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Edinburgh was rightly chosen for the ISIR conference this year, since it must now rank as the world leader in intelligence research.

120 delegates gathered in the grand surroundings of the Royal Society of Edinburgh, bathed in the almost perpetual Northern sunlight of this noble city, to start at the beginning, which was 530 million years ago with a synapse complexity expansion, which itself was followed by a genome duplication event 30 million years later. It was the mutation of all mutations, since the duplication then duplicated again, and it is from that freak 4 duplicated genomes that all vertebrate life descends. Truly, our ancestry depends upon a mistake, and we are the spawn of error.

synapse

Seth Grant explained how the synapse functioned. Synapses are the junction boxes through which brain cells communicate with each other. One cell has a long connecting axon coming out of it which ends in several synapses right next to other brain cells and clasps them together. The transmission has to leap a tiny synaptic gap by chemical means. Most drugs operate by affecting this synaptic gap. I confess that when I learned physiology I was a very poor student and thought of it as no more than a messy junction box, and would have preferred it to be made of copper wires rather than a chemical exchange soup. Wrong, wrong, utterly wrong. In fact, the synapse takes the digital signal from the nerve and converts it into a highly informative analogue signal depending on the time intervals of the arriving digital signals. The synapse counts, and then draws a graph. This exquisitely informative shape provides patterns, and even a 9 by 9 array of synaptic receptor will provide a rich mental map of every move an organism takes, like a film. It is a Youtube of events registered at the synaptic level. Given that there are so many receptors, each with different triggering sensitivities, complex computation can be carried out at the synaptic level. In short, it was good to hear all this laid out before us. The relays are doing a lot of the thinking.

Seth Grant went on to discuss a puzzle: why does schizophrenia have such a late onset? Autism reveals itself very early. Attention deficits and other problems are detectable at 3 years of age, and by 11 years of age most of the psychological problems a child may have are already evident. Schizophrenia, on the other hand, seems to come almost out of the blue in the 17 to 25 year period. How can the heritable susceptibility lie dormant so long, and what triggers the breakdown?

Skene, NG, Roy, M & Grant, SG 2017, ‘A genomic lifespan program that reorganises the young adult brain is targeted in schizophrenia’ eLIFE, vol 6. DOI: 10.7554/eLife.17915

The genetic mechanisms regulating the brain and behaviour across the lifespan are poorly understood. We found that lifespan transcriptome trajectories describe a calendar of gene regulatory events in the brain of humans and mice. Transcriptome trajectories defined a sequence of gene expression changes in neuronal, glial and endothelial cell-types, which enabled prediction of age from tissue samples. A major lifespan landmark was the peak change in trajectories occurring in humans at 26 years and in mice at 5 months of age. This species-conserved peak was delayed in females and marked a reorganization of expression of synaptic and schizophrenia-susceptibility genes. The lifespan calendar predicted the characteristic age of onset in young adults and sex differences in schizophrenia. We propose a genomic program generates a lifespan calendar of gene regulation that times age-dependent molecular organization of the brain and mutations that interrupt the program in young adults cause schizophrenia.

Schizophrenia tends to run in families and it is likely that different combinations of faulty genes that affect the connections between nerve cells increase the chance of having the disease. Until now, scientists have assumed that certain situations and environmental factors trigger the condition, but it was unknown if genes could influence the age at which the disease will begin.

To explore whether genes in the brain change at certain time points, Skene et al. examined how the genes are turned on and off across the lifespan of healthy mice and humans. The results showed that in both mice and humans, a ‘genetic lifespan calendar’ controlled every cell type in the brain and directed the way they worked at different ages. The timing was so precise that it was possible tell the age of a mouse or a person simply by looking at the way the genes were expressed in a tissue sample.

Skene et al. then studied how the genetic lifespan calendar controlled the genes damaged in schizophrenia, and found that the calendar caused a major reorganization of the genes at the time when the symptoms started. This suggests that the genetic lifespan calendar is a crucial factor that can determine at what age the disease will start.

The next step will be to study how the genetic lifespan calendar programs changes throughout the brain and to explore if it could be manipulated to change how the brain ages. This could help to develop new types of treatments for schizophrenia and other conditions of the brain.

https://www.research.ed.ac.uk/portal/files/43307105/elife_17915_v1.pdf

It could be that mutation load accumulates in post-synaptic proteins, and gene regulation changes a lot during that period, so that brains also change considerably, and it is enough to trigger a major disorder in the vulnerable 1%. Since therapies might not be able to target all the specific causes of schizophrenia, it might be better to find a pharmacological way (for genetically vulnerable teenagers) of slowing down the general gene regulation changes until such time as the person is more resilient. I likened it to being a good mountaineer, but lacking oxygen as you get experienced enough to climb the highest peaks.

What this lecture shows is that real subjects develop and are altered by discoveries in related fields. Essentially, we are studying the brain, and doing so with the best tools available. The tool set has expanded considerably in the last decade. This should boost our understanding, as when a walker in a city discovers that the edge of their familiar neighbourhood links to other neighbourhoods in ways they had not realized. I call it the London Underground Pop Up phenomenon. Places formerly seen as disparate countries with their tube station capitals are revealed, by one long intrepid walk, to be adjoining principalities in a grander continent.

 
• Category: Science • Tags: Genetics, Schizophrenia 
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  1. dearieme says:

    “the almost perpetual Northern sunlight of this noble city”: quite right. You can finish work about six or six-thirty, have a quick, early dinner, and then get in a round of golf, or an evening’s croquet, or a walk in the hills or on the beaches. Or a spot of sailing – whatever appeals in summer.

    The price you pay is that Spring comes late.

    I know nothing about the workings of the brain. I’ll try to be a good student, doc. But I’m getting old and dimmer. Perhaps you’ll touch on that too?

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  2. Much more to come on ageing, but do not despair, brighter minds live longer.

    Read More
    • Replies: @Wizard of Oz
    There's a paper to be written, if it hasn't been already (maybe just as a humble piece of work for a Masters degree), on the positive effects of smart hones on the ageing brain.

    I refer to both the reinforcement effects on specific memories and on the maintenance of mental agility. One can surely get both combined if you search your mind for a name or quote or formula and, not achieving satisfaction, quickly but with concentration choose the key words and/or phrases to put into one's Google search line on one's home page.

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  3. TheJester says:

    Schizophrenia tends to run in families and it is likely that different combinations of faulty genes that affect the connections between nerve cells increase the chance of having the disease. Until now, scientists have assumed that certain situations and environmental factors trigger the condition, but it was unknown if genes could influence the age at which the disease will begin.

    Dr. Thompson,

    It seems that the claim is that schizophrenia may be epigenetic as a function of the environment and high mutational loads operating against a hitherto unknown genetic calendar governing gene expressions within the brain. Sounds almost too complex to describe.

