into promotion focus / mania and starts weaving narratives and having false prototypical memories of events/happenings.
de Vries, M., Holland, R., Chenier, T., Starr, M., & Winkielman, P. (2010). Happiness Cools the Warm Glow of Familiarity: Psychophysiological Evidence That Mood Modulates the Familiarity-Affect Link Psychological Science DOI: 10.1177/0956797609359878
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Dec 2nd
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I have blogged extensively about the Autism and Schizophrenia as opposites on a continuum theory. I remember first putting this theory in words in an article 3 yrs back on the mouse trap titled Autism and Schizophrenia: the two cultures. That 2006 article, in turn, was inspired by Daniel Nettle’s 2005 article in Journal of Research in Personality where Nettle had also proposed the dichotomy and that paper helped crystallize my thoughts on the subject, a theory which I had been building on my own and now supported by someone like Nettle who I respect a lot. Important to note that at that time I was blissfully unaware of Badcock or Crespi and their work. It is to the credit of Badcock that he had published in 2006 his own theory of Autism and Schizophrenia as opposites on a continuum based on parental imprinting of genes and proposed a mechanism. Crespi I guess got involved in Badcocks’s efforts later on and gave it more experimental and theoretic grounding. I firts became aware of Badcock and Crespi’s work in early 2008.
The wider world became aware of the Autism/Schizophrenia dichotomy sometime in late 2008 (November 2008) . at that time too, I was a little disappointed because most of the coverage did not mention Daniel Nettle, who I think should be credited for this work and line of reasoning too. As a consolation, some reports did mention Chris Frith who has also been partly supporting the thesis.
I wanted to give a historical perspective, because I am sure the recent Crespi article would be grabbed on by mainstream media and the pioneers Chris Frith/Nettle perhaps overlooked- but to me they too are heroes for having come up with such profound early insights. this is not to discredit teh work of Badcock and Crespi- they are doing a thorough job of convincing the skeptics and delineating the exact mechanism and genetics involved.
While we are on the topic of historical perspective , let me also pat myself on the back. In May 2008, a study came out that de novo Copy Number Variations’s (CNVs) were quite high in schizophrenics and they are in the same region as that for autistics who also have high CNVs in the same region. While some took that result to imply that Schizophrenia and Autism are same and are not different, I persisted and proposed a mechanism, whereby they could still be opposites : To quote:
Now as it happens previous research has also found that CNVs are also found to a higher extent in autistics. Moreover, research has indicated that the same chromosomal regions have CNVs in both Autism and Schizophrenia. To me this is exciting news. Probably the chromosomal region (neurexin related is one such region) commonly involved in both schizophrenia and autism is related to cognitive style, creativity and social thinking. Qualitatively (deletions as opposed to duplications) and quantitatively (more duplications) different type of CNVs may lead to differential eruption of either Schizophrenia or Autism as the same underlying neural circuit gets affected due to CNVs, though in a different qualitative and quantitative way.
Now one and half year later Crespi et al report the results of their study which has found exactly the same- that is, if deletions in some locus lead to autism, duplications lead to schizophrenia and vice versa. That to me is clinching evidence of my thesis. Who says Science does not happen on blogs- I proposed something to flow as a consequence of theory and exactly the same thing is found as per the hypothesis. I feel vindicated and emotional to some extent. Loves labor has not been lost to deaf ears.
Let us then return to the new and latest study that has sort of proven that Autism and Schizophrenia are opposites, genetically. Crespi et al, report in the latest PNAS edition that comparative genomics leads to that conclusion. What Crespi et al did was look at theCNV s and the locus whee CNV in both Autism and Schizophrenia are involved and sure enough they found the pattern I had proposed. I’ll now quote from the abstract and the article extensively:
We used data from studies of copy-number variants (CNVs), singlegene associations, growth-signaling pathways, and intermediate phenotypes associated with brain growth to evaluate four alternative hypotheses for the genomic and developmental relationships between autism and schizophrenia: (i) autism subsumed in schizophrenia, (ii) independence, (iii) diametric, and (iv) partialoverlap. Data from CNVs provides statistical support for the hypothesis that autism and schizophrenia are associated with reciprocal variants, such that at four loci, deletions predispose to one disorder, whereas duplications predispose to the other. Data from single-gene studies are inconsistent with a hypothesis based on independence, in that autism and schizophrenia share associated genes more often than expected by chance. However, differentiation between the partial overlap and diametric hypotheses using these data is precluded by limited overlap in the specific genetic markers analyzed in both autism and schizophrenia. Evidence from the effects of risk variants on growth-signaling pathways shows that autism-spectrum conditions tend to be associated with upregulation of pathways due to loss of function mutations in negative regulators, whereas schizophrenia is associated with reduced pathway activation. Finally, data from studies of head and brain size phenotypes indicate that autism is commonly associated with developmentally-enhanced brain growth, whereas schizophrenia is characterized, on average, by reduced brain growth.These convergent lines of evidence appear most compatible with the hypothesis that autism and schizophrenia represent diametric conditions with regard to their genomic underpinnings, neurodevelopmental bases, and phenotypic manifestations as reflecting under-development versus dysregulated over-development of the human social brain.