    My father was diagnosed with schizophrenia in his early 30s in the 1950s; the diagnosis was that he was incurable. I had the privilege of understudying his schizophrenia as I grew up. Fortunately, no one else in the family line before or after has been diagnosed with schizophrenia … an odd duck, perhaps, although I do find some of my relatives strange. (I’m sure they would return the compliment :-)

    What this lecture shows is that real subjects develop and are altered by discoveries in related fields. Essentially, we are studying the brain, and doing so with the best tools available. The tool set has expanded considerably in the last decade. This should boost our understanding, as when a walker in a city discovers that the edge of their familiar neighbourhood links to other neighbourhoods in ways they had not realized. I call it the London Underground Pop Up phenomenon. Places formerly seen as disparate countries with their tube station capitals are revealed, by one long intrepid walk, to be adjoining principalities in a grander continent.

    The above caught my eye. It seems to describe my father’s progressive sense of renewable awareness as he aged. He had a massive library that covered the Greek classics, through the Romans, to contemporary times. He read about things, experienced things (including WWII), and noticed things. He was always discovering that he lived in “disparate countries” that constantly required new understandings … as well as the realization that most everything he had previously known and had accepted as true was now false.

    How does one deal with losing confidence, not only in your own judgement but also in your sense of perception? It would seem, at the point, that everything is up for grabs.

    Was my father crazy … or, was the world that he perceived undecipherable because it is undecipherable? The history of science and human relations would suggest the latter, which would mean the rest of us might to too quick to judgement regarding what is real.

    Perhaps ignorance is bliss … the fact that most of us live with highly filtered and inconsistent presumptions about reality that help keep us “balanced” … and within the DSM-defined boundaries of what is considered functional.

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  4. jake n says:

    Are you guys planning on uploading these brilliant lectures on youtube? I’d love to watch them.

    Read More
    • Replies: @James Thompson
    I am afraid that they were not recorded, but I will ask for the slide decks.
    , @James Thompson
    I am afraid that they were not recorded, but I will ask for the slide decks.
    , @jake N
    Thanks! That would be great.
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  5. @jake n
    Are you guys planning on uploading these brilliant lectures on youtube? I'd love to watch them.

    I am afraid that they were not recorded, but I will ask for the slide decks.

    Read More
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  6. The brain being an electrochemical–that is, physica–mechanism, and every state of a physical mechanism being determined by the previous state, our thughts would seem to be determined and therefore not precisely thoughts. If this is not true, tell me why it is not.A neurotransmitter cannnot decide whether to diffuse across a gap any more than a bowling ball can decide to fall sideways, no? Therefore we cannnot think, QED. This tracks well with most of political commentary.

    Read More
    • Replies: @anon
    Fred,
    Uhm... quantum mechanics? Just kidding, I'm more and more of the Bohmian persuasion which claims that QM is actually deterministic if you posit the existence of a pilot wave.
    , @Wizard of Oz
    Try reading The Mind Matters by David Hodgson who sadly died at 72 only months after retiring from the New South Wales Court of Appeal. He had topped NSW in mathematics at the Matriculation/Higher School Certificate level about 1957 and later became a Rhodes Scholar noted as his best ever student by one Oxford philosophy prof. While on the bench he taught himself Quantum Mechanics and incorporated what he got from that into his "The Mind Matters". Frequent commenter CanSpeccy has I think read more of it than I and I don't think bought it all. However, it could only be good for the brain to have a go at it.
    , @utu

    Therefore we cannnot think
     
    What is "we" that "can" or "cannot" in this sentence? The issue of free will is intractable. Either we have it or we do not. In materialistic world to which you and Dr. Thompson most likely subscribe there is no free will. Consciousness is just an epiphenomenon w/o any practical consequences. We are just philosophizing zombies whose philosophizing is inconsequential. Bertrand Russel rejected the no free will posture on practical grounds: life with a belief in no free will would be impossible. But where form can we get free will? Only from God. It must be postulated and the materialistic framework must be abandoned. You have to postulate the free will and step outside the materialist framework. God gave you free will. Take it or leave it. And obviouly you can leave it as a philosophizing zombie whose philosophizing even if full of antinomies and contradictions have no consequences. "You" "can" say and think whatever you "want" because it is not in your control anyway and your belief in free will is just a pretense if you subscribe to materialism.

    Somebody already brought up quantum physics that it could save free will in deterministic world:

    http://www.informationphilosopher.com/freedom/history/
    In his Gifford Lectures of 1927, Arthur Stanley Eddington had described himself as unable "to form a satisfactory conception of any kind of law or causal sequence which shall be other than deterministic." Eddington had already established himself as the leading interpreter of the new relativity and quantum physics. His astronomical measurements of light bending as it passes the sun had confirmed Einstein's general relativity theory.

    A year later, in response to Heisenberg's uncertainty principle, Eddington revised his lectures for publication as The Nature of the Physical World. There he announced "It is a consequence of the advent of the quantum theory that physics is no longer pledged to a scheme of deterministic law," and enthusiastically identified indeterminism with freedom of the will.

    But Eddington left himself open to the charge since Epicurus' time, that chance could not be identified with freedom. He was apparently unaware of the work of William James or Henri Poincaré to make deliberation a two-stage process - first random possibilities, then a choice. A decade later, in his 1939 book The Philosophy of Physical Science, just a few years before his death, he reluctantly concluded there is no "halfway house" between randomness and determinism - an echo of Hume's "no medium betwixt chance and an absolute necessity."
     
    , @Rurik
    Hey Fred, it's your ol' pal Rurik,

    The brain being an electrochemical–that is, physica–mechanism, and every state of a physical mechanism being determined by the previous state, our thughts would seem to be determined and therefore not precisely thoughts. If this is not true, tell me why it is not.A neurotransmitter cannnot decide whether to diffuse across a gap any more than a bowling ball can decide to fall sideways, no? Therefore we cannnot think, QED.
     
    Why, if our thoughts are determined, (as they indeed are) do they stop being thoughts?

    I'm thinking right now that I'm going to write this next word; lomatricine.

    I thought up that 'word', and in doing so, brought to bear all of my respective nature and nurture, all of which are a consequence of what transpired previously. There is no way I could have thought of that word, were it not for what I was born as, and the life and experiences I've lived subsequently.

    If there were such a thing as free will, then you'd be able to think in anyway possible. You'd be literally free to think as a Somali teenage girl, or have a thought that your typical Oprah fan would have on any given day. But you can't do that, because you're limited by being Fred, and having been born with your particular gifts and proclivities and penchants, some of which are a consequence of your 'nurture', which to say is the experiences you've had over your years.