Copy Number Data. Rare copy-number variants (CNVs) at seven loci, 1q21.1, 15q13.3, 16p11.2, 16p13.1, 17p12, 22q11.21, and 22q13.3 (Tables S1 and S2), have been independently ascertained and associated with autism and schizophrenia in a sufficient number of microarray-based comparative genomic hybridization (aCGH) and SNP-based studies to allow statistical analysis of the frequencies of deletions versus duplications in these two conditions (Table 1, Tables S3–S9). For five of the loci (1q21.1, 16p11.2, 16p13.1, 22q11.21, and 22q13.3), specific risk variants have been statistically supported for both autism and schizophrenia using case-control comparisons, which allows direct evaluation of the alternative hypotheses in Fig. 1. One locus (16p13.1) supports a model of overlap, and four loci support the reciprocal model, such that deletions are associated with increased risk of autism and duplications with increased risk of schizophrenia (16p11.2, 22q13.3), or deletions are associated with increased risk of schizophrenia and duplications with increased risk of autism (1q21.1, 22q11.21). For 1q21.1 and 22q11.21, contingency table analyses also indicate highly significant differences in the frequencies of deletions compared with duplications for the two disorders, such that schizophrenia is differentially associated with deletions and autism with duplications. By contrast, for 16p11.2 and 22q13.3 such analyses show that autism is differentially associated with deletions and schizophrenia with duplications.
I cannot cut n paste the table, but a look at the table clears all doubts. They also look at gene association data and come to a similar conclusion ruling out model A (autism, subsumed in schizophrenia) or model B (autism and schizophrenia are independent of each other).
Models 1C (diametric) and 1D (overlapping) both predict broad overlap in risk genes between autism and schizophrenia, and do not necessarily predict an absence or paucity of genes affecting one condition but not the other. In theory, these models can be differentiated by using data on specific risk alleles for specific loci (such as single-nucleotide polymorphisms, haplotypes, or genotypes), which should be partially shared under the overlapping model but different under the diametric model. For the genes DAO, DISC1, GRIK2, GSTM1, and MTHFR, the same allele, genotype, or haplotype was associated with both autism and schizophrenia, and for the genes AHI1, APOE, DRD1, FOXP2, HLA-DRB1, and SHANK3, alternative alleles, genotypes, or haplotypes at the same loci appear to mediate risk of these two conditions (SI Text). For the other genes that have been associated with both conditions, heterogeneity in the genetic markers used, heterogeneity among results from multiple studies of the same genes, and the general lack of functional information preclude interpretation in terms of shared or alternative risk factors.
Models of autism as a subset of schizophrenia (Fig. 1A), and autism and schizophrenia as independent or separate (model 1B), can be rejected with some degree of confidence, but models involving diametric etiology (model 1C) or partial overlap (model 1D) cannot be clearly rejected. Taken together, most of the data and analyses described here appear to support the hypothesis of autism and schizophrenia as diametric conditions, based primarily on the findings that reciprocal variants at 1q21.1, 16p11.2, 22q11.21, and 22q13.3 represent statistically-supported, highly-penetrant risk factors for the two conditions (Table 1), and that for a number of genes, alternative alleles or haplotypes appear to mediate risk of autism versus schizophrenia. Additional lines of evidence supporting the diametric hypothesis, from previous studies of autism and schizophrenia, include:
- 1. Data showing notable rarity of familial coaggregation of autism with schizophrenia (38), in contrast, for example, to strong patterns of co-occurance within pedigrees of schizophrenia, schizoaffective disorder, and bipolar disorder (39).