    If our will were free, we could think in anyway and everyway we liked, and be free to have thoughts that would transcend Aristotle. But we can't, because our will, and our minds are limited in exactly the way you point out, being as our brains are organic, and subject to those limitations.

    So the act of thinking, is not any less so because of those limitations. We do indeed think, but it's like a dog thinks, (I want food, I want pussy, that other dog better watch out or I'm gonna whup some arse). What it isn't like is how a God would think, iow unlimited by mortal flesh.

    We are mortal, and limited. But that doesn't stop us from thinking of words like lomatricine. if it suits our whim.

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  7. hyperbola says:

    The most advanced city in “intelligence research” can only muster 120 delegates??? Sounds like this is a dying field.

    As for schixophrenia, transcriptomic studies are not new and we have known for some time that transcription of substantial numbers of genes are involved. Amongst these are genes involved in red blood cells. Other work identifies OxPhos and mitochondria. Recent work comes from all over the world, far beyond Edinburgh. We have known for at least a decade that epigenetic effects on transcription levels are observed in other “late-onset” diseases such as breast cancer. Then there is, of course, the added complication that levels of transcribed RNA do NOT correlate particularly well with the levels of expressed proteins in many cases. This paper does not appear to be a major breakthrough.

    PLoS One. 2018 Jul 17;13(7):e0200003. doi: 10.1371/journal.pone.0200003. eCollection 2018.
    Inference of cell type content from human brain transcriptomic datasets illuminates the effects of age, manner of death, dissection, and psychiatric diagnosis.
    Hagenauer MH1, Schulmann A2, Li JZ3, Vawter MP4, Walsh DM4, Thompson RC1, Turner CA1, Bunney WE4, Myers RM5, Barchas JD6, Schatzberg AF7, Watson SJ1, Akil H1.
    Abstract
    Psychiatric illness is unlikely to arise from pathology occurring uniformly across all cell types in affected brain regions. Despite this, transcriptomic analyses of the human brain have typically been conducted using macro-dissected tissue due to the difficulty of performing single-cell type analyses with donated post-mortem brains. To address this issue statistically, we compiled a database of several thousand transcripts that were specifically-enriched in one of 10 primary cortical cell types in previous publications. Using this database, we predicted the relative cell type content for 833 human cortical samples using microarray or RNA-Seq data from the Pritzker Consortium (GSE92538) or publicly-available databases (GSE53987, GSE21935, GSE21138, CommonMind Consortium). These predictions were generated by averaging normalized expression levels across transcripts specific to each cell type using our R-package BrainInABlender (validated and publicly-released on github). Using this method, we found that the principal components of variation in the datasets strongly correlated with the predicted neuronal/glial content of the samples. This variability was not simply due to dissection-the relative balance of brain cell types appeared to be influenced by a variety of demographic, pre- and post-mortem variables. Prolonged hypoxia around the time of death predicted increased astrocytic and endothelial gene expression, illustrating vascular upregulation. Aging was associated with decreased neuronal gene expression. Red blood cell gene expression was reduced in individuals who died following systemic blood loss. Subjects with Major Depressive Disorder had decreased astrocytic gene expression, mirroring previous morphometric observations. Subjects with Schizophrenia had reduced red blood cell gene expression, ……

    [MORE]

    Int J Mol Sci. 2017 Aug 4;18(8). pii: E1711. doi: 10.3390/ijms18081711.
    Epigenomics of Major Depressive Disorders and Schizophrenia: Early Life Decides.
    Hoffmann A1, Sportelli V2, Ziller M3, Spengler D4.
    Author information
    Abstract
    Brain development is guided by the interactions between the genetic blueprint and the environment. Epigenetic mechanisms, especially DNA methylation, can mediate these interactions and may also trigger long-lasting adaptations in developmental programs that increase the risk of major depressive disorders (MDD) and schizophrenia (SCZ). Early life adversity is a major risk factor for MDD/SCZ and can trigger persistent genome-wide changes in DNA methylation at genes important to early, but also to mature, brain function, including neural proliferation, differentiation, and synaptic plasticity, among others. Moreover, genetic variations controlling dynamic DNA methylation in early life are thought to influence later epigenomic changes in SCZ. This finding corroborates the high genetic load and a neurodevelopmental origin of SCZ and shows that epigenetic responses to the environment are, at least in part, genetically controlled. Interestingly, genetic variants influencing DNA methylation are also enriched in risk variants from genome-wide association studies (GWAS) on SCZ supporting a role in neurodevelopment. Overall, epigenomic responses to early life adversity appear to be controlled to different degrees by genetics in MDD/SCZ, even though the potential reversibility of epigenomic processes may offer new hope for timely therapeutic interventions in MDD/SCZ…..

    Can J Psychiatry. 2016 Aug;61(8):457-69. doi: 10.1177/0706743716648290.
    Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia: Possible Interactions with Cellular Processes.
    Bergman O1, Ben-Shachar D2.
    Abstract
    Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate molecules by the oxidative phosphorylation system (OXPHOS). Linked to numerous signaling pathways and cellular functions, mitochondria, and OXPHOS in particular, are involved in neuronal development, connectivity, plasticity, and differentiation. Impairments in a variety of mitochondrial functions have been described in different general and psychiatric disorders, including schizophrenia (SCZ), a severe, chronic, debilitating illness that heavily affects the lives of patients and their families. This article reviews findings emphasizing the role of OXPHOS in the pathophysiology of SCZ. Evidence accumulated during the past few decades from imaging, transcriptomic, proteomic, and metabolomic studies points at OXPHOS deficit involvement in SCZ……

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    • Replies: @scientificbubble
    Indeed the " field is dying " .

    The myriad of well paid and well considered basic bioscientists has costed the USA and EU hundreds of billions of dollars and euros in the last 3 decades , and has produced millions of " impact " papers about the human brain and genoma , what has granted the authors good academic and research careers , but whose relevance for the mental patients or for the psychiatric clinicians has been very little -

    In fact if you add to the mad scientists the mad bureaucrats , with their DSM , and management delusions , you will understand why clinical psychiatry is in shambles .

    Modern psychiatrists don `t ask anylonger to the patients for their human feelings and ideas , for their ways of adaptation , their behavior . Modern clinicians only worry for serotonin , synapses , genome , brain images ...... How is your serotonin ? madam ....I `m affraid your genome is not regulating well your synapses .... you know .....
    , @puropedo
    https://www.plos.org/publication-fees

    publishing in plos costs from 1,600 to 3000 US $ per paper , according to the area .


    Most of the basic sciences studies on brain diseases are done with rats . The brain of a rat wheighs 0,5 gr. the human brain wheighs 1,500 gr , so is 3000 thousand time heavier .

    The results with rats are not extrapolable to humans . No comparison .

    Schizophrenia is a syndrome , Depression is a syndrome .... like so many medical and psychiatric conditions .
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  8. @jake n
    Are you guys planning on uploading these brilliant lectures on youtube? I'd love to watch them.