- 2. Psychiatric contrasts of Smith-Magenis syndrome with Potocki-Lupski syndrome (due to the reciprocal duplication at the Smith-Magenis locus), Williams syndrome with cases of Williams-syndrome region duplication, and Klinefelter syndrome with Turner syndrome, each of which tends to involve psychotic-affective spectrum phenotypes in the former syndrome, and autistic spectrum conditions in the latter (5, 40).
- 3. Effects of autism and schizophrenia risk alleles on common growth-signaling pathways, such that autism has been associated with loss of function in genes, such as FMR1, NF1, PTEN, TSC1, and TSC2 that act as negative regulators of the PI3K, Akt, mTOR, or other growth-signaling pathways (41–45), whereas schizophrenia tends to be associated with reduced function or activity of genes that up-regulate the PI3K, Akt, and other growth-related pathways (46–49).
- 4. Increased average head size, childhood brain volume, or cortical thickness in individuals with: (i) idiopathic autism (50–53), (ii) the autism-associated duplications at 1q21.1 (17) and 16p13.1 (32) and the autism-associated deletions at 6p11.2 (31), and (iii) autism due to loss of function (or haploinsufficiency) of FMR1 (54), NF1 (55), PTEN (56) and RNF135 (57). By contrast, reduced average values for brain size and cortical thickness, due to some combination of reduced growth and accelerated gray matter loss, have been demonstrated with notable consistency across studies of schizophrenia (58–62), and such reduced head or brain size has also been associated with the schizophrenia-linked CNVs at 1q21.1 and 22q11.21 (17, 63, 64), and with deletions of 16p13.1 (65).
I am more than pleased with these results. Badcock too is. You can read his comments here. What about you? What would it take to convince you?
Crespi, B., Stead, P., & Elliot, M. (2009). Evolution in Health and Medicine Sackler Colloquium: Comparative genomics of autism and schizophrenia Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0906080106
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Nov 21st
I recently came across this TED talk by Devdatt Patnaik, A chief Belief Officer in an Indian industry group and was fascinated by his description of the distinction between logos based ‘the’ world which is objective, logical, universal, factual and science based and mythos based ‘my’ world which is subjective,emotional, personal, belief-based and mythological in nature. while ‘the’ world tries to answer ‘how’, ‘my’ world tires to answer ‘why’.
To me the same is true of Autism and Psychosis dichotomy. While autistic frame of reference is rooted in ‘the’ world – trying to apply a science based approach even to the mind and mental; the psychotic frame of reference becomes detached from ‘the’ world and is totally enamored by the subjective depths of ‘my’ world -attributing mental properties to physical things too.
Devdatt, later on goes to contrast East Vs West Myths and here at the second order , though we are talking of mythos and not of logos and are in the psychotic/mythic world , we see a difference in focus, between the eastern traditions and the western traditions. While the east is portrayed as more spiritual and renunciation-believing in multiple lives and thus multiple chances; the west is depicted as more materialistic and ambitious and believing in one and only life and thus believing in only one chance of redemption -and though this dichotomy may be simplistic it does bring into focus the fact that the cultures do differ profoundly.
The difference between cultures and mythologies, and the people shaped from them thereof, is important in light of a new study , for eg., that demonstrates that most of the behavioral research is carried on with WEIRD people! WEIRD stands for Western, Educated, Industrial, Rich and Democratic subjects and the paper claims that these WEIRD subjects are outliers and not representative of the general population. If much of the scientific and psychological research is done on WEIRD subjects (which is a fact) and if WEIRD are not representative of the population (which seems reasonable given the differences in culture and the ability of culture to shape people) , than that raises a more serious questions on the results of behavioral studies than the voodoo correlations paper raised questions about the fMRI studies.
Devdutt, though seems to be slightly biased towards Indian culture, but the TED talk is worth a watch. And you may also find one of my earlier post relating Indian culture,religion, and Autism, Schizophrenia quite pertinent here.
Do you think Devdutt is right when he stresses differences in cultures and myths? If so, do you think Culture shapes people? and if so do you believe with Norenzayan et al that if we just do studies based on WEIRD subjects, our results are not representative but skewed. Lot of questions to think about!