    I am afraid that they were not recorded, but I will ask for the slide decks.

    Read More
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  9. Was there discussion of comorbidities such as anorexia?

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    • Replies: @James Thompson
    No, but it was only a summary lecture, and schizophrenia was taken as an important examplar of a general point.
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  10. @Philip Owen
    Was there discussion of comorbidities such as anorexia?

    No, but it was only a summary lecture, and schizophrenia was taken as an important examplar of a general point.

    Read More
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  11. anon[693] • Disclaimer says:
    @Frederick V. Reed
    The brain being an electrochemical--that is, physica--mechanism, and every state of a physical mechanism being determined by the previous state, our thughts would seem to be determined and therefore not precisely thoughts. If this is not true, tell me why it is not.A neurotransmitter cannnot decide whether to diffuse across a gap any more than a bowling ball can decide to fall sideways, no? Therefore we cannnot think, QED. This tracks well with most of political commentary.

    Fred,
    Uhm… quantum mechanics? Just kidding, I’m more and more of the Bohmian persuasion which claims that QM is actually deterministic if you posit the existence of a pilot wave.

    Read More
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  12. anon[693] • Disclaimer says:

    Dr. Thompson,
    My mental model of the synapse probably matches your previous one, but your description has me intrigued. Do you have a reference to recommend for a more up-to-date picture of the synapse? My knowledge is about 10 years out of date.

    Read More
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  13. jake N says:
    @jake n
    Are you guys planning on uploading these brilliant lectures on youtube? I'd love to watch them.

    Thanks! That would be great.

    Read More
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  14. Yes, but what does this have to do with proving that blacks are inferior?

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  15. @James Thompson
    Much more to come on ageing, but do not despair, brighter minds live longer.

    There’s a paper to be written, if it hasn’t been already (maybe just as a humble piece of work for a Masters degree), on the positive effects of smart hones on the ageing brain.

    I refer to both the reinforcement effects on specific memories and on the maintenance of mental agility. One can surely get both combined if you search your mind for a name or quote or formula and, not achieving satisfaction, quickly but with concentration choose the key words and/or phrases to put into one’s Google search line on one’s home page.

    Read More
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  16. @Frederick V. Reed
    The brain being an electrochemical--that is, physica--mechanism, and every state of a physical mechanism being determined by the previous state, our thughts would seem to be determined and therefore not precisely thoughts. If this is not true, tell me why it is not.A neurotransmitter cannnot decide whether to diffuse across a gap any more than a bowling ball can decide to fall sideways, no? Therefore we cannnot think, QED. This tracks well with most of political commentary.

    Try reading The Mind Matters by David Hodgson who sadly died at 72 only months after retiring from the New South Wales Court of Appeal. He had topped NSW in mathematics at the Matriculation/Higher School Certificate level about 1957 and later became a Rhodes Scholar noted as his best ever student by one Oxford philosophy prof. While on the bench he taught himself Quantum Mechanics and incorporated what he got from that into his “The Mind Matters”. Frequent commenter CanSpeccy has I think read more of it than I and I don’t think bought it all. However, it could only be good for the brain to have a go at it.

    Read More
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  17. Nothing about the theory that each neuron ‘thinks’, that is, processes information:
    Roger Penrose, ‘The Emperor’s New Mind, Concerning computers, minds, and the laws of physics’, 1989 Oxford
    Penrose is a phycisist, his book is interesting as the question of free will and quantum mechanics, where causality has been replaced by probablity, is discussed.

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  18. I think that Seth Grant is the best person on this, though his papers are very technical.

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  19. Sean says:

    The https://en.wikipedia.org/wiki/Complement_component_4 variant for increased inflammatory signalling is the most implicated of hundreds of genes thought to be involved in causing schizophrenia, according to The Inflamed Mind by Edward Bullmore. He also says maternal, fetal, and neonatal infections are implicated in schizophrenia, and being born at certain times of the year is too. Case closed.

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  20. Orates says:

    If you want to understand a little bit of schizophrenia from the clinical and phenomenological point of view you have to read :

    Interpretation of schizophrenia

    Silvano Arieti

    first edition 1955

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  21. Close to unintelligible, academic gobbledygook, even the photo is dreadful.

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  22. @hyperbola
    The most advanced city in "intelligence research" can only muster 120 delegates??? Sounds like this is a dying field.

    As for schixophrenia, transcriptomic studies are not new and we have known for some time that transcription of substantial numbers of genes are involved. Amongst these are genes involved in red blood cells. Other work identifies OxPhos and mitochondria. Recent work comes from all over the world, far beyond Edinburgh. We have known for at least a decade that epigenetic effects on transcription levels are observed in other "late-onset" diseases such as breast cancer. Then there is, of course, the added complication that levels of transcribed RNA do NOT correlate particularly well with the levels of expressed proteins in many cases. This paper does not appear to be a major breakthrough.


    PLoS One. 2018 Jul 17;13(7):e0200003. doi: 10.1371/journal.pone.0200003. eCollection 2018.
    Inference of cell type content from human brain transcriptomic datasets illuminates the effects of age, manner of death, dissection, and psychiatric diagnosis.
    Hagenauer MH1, Schulmann A2, Li JZ3, Vawter MP4, Walsh DM4, Thompson RC1, Turner CA1, Bunney WE4, Myers RM5, Barchas JD6, Schatzberg AF7, Watson SJ1, Akil H1.
    Abstract
    Psychiatric illness is unlikely to arise from pathology occurring uniformly across all cell types in affected brain regions. Despite this, transcriptomic analyses of the human brain have typically been conducted using macro-dissected tissue due to the difficulty of performing single-cell type analyses with donated post-mortem brains. To address this issue statistically, we compiled a database of several thousand transcripts that were specifically-enriched in one of 10 primary cortical cell types in previous publications. Using this database, we predicted the relative cell type content for 833 human cortical samples using microarray or RNA-Seq data from the Pritzker Consortium (GSE92538) or publicly-available databases (GSE53987, GSE21935, GSE21138, CommonMind Consortium). These predictions were generated by averaging normalized expression levels across transcripts specific to each cell type using our R-package BrainInABlender (validated and publicly-released on github). Using this method, we found that the principal components of variation in the datasets strongly correlated with the predicted neuronal/glial content of the samples. This variability was not simply due to dissection-the relative balance of brain cell types appeared to be influenced by a variety of demographic, pre- and post-mortem variables. Prolonged hypoxia around the time of death predicted increased astrocytic and endothelial gene expression, illustrating vascular upregulation. Aging was associated with decreased neuronal gene expression. Red blood cell gene expression was reduced in individuals who died following systemic blood loss. Subjects with Major Depressive Disorder had decreased astrocytic gene expression, mirroring previous morphometric observations. Subjects with Schizophrenia had reduced red blood cell gene expression, ......


    Int J Mol Sci. 2017 Aug 4;18(8). pii: E1711. doi: 10.3390/ijms18081711.
    Epigenomics of Major Depressive Disorders and Schizophrenia: Early Life Decides.
    Hoffmann A1, Sportelli V2, Ziller M3, Spengler D4.
    Author information
    Abstract
    Brain development is guided by the interactions between the genetic blueprint and the environment. Epigenetic mechanisms, especially DNA methylation, can mediate these interactions and may also trigger long-lasting adaptations in developmental programs that increase the risk of major depressive disorders (MDD) and schizophrenia (SCZ). Early life adversity is a major risk factor for MDD/SCZ and can trigger persistent genome-wide changes in DNA methylation at genes important to early, but also to mature, brain function, including neural proliferation, differentiation, and synaptic plasticity, among others. Moreover, genetic variations controlling dynamic DNA methylation in early life are thought to influence later epigenomic changes in SCZ. This finding corroborates the high genetic load and a neurodevelopmental origin of SCZ and shows that epigenetic responses to the environment are, at least in part, genetically controlled. Interestingly, genetic variants influencing DNA methylation are also enriched in risk variants from genome-wide association studies (GWAS) on SCZ supporting a role in neurodevelopment. Overall, epigenomic responses to early life adversity appear to be controlled to different degrees by genetics in MDD/SCZ, even though the potential reversibility of epigenomic processes may offer new hope for timely therapeutic interventions in MDD/SCZ.....



    Can J Psychiatry. 2016 Aug;61(8):457-69. doi: 10.1177/0706743716648290.
    Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia: Possible Interactions with Cellular Processes.
    Bergman O1, Ben-Shachar D2.
    Abstract
    Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate molecules by the oxidative phosphorylation system (OXPHOS). Linked to numerous signaling pathways and cellular functions, mitochondria, and OXPHOS in particular, are involved in neuronal development, connectivity, plasticity, and differentiation. Impairments in a variety of mitochondrial functions have been described in different general and psychiatric disorders, including schizophrenia (SCZ), a severe, chronic, debilitating illness that heavily affects the lives of patients and their families. This article reviews findings emphasizing the role of OXPHOS in the pathophysiology of SCZ. Evidence accumulated during the past few decades from imaging, transcriptomic, proteomic, and metabolomic studies points at OXPHOS deficit involvement in SCZ......

    Indeed the ” field is dying ” .

    The myriad of well paid and well considered basic bioscientists has costed the USA and EU hundreds of billions of dollars and euros in the last 3 decades , and has produced millions of ” impact ” papers about the human brain and genoma , what has granted the authors good academic and research careers , but whose relevance for the mental patients or for the psychiatric clinicians has been very little –

    In fact if you add to the mad scientists the mad bureaucrats , with their DSM , and management delusions , you will understand why clinical psychiatry is in shambles .

    Modern psychiatrists don `t ask anylonger to the patients for their human feelings and ideas , for their ways of adaptation , their behavior . Modern clinicians only worry for serotonin , synapses , genome , brain images …… How is your serotonin ? madam ….I `m affraid your genome is not regulating well your synapses …. you know …..

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  23. mike k says:

    Elaborate fantasies of materialist technocrats, who wish to reduce humans and their behaviors to the level of predictable machines. The article is simply unprovable nonsense, in spite of it’s high sounding pretensions.

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  24. They say “the winner’s write history,” it is absolutely true, and the most egregious example in modern times has to be the mainstream (mis)understanding of Adolf Hitler and pre-WWII Germany. Adolf Hitler was actually a vegetarian, animal-lover, an author, an artist, a political activist, economic reformer and nominated for a Nobel Peace prize. He enacted the world’s first anti-animal cruelty, anti-pollution, and anti-smoking.

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    • Troll: Wizard of Oz
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  25. Perhaps articles should begin by signifying what the lead acronym is. Just throwing some initials up may beg us to think, or just skip to the comments as is usually the case.
    So ISRA is that short for…. just add two letters and voila….the center of attention once again.

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  26. “a synapse complexity expansion, which itself was followed by a genome duplication event 30 million years later. It was the mutation of all mutations, since the duplication then duplicated again, and it is from that freak 4 duplicated genomes that all vertebrate life descends.”

    This is Just-So-Storyism of a high order.From the confident tone you would think the author was there.

    “A” mutation? A synapse requires a stable gap, the production of a neurotransmitter, a storage mechanism, a mechanism to release it into the gap on arrival of a signal from upstream, receptors on the other side, and a mechanism by which the binding of the transmitter causes initiation of a downstream signal, sodium in, potassium out. I suppose acetylcholinesterase or some such might miraculously been added later to clean up. None of this would work without the rest being already in place. Many complex simultaneous mutations. Butin fairness I suppose the author has examined many fossilized synapses.

    Read More
    • Replies: @res
    That sound bite does seem overly glibly certain, but such is the nature of popular communication.

    Here is some of the substance behind that claim. Also from Seth Grant. https://www.researchgate.net/publication/284546510_The_molecular_evolution_of_the_vertebrate_behavioural_repertoire
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  27. utu says:
    @Frederick V. Reed
    The brain being an electrochemical--that is, physica--mechanism, and every state of a physical mechanism being determined by the previous state, our thughts would seem to be determined and therefore not precisely thoughts. If this is not true, tell me why it is not.A neurotransmitter cannnot decide whether to diffuse across a gap any more than a bowling ball can decide to fall sideways, no? Therefore we cannnot think, QED. This tracks well with most of political commentary.

    Therefore we cannnot think

    What is “we” that “can” or “cannot” in this sentence? The issue of free will is intractable. Either we have it or we do not. In materialistic world to which you and Dr. Thompson most likely subscribe there is no free will. Consciousness is just an epiphenomenon w/o any practical consequences. We are just philosophizing zombies whose philosophizing is inconsequential. Bertrand Russel rejected the no free will posture on practical grounds: life with a belief in no free will would be impossible. But where form can we get free will? Only from God. It must be postulated and the materialistic framework must be abandoned. You have to postulate the free will and step outside the materialist framework. God gave you free will. Take it or leave it. And obviouly you can leave it as a philosophizing zombie whose philosophizing even if full of antinomies and contradictions have no consequences. “You” “can” say and think whatever you “want” because it is not in your control anyway and your belief in free will is just a pretense if you subscribe to materialism.

    Somebody already brought up quantum physics that it could save free will in deterministic world:

    http://www.informationphilosopher.com/freedom/history/
    In his Gifford Lectures of 1927, Arthur Stanley Eddington had described himself as unable “to form a satisfactory conception of any kind of law or causal sequence which shall be other than deterministic.” Eddington had already established himself as the leading interpreter of the new relativity and quantum physics. His astronomical measurements of light bending as it passes the sun had confirmed Einstein’s general relativity theory.