Joseph Henrich, Steven J. Heine, & Ara Norenzayan (2009). The Weirdest People in the World? Behavioral and Brain Sciences
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Nov 9th
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Two main underlying deficits have been proposed in autism- one concerning an inactive or non-existent Theory of Mind module and another a tendency towards Weak Central Coherence. ToM defects reflect in the communicative, social and imaginative deficits seen in autistics; while the savant skills as well as restrictive and repetitive behavior (restricted repertoire of interests ;obsessive desire for sameness – islets of ability – idiot savant abilities – excellent rote memory – preoccupation with parts of objects ) are best explained by taking recourse to the Autism-as-a cognitive-style having weak Central Coherence argument. I’ve discussed the crucial aspects of both of these two dimensions in y series of posts on autism and psychosis and shown how they have to be seen on a continuum and more as deviation from the normal range with one end as autism and the other as psychosis. We also know that psychosis itself is two dimensional with one dimension being that of schizophrenic spectrum and the other the bipolar spectrum. Thus what I propose is that we start seeing Autism also as a two dimensional disorder with TOM defect subtype a mirror image of schizophrenia; while the Weak CC subtype a mirror image of bipolar or manic depressive phenotype. Here are autistic and psychotic features on these dimensions (from Autism, Happe, the autistic deficits and assets table):
- ordering behavioural pictures (Baron-Cohen et al. 1986) vs ordering mentalistic pictures understanding “see” (Perner et al. 1989)
- understanding “know” protoimperative pointing (Baron-Cohen 1989c) vs protodeclarative pointing sabotage (Sodian & Frith 1992)
- deception false photographs (Leekam & Perner 1991, Leslie & Thaiss 1992) vs. false beliefs recognising happiness and sadness (Baron-Cohen et al. 1993a)
- recognizing surprise object occlusion (Baron-Cohen 1992) vs. information occlusion
- literal expression (Happé 1993) vs. metaphorical expression
- elicited structured play (Wetherby & Prutting 1984)vs. spontaneous pretend play
- instrumental gestures (Attwood et al. 1988) vs. expressive gestures
- talking about desires and emotions (Tager-Flusberg 1993) vs. talking about beliefs and ideas
- using person as tool (Phillips 1993) vs. using person as receiver of information
- showing “active” sociability (Frith et al. 1994) vs. showing “interactive” sociability
It is also pertinent in this regard to revisit the question of co-occurrence of autism and schizophrenia. Happe maintains that psychois can only be relaibly seen in Asperge’s group who might have a late developing ToMm ability. To quote:
The higher incidence of psychiatric disorders in this group (asperger’s group) (Tantam 1991, Szatmari et al. 1989b) is well explained by this hypothesis. Depression will be more common since these people have greater insight into their own difficulties and their own feelings and thoughts. Positive symptoms of psychosis, such as hallucinations and delusions would be found only in Asperger’s syndrome cases by this account, if one takes Frith & Frith’s (1991) view of these symptoms as resulting from an “over-active” theory of mind. Asperger’s syndrome people, who gain theory of mind late and therefore abnormally, may be at high risk for having their theory of mind “go wrong”. On this hypothesis it would be impossible for a Kanner-type autistic person (who has no theory of mind) to show these psychotic or positive symptoms. In this sense (according to Frith & Frith’s theory) Asperger’s syndrome would be something of a midpoint between autism and (positive or florid) schizophrenia; while the former is due to a lack of theory of mind, and the latter due to over-active theory of mind, some people with Asperger’s syndrome may show both the scars of early lack and the florid symptoms of late acquired theory of mind working abnormally hard.
There is some preliminary evidence to support the suggestion that the term “Asperger’s syndrome” could meaningfully be restricted to those subjects with autism who have achieved some ability to think about thoughts. Ozonoff et al. (1991) found that their group labelled (perhaps arguably) as having Asperger’s syndrome did not show impairments relative to controls.
It is interesting to note the ‘over-active’ theory of mind reference to Frith and Frith. I could not locate that paper but came across another paper by Abu-akkel that propose over-active ToM as a mechanism of psychosis. There are also some full text related articles available online that may be of interest to the serious reader. As for me, it is heartening to note that others concur with the theory of autism and psychosis as opposites on a continuum.