    A year later, in response to Heisenberg’s uncertainty principle, Eddington revised his lectures for publication as The Nature of the Physical World. There he announced “It is a consequence of the advent of the quantum theory that physics is no longer pledged to a scheme of deterministic law,” and enthusiastically identified indeterminism with freedom of the will.

    But Eddington left himself open to the charge since Epicurus’ time, that chance could not be identified with freedom. He was apparently unaware of the work of William James or Henri Poincaré to make deliberation a two-stage process – first random possibilities, then a choice. A decade later, in his 1939 book The Philosophy of Physical Science, just a few years before his death, he reluctantly concluded there is no “halfway house” between randomness and determinism – an echo of Hume’s “no medium betwixt chance and an absolute necessity.”

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  28. utu says:

    “simply by looking at the way the genes were expressed in a tissue sample”

    Could anybody explain this? How gene expression is determined? Genes do not change but apparently one tissue id different form another tissue.

    “genomic lifespan program”

    Does it have a definition or is it a candidate for a new buzz word?

    Read More
    • Replies: @res

    Could anybody explain this? How gene expression is determined?
     
    https://en.wikipedia.org/wiki/Gene_expression#Measurement


    “genomic lifespan program”
     
    Does it have a definition or is it a candidate for a new buzz word?
     
    Looks like a candidate to me. Also see "genetic lifespan calendar."

    Seems like a useful phrase. I think it is fairly well defined in the final sentence of the abstract:

    We propose a genomic program generates a lifespan calendar of gene regulation that times age-dependent molecular organization of the brain
     
    , @hyperbola
    The basic set of genes is unchanged, BUT the expression of those genes changes dramatically depending on what cell type is involved and the "envieonment in which the cell finds itself. Estimates seem to be that of the roughly 19,000 human genes only about half are expressed in any given cell type. Expression levels within a given cell type are also changed depending on the environment of the cell, which includes even the other types of cells with which a given cell interacts, e.g. glial cells in the brain that interact with neurons.

    Neuroglia, also called glial cells or simply glia, are non-neuronal cells in the central nervous system (brain and spinal cord) and the peripheral nervous system. They maintain homeostasis, form myelin, and provide support and protection for neurons.[1]
    https://en.wikipedia.org/wiki/Neuroglia

    What determines observed expression levels? This includes at least control of transcription (DNA to RNA), control of translation (RNA to protein) and catabolism of proteins (removal of proteins). Each of these may in turn have several contributions, e.g. overall chromosome structure and epigenetic (methylation) changes in DNA can both influence transcription. All of these factors can interact.

    Much simplified, but perhaps this serves to remind us that a living cell involves MUCH more than simply a gene catalogue. To top matters off, although a de-nucleated cell cannot reproduce itself, many cell activities can be kept "alive" for months in a test tube under suitable conditions.
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  29. faketimes says:

    Fedor Dostoyevski ( 1821-1881 ) Demons :

    . Reason has never had the power to define good and evil, or even to distinguish between good and evil, even approximately; on the contrary, it has always mixed them up in a disgraceful and pitiful way; science has even given the solution by the fist. This is particularly characteristic of the half-truths of science, the most terrible scourge of humanity, unknown till this century, and worse than plague, famine, or war. A half-truth is a despot… such as has never been in the world before. A despot that has its priests and its slaves, a despot to whom all do homage with love and superstition hitherto inconceivable, before which science itself trembles and cringes in a shameful way.”

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  30. res says:
    @Frederick V. Reed
    “a synapse complexity expansion, which itself was followed by a genome duplication event 30 million years later. It was the mutation of all mutations, since the duplication then duplicated again, and it is from that freak 4 duplicated genomes that all vertebrate life descends.”

    This is Just-So-Storyism of a high order.From the confident tone you would think the author was there.

    “A” mutation? A synapse requires a stable gap, the production of a neurotransmitter, a storage mechanism, a mechanism to release it into the gap on arrival of a signal from upstream, receptors on the other side, and a mechanism by which the binding of the transmitter causes initiation of a downstream signal, sodium in, potassium out. I suppose acetylcholinesterase or some such might miraculously been added later to clean up. None of this would work without the rest being already in place. Many complex simultaneous mutations. Butin fairness I suppose the author has examined many fossilized synapses.

    That sound bite does seem overly glibly certain, but such is the nature of popular communication.

    Here is some of the substance behind that claim. Also from Seth Grant. https://www.researchgate.net/publication/284546510_The_molecular_evolution_of_the_vertebrate_behavioural_repertoire

    Read More
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  31. res says:
    @utu

    "simply by looking at the way the genes were expressed in a tissue sample"
     
    Could anybody explain this? How gene expression is determined? Genes do not change but apparently one tissue id different form another tissue.

    "genomic lifespan program"
     
    Does it have a definition or is it a candidate for a new buzz word?

    Could anybody explain this? How gene expression is determined?

    https://en.wikipedia.org/wiki/Gene_expression#Measurement

    “genomic lifespan program”

    Does it have a definition or is it a candidate for a new buzz word?

    Looks like a candidate to me. Also see “genetic lifespan calendar.”

    Seems like a useful phrase. I think it is fairly well defined in the final sentence of the abstract:

    We propose a genomic program generates a lifespan calendar of gene regulation that times age-dependent molecular organization of the brain

    Read More
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  32. hyperbola says:
    @utu

    "simply by looking at the way the genes were expressed in a tissue sample"
     
    Could anybody explain this? How gene expression is determined? Genes do not change but apparently one tissue id different form another tissue.

    "genomic lifespan program"
     
    Does it have a definition or is it a candidate for a new buzz word?

    The basic set of genes is unchanged, BUT the expression of those genes changes dramatically depending on what cell type is involved and the “envieonment in which the cell finds itself. Estimates seem to be that of the roughly 19,000 human genes only about half are expressed in any given cell type. Expression levels within a given cell type are also changed depending on the environment of the cell, which includes even the other types of cells with which a given cell interacts, e.g. glial cells in the brain that interact with neurons.

    Neuroglia, also called glial cells or simply glia, are non-neuronal cells in the central nervous system (brain and spinal cord) and the peripheral nervous system. They maintain homeostasis, form myelin, and provide support and protection for neurons.[1]

    https://en.wikipedia.org/wiki/Neuroglia

    What determines observed expression levels? This includes at least control of transcription (DNA to RNA), control of translation (RNA to protein) and catabolism of proteins (removal of proteins). Each of these may in turn have several contributions, e.g. overall chromosome structure and epigenetic (methylation) changes in DNA can both influence transcription. All of these factors can interact.

    Much simplified, but perhaps this serves to remind us that a living cell involves MUCH more than simply a gene catalogue. To top matters off, although a de-nucleated cell cannot reproduce itself, many cell activities can be kept “alive” for months in a test tube under suitable conditions.

    Read More
    • Replies: @utu
    Thanks!
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  33. utu says:
    @hyperbola
    The basic set of genes is unchanged, BUT the expression of those genes changes dramatically depending on what cell type is involved and the "envieonment in which the cell finds itself. Estimates seem to be that of the roughly 19,000 human genes only about half are expressed in any given cell type. Expression levels within a given cell type are also changed depending on the environment of the cell, which includes even the other types of cells with which a given cell interacts, e.g. glial cells in the brain that interact with neurons.

    Neuroglia, also called glial cells or simply glia, are non-neuronal cells in the central nervous system (brain and spinal cord) and the peripheral nervous system. They maintain homeostasis, form myelin, and provide support and protection for neurons.[1]
    https://en.wikipedia.org/wiki/Neuroglia

    What determines observed expression levels? This includes at least control of transcription (DNA to RNA), control of translation (RNA to protein) and catabolism of proteins (removal of proteins). Each of these may in turn have several contributions, e.g. overall chromosome structure and epigenetic (methylation) changes in DNA can both influence transcription. All of these factors can interact.

    Much simplified, but perhaps this serves to remind us that a living cell involves MUCH more than simply a gene catalogue. To top matters off, although a de-nucleated cell cannot reproduce itself, many cell activities can be kept "alive" for months in a test tube under suitable conditions.

    Thanks!

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  34. Childhood trauma. Abuse or perception of negligence. 90% fit the model, my uncle and brother (negligence) included.

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  35. puropedo says:
    @hyperbola
    The most advanced city in "intelligence research" can only muster 120 delegates??? Sounds like this is a dying field.

    As for schixophrenia, transcriptomic studies are not new and we have known for some time that transcription of substantial numbers of genes are involved. Amongst these are genes involved in red blood cells. Other work identifies OxPhos and mitochondria. Recent work comes from all over the world, far beyond Edinburgh. We have known for at least a decade that epigenetic effects on transcription levels are observed in other "late-onset" diseases such as breast cancer. Then there is, of course, the added complication that levels of transcribed RNA do NOT correlate particularly well with the levels of expressed proteins in many cases. This paper does not appear to be a major breakthrough.


    PLoS One. 2018 Jul 17;13(7):e0200003. doi: 10.1371/journal.pone.0200003. eCollection 2018.
    Inference of cell type content from human brain transcriptomic datasets illuminates the effects of age, manner of death, dissection, and psychiatric diagnosis.
    Hagenauer MH1, Schulmann A2, Li JZ3, Vawter MP4, Walsh DM4, Thompson RC1, Turner CA1, Bunney WE4, Myers RM5, Barchas JD6, Schatzberg AF7, Watson SJ1, Akil H1.
    Abstract
    Psychiatric illness is unlikely to arise from pathology occurring uniformly across all cell types in affected brain regions. Despite this, transcriptomic analyses of the human brain have typically been conducted using macro-dissected tissue due to the difficulty of performing single-cell type analyses with donated post-mortem brains. To address this issue statistically, we compiled a database of several thousand transcripts that were specifically-enriched in one of 10 primary cortical cell types in previous publications. Using this database, we predicted the relative cell type content for 833 human cortical samples using microarray or RNA-Seq data from the Pritzker Consortium (GSE92538) or publicly-available databases (GSE53987, GSE21935, GSE21138, CommonMind Consortium). These predictions were generated by averaging normalized expression levels across transcripts specific to each cell type using our R-package BrainInABlender (validated and publicly-released on github). Using this method, we found that the principal components of variation in the datasets strongly correlated with the predicted neuronal/glial content of the samples. This variability was not simply due to dissection-the relative balance of brain cell types appeared to be influenced by a variety of demographic, pre- and post-mortem variables. Prolonged hypoxia around the time of death predicted increased astrocytic and endothelial gene expression, illustrating vascular upregulation. Aging was associated with decreased neuronal gene expression. Red blood cell gene expression was reduced in individuals who died following systemic blood loss. Subjects with Major Depressive Disorder had decreased astrocytic gene expression, mirroring previous morphometric observations. Subjects with Schizophrenia had reduced red blood cell gene expression, ......


    Int J Mol Sci. 2017 Aug 4;18(8). pii: E1711. doi: 10.3390/ijms18081711.
    Epigenomics of Major Depressive Disorders and Schizophrenia: Early Life Decides.
    Hoffmann A1, Sportelli V2, Ziller M3, Spengler D4.
    Author information
    Abstract
    Brain development is guided by the interactions between the genetic blueprint and the environment. Epigenetic mechanisms, especially DNA methylation, can mediate these interactions and may also trigger long-lasting adaptations in developmental programs that increase the risk of major depressive disorders (MDD) and schizophrenia (SCZ). Early life adversity is a major risk factor for MDD/SCZ and can trigger persistent genome-wide changes in DNA methylation at genes important to early, but also to mature, brain function, including neural proliferation, differentiation, and synaptic plasticity, among others. Moreover, genetic variations controlling dynamic DNA methylation in early life are thought to influence later epigenomic changes in SCZ. This finding corroborates the high genetic load and a neurodevelopmental origin of SCZ and shows that epigenetic responses to the environment are, at least in part, genetically controlled. Interestingly, genetic variants influencing DNA methylation are also enriched in risk variants from genome-wide association studies (GWAS) on SCZ supporting a role in neurodevelopment. Overall, epigenomic responses to early life adversity appear to be controlled to different degrees by genetics in MDD/SCZ, even though the potential reversibility of epigenomic processes may offer new hope for timely therapeutic interventions in MDD/SCZ.....



    Can J Psychiatry. 2016 Aug;61(8):457-69. doi: 10.1177/0706743716648290.
    Mitochondrial Oxidative Phosphorylation System (OXPHOS) Deficits in Schizophrenia: Possible Interactions with Cellular Processes.
    Bergman O1, Ben-Shachar D2.
    Abstract
    Mitochondria are key players in the generation and regulation of cellular bioenergetics, producing the majority of adenosine triphosphate molecules by the oxidative phosphorylation system (OXPHOS). Linked to numerous signaling pathways and cellular functions, mitochondria, and OXPHOS in particular, are involved in neuronal development, connectivity, plasticity, and differentiation. Impairments in a variety of mitochondrial functions have been described in different general and psychiatric disorders, including schizophrenia (SCZ), a severe, chronic, debilitating illness that heavily affects the lives of patients and their families. This article reviews findings emphasizing the role of OXPHOS in the pathophysiology of SCZ. Evidence accumulated during the past few decades from imaging, transcriptomic, proteomic, and metabolomic studies points at OXPHOS deficit involvement in SCZ......

    https://www.plos.org/publication-fees

    publishing in plos costs from 1,600 to 3000 US $ per paper , according to the area .