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Oct 21st
Jonah Lehrer, has an article in this week’s Nature News, (find a PDF here) , regarding 30 or so cognitively enhanced mice strains that have been bred and genetically engineered. As Lehrer very elaborately documents, all these have enhanced LTP as an intervening mechanism that leads to improvements in learning and memory. Most of the genes involved affcet the LTP mechanism in one way or the other to breed super mnemonist mice. However, from the time of Luria, t has been well known that those who have enhanced memory also suffer from some of its disadvantages and that the ability to forget is also very important.
Little is known about the side effects and tradeoffs of both the current usage or the drugs in development, but initial clues offered by smart mice raise concerns. The Hras strain developed in Silva’s lab might be good at learning, but its fear response for a relatively benign stimulus would be counterproductive for a wild mouse. Its enhanced memory is both a blessing and a burden. Silva cites other strains of smart mice that excel at solving complex exercises, such as the Morris water maze, but that struggle with simpler mazes. “It’s as if they remember too much,” he says — possibly taking in irrelevant information such as the position of windows or lights but missing the big clues. Farah sees a parallel between these mice and one of the few case studies of an individual with profoundly enhanced memory. In the early 1920s, the Russian neurologist Alexander Luria began studying the learning skills of a newspaper reporter called Solomon Shereshevsky, who had been referred to the doctor by his editor. Shereshevsky had such a perfect memory that he often struggled to forget irrelevant details. After a single read of Dante’s Divine Comedy, he was able to recite the complete poem by heart. Although thisLittle is known about the side effects and tradeoffs of both the current usage or the drugs in development, but initial clues offered by smart mice raise concerns. The Hras strain developed in Silva’s lab might be good at learning, but its fear response for a relatively benign stimulus would be counterproductive for a wild mouse. Its enhanced memory is both a blessing and a burden. Silva cites other strains of smart mice that excel at solving complex exercises, such as the Morris water maze, but that struggle with simpler mazes. “It’s as if they remember too much,” he says — possibly taking in irrelevant information such as the position of windows or lights but missing the big clues.
Farah sees a parallel between these mice and one of the few case studies of an individual with profoundly enhanced memory. In the early 1920s, the Russian neurologist Alexander Luria began studying the learning skills of a newspaper reporter called Solomon Shereshevsky, who had been referred to the doctor by his editor. Shereshevsky had such a perfect memory that he often struggled to forget irrelevant details. After a single read of Dante’s Divine Comedy, he was able to recite the complete poem by heart. Although this flawless memory occasionally helped Shereshevsky at work — he never needed to take notes — Luria also documented the profound disadvantages of such a capacious memory. Shereshevsky, for instance, was almost entirely unable to grasp metaphors, as his mind was so fixated on particulars. When he tried to read poetry, for example, “the obstacles to his understanding were overwhelming”, Luria wrote in his book The Mind of a Mnemonist. “Each expression gave rise to a remembered image; this, in turn, would conflict with another image that had been evoked.”
For Luria, Shereshevsky’s struggles were a powerful reminder that the ability to forget is as important as the ability to remember. Enhancing human memory in individuals without severe cognitive defects might prove counterproductive.
It is interesting to pause here and note that many savants who have excellent memory are also autistic and that schizophrenics on the opposite end of the spectrum are characterized by too much reliance of metaphors and too much generalizations and abstractions. Further Martha Farah notes the following:
Many scientists are concerned that the animal models of enhanced cognition might obscure subtle side effects, which can’t be studied in rodents or primates. Farah is currently looking at the trade-off between enhanced attention — she gives human subjects a mild amphetamine — and performance on creative tasks. Other researchers have used computer models to show that memory is actually optimized by slight imperfections, as they allow one to see connections between different but related events9. “The brain seems to have made a compromise in that having a more accurate memory interferes with the ability to generalize,” Farah says. “You need a little noise in order to be able to think abstractly, to get beyond the concrete and literal.”
Again, one can easily see the correlations with Autism and Schizophrenia- one end marked by too narrow a focus , while the other marked by too much noise and divergent creativity. I would have been happy to incorporate the more LTP as autistic and less LTP as schizophrenics, but it flies in face of my earlier findings regarding experience dependent plasticity in autism and schizophrenia where the conclusions were just the revers. Yet, it is clear that synaptic plasticity is a majo mechanism involved in the autism/psychosis differentiation. Do let me know if you can reconcile the new findings with the older ones to come up with the right LTP and psychosis/autism relationship.
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