    Most of the basic sciences studies on brain diseases are done with rats . The brain of a rat wheighs 0,5 gr. the human brain wheighs 1,500 gr , so is 3000 thousand time heavier .

    The results with rats are not extrapolable to humans . No comparison .

    Schizophrenia is a syndrome , Depression is a syndrome …. like so many medical and psychiatric conditions .

    Read More
    • Replies: @dearieme
    " The brain of a rat wheighs 0,5 gr. the human brain wheighs 1,500 gr , so is 3000 thousand time heavier .

    The results with rats are not extrapolable to humans . No comparison ."

    False logic. Your conclusion may be right but your reasoning is wrong. There are examples in physics and engineering where scaling up over three orders of magnitude has worked.
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  36. dearieme says:
    @puropedo
    https://www.plos.org/publication-fees

    publishing in plos costs from 1,600 to 3000 US $ per paper , according to the area .


    Most of the basic sciences studies on brain diseases are done with rats . The brain of a rat wheighs 0,5 gr. the human brain wheighs 1,500 gr , so is 3000 thousand time heavier .

    The results with rats are not extrapolable to humans . No comparison .

    Schizophrenia is a syndrome , Depression is a syndrome .... like so many medical and psychiatric conditions .

    ” The brain of a rat wheighs 0,5 gr. the human brain wheighs 1,500 gr , so is 3000 thousand time heavier .

    The results with rats are not extrapolable to humans . No comparison .”

    False logic. Your conclusion may be right but your reasoning is wrong. There are examples in physics and engineering where scaling up over three orders of magnitude has worked.

    Read More
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  37. Rurik says:
    @Frederick V. Reed
    The brain being an electrochemical--that is, physica--mechanism, and every state of a physical mechanism being determined by the previous state, our thughts would seem to be determined and therefore not precisely thoughts. If this is not true, tell me why it is not.A neurotransmitter cannnot decide whether to diffuse across a gap any more than a bowling ball can decide to fall sideways, no? Therefore we cannnot think, QED. This tracks well with most of political commentary.

    Hey Fred, it’s your ol’ pal Rurik,

    The brain being an electrochemical–that is, physica–mechanism, and every state of a physical mechanism being determined by the previous state, our thughts would seem to be determined and therefore not precisely thoughts. If this is not true, tell me why it is not.A neurotransmitter cannnot decide whether to diffuse across a gap any more than a bowling ball can decide to fall sideways, no? Therefore we cannnot think, QED.

    Why, if our thoughts are determined, (as they indeed are) do they stop being thoughts?

    I’m thinking right now that I’m going to write this next word; lomatricine.

    I thought up that ‘word’, and in doing so, brought to bear all of my respective nature and nurture, all of which are a consequence of what transpired previously. There is no way I could have thought of that word, were it not for what I was born as, and the life and experiences I’ve lived subsequently.

    If there were such a thing as free will, then you’d be able to think in anyway possible. You’d be literally free to think as a Somali teenage girl, or have a thought that your typical Oprah fan would have on any given day. But you can’t do that, because you’re limited by being Fred, and having been born with your particular gifts and proclivities and penchants, some of which are a consequence of your ‘nurture’, which to say is the experiences you’ve had over your years.

    If our will were free, we could think in anyway and everyway we liked, and be free to have thoughts that would transcend Aristotle. But we can’t, because our will, and our minds are limited in exactly the way you point out, being as our brains are organic, and subject to those limitations.

    So the act of thinking, is not any less so because of those limitations. We do indeed think, but it’s like a dog thinks, (I want food, I want pussy, that other dog better watch out or I’m gonna whup some arse). What it isn’t like is how a God would think, iow unlimited by mortal flesh.

    We are mortal, and limited. But that doesn’t stop us from thinking of words like lomatricine. if it suits our whim.

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  38. mcohen says:

    thoughts are not detetmined they are a simply a conversation.one for one starting at the top.for Aviv.

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  39. Factorize says:

    July 23, 2018: the day that changed everything.
    This one probably should be Open Access; it is too important not to be.

    Does anyone have the $5000 to give this one to the people?

    https://www.nature.com/articles/s41588-018-0147-3

    Read More
    • Replies: @res
    The supplementary material (207 page PDF and spreadsheet) is freely available (bottom of your link).

    The DOI for the paper is 10.1038/s41588-018-0147-3
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  40. res says:
    @Factorize
    July 23, 2018: the day that changed everything.
    This one probably should be Open Access; it is too important not to be.

    Does anyone have the $5000 to give this one to the people?

    https://www.nature.com/articles/s41588-018-0147-3

    The supplementary material (207 page PDF and spreadsheet) is freely available (bottom of your link).

    The DOI for the paper is 10.1038/s41588-018-0147-3

    Read More
    • Replies: @Factorize
    Good one res!

    Look at the Figures! I do not think I have ever seen a Manhattan plot like that before.
    Everything is genome wide significant?
    For about 10 years, these plots had NO genome wide-significant SNPs: anything shown in the plots did not replicate.

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  41. Factorize says:
    @res
    The supplementary material (207 page PDF and spreadsheet) is freely available (bottom of your link).

    The DOI for the paper is 10.1038/s41588-018-0147-3

    Good one res!

    Look at the Figures! I do not think I have ever seen a Manhattan plot like that before.
    Everything is genome wide significant?
    For about 10 years, these plots had NO genome wide-significant SNPs: anything shown in the plots did not replicate.

    Read More
    • Replies: @Factorize
    This is such a massively massively important moment for humanity. I am sure others more linguistically gifted will be able to express this awe better, though when looking directly into infinity it is not an especially favorable time to be eloquent. No other time in the history of the universe is even close in comparability to what is now imminent. I sincerely hope that other people are paying close attention to what is important and not to various other trivial diversions.
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  42. Factorize says:
    @Factorize
    Good one res!

    Look at the Figures! I do not think I have ever seen a Manhattan plot like that before.
    Everything is genome wide significant?
    For about 10 years, these plots had NO genome wide-significant SNPs: anything shown in the plots did not replicate.

    This is such a massively massively important moment for humanity. I am sure others more linguistically gifted will be able to express this awe better, though when looking directly into infinity it is not an especially favorable time to be eloquent. No other time in the history of the universe is even close in comparability to what is now imminent. I sincerely hope that other people are paying close attention to what is important and not to various other trivial diversions.

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  43. Factorize says:

    res, does Nature Genetics publish peer reviews? I cannot see it on their website. Might be very interesting to see what comments the reviewers made.

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