Results 1 to 4 of 4

Thread: Genes Unravel Mystery of Schizophrenia

  1. #1
    Member
    Join Date
    Aug 2007
    Last Online
    Saturday, April 28th, 2018 @ 05:23 AM
    Ethnicity
    Katarinensische
    Subrace
    Dinarid
    Gender
    Age
    42
    Family
    Single adult
    Posts
    1,243
    Thanks Thanks Given 
    0
    Thanks Thanks Received 
    1
    Thanked in
    1 Post

    Post Linkage of schizophrenia to markers on chromosome 13 in Caucasian but not Oriental

    Am J Hum Genet. 1999 Oct;65(4):1096-103.


    Linkage of familial schizophrenia to chromosome 13q32.

    Brzustowicz LM, Honer WG, Chow EW, Little D, Hogan J, Hodgkinson K, Bassett AS.

    Center for Molecular and Behavorial Neuroscience, Rutgers University, Newark, New Jersey 07102, USA brzustowicz@axon.rutgers.edu

    Over the past 4 years, a number of investigators have reported findings suggestive of linkage to schizophrenia, with markers on chromosomes 13q32 and 8p21, with one recent study by Blouin et al. reporting significant linkage to these regions. As part of an ongoing genome scan, we evaluated microsatellite markers spanning chromosomes 8 and 13, for linkage to schizophrenia, in 21 extended Canadian families. Families were analyzed under autosomal dominant and recessive models, with broad and narrow definitions of schizophrenia. All models produced positive LOD scores with markers on 13q, with higher scores under the recessive models. The maximum three-point LOD scores were obtained under the recessive-broad model: 3.92 at recombination fraction (theta).1 with D13S793, under homogeneity, and 4.42 with alpha=.65 and straight theta=0 with D13S793, under heterogeneity. Positive LOD scores were also obtained, under all models, for markers on 8p. Although a maximum two-point LOD score of 3.49 was obtained under the dominant-narrow model with D8S136 at straight theta=0.1, multipoint analysis with closely flanking markers reduced the maximum LOD score in this region to 2. 13. These results provide independent significant evidence of linkage of a schizophrenia-susceptibility locus to markers on 13q32 and support the presence of a second susceptibility locus on 8p21.

  2. #2
    Member
    Join Date
    Aug 2007
    Last Online
    Saturday, April 28th, 2018 @ 05:23 AM
    Ethnicity
    Katarinensische
    Subrace
    Dinarid
    Gender
    Age
    42
    Family
    Single adult
    Posts
    1,243
    Thanks Thanks Given 
    0
    Thanks Thanks Received 
    1
    Thanked in
    1 Post

    Post Linkage of schizophrenia to markers on chromosome 13 in Caucasian but not Oriental

    Hum Genet. 1997 Mar;99(3):417-20.


    Suggestive evidence for linkage of schizophrenia to markers on chromosome 13 in Caucasian but not Oriental populations.

    Lin MW, Sham P, Hwu HG, Collier D, Murray R, Powell JF.

    Department of Psychological Medicine and Neuroscience, Institute of Psychiatry, London, UK. mlin@hgmp.mrc.ac.uk

    Previously we reported suggestive evidence for linkage of schizophrenia to markers on chromosome 13q14.1-q32. We have now studied an additional independent sample of 44 pedigrees consisting of 34 Taiwanese, 9 English and 1 Welsh family in an attempt to replicate this finding. Narrow and broad models based on Research Diagnostic Criteria or the Diagnostic and Statistical Manual of Mental Disorders, third edition, revised, were used to define the schizophrenia phenotype. Under a dominant genetic model, two-point lod scores obtained for most of the markers were negative except that marker D13S122 gave a total lod score of 1.06 (theta = 0.2, broad model). As combining pedigrees from different ethnic origins may be inappropriate, we combined this replication sample and our original sample, and then divided the total sample into Caucasian (English and Welsh pedigrees) and Oriental (Taiwanese and Japanese pedigrees) groups. The Caucasian pedigrees produced maximized admixture two-point lod scores (A-lod) of 1.41 for the marker D13S119 (theta = 0.2, alpha = 1.0) and 1.54 for D13S128 (theta = 0, alpha = 0.3) with nearby markers also producing positive A-lod scores. When five-point model-free linkage analysis was applied to the Caucasian sample, a maximum lod score of 2.58 was obtained around the markers D13S122 and D13S128, which are located on chromosome 13q32. The linkage results for the Oriental group were less positive than the Caucasian group. Our results again suggest that there is a potential susceptibility locus for schizophrenia on chromosome 13q14.1-q32, especially in the Caucasian population.

  3. #3
    You are not wrong, who deem / That my days have been a dream Johannes de León's Avatar
    Join Date
    Mar 2004
    Last Online
    Sunday, April 15th, 2012 @ 11:03 AM
    Ethnicity
    Iberian
    Subrace
    Atlanto-Baskid
    Location
    Terra Firma
    Gender
    Politics
    Nationalism
    Posts
    1,477
    Thanks Thanks Given 
    0
    Thanks Thanks Received 
    1
    Thanked in
    1 Post

    Post Genes Unravel Mystery of Schizophrenia

    Genes unravel mystery of schizophrenia
    Reuters

    Psychotic mice that flee other mice may offer insights into diseases such as schizophrenia, U.S. researchers say.

    The team at University of Texas Southwestern Medical Center and the Cincinnati Children's Hospital Medical Center published their research in the current issue of the journal Proceedings of the National Academy of Sciences.

    The genetically engineered mice have mutations in two key genes that make them suffer from psychosis, a condition where there is an altered sense of reality.

    Humans suffering from psychosis, for example, may have hallucinations, have paranoid or delusional thoughts, or may exhibit changes of behaviour.


    Faulty genes that turn sociable mice into antisocial ones may help researchers understand psychosis and schizophrenia (Image: iStockphoto)

    Psychosis is one symptom of shizophrenia, a condition that usually shows up in early adulthood that affects a person's ability to manage emotions, interact with others and think clearly.

    The researchers looked at mutations in mice that were the same as those found in a Canadian family with a history of schizophrenia, and involve two poorly understood genes.

    "These mice display certain deficits that are potentially consistent with schizophrenia," said Dr Steven McKnight, chairman of biochemistry at the University of Texas Southwestern Medical Center and leader of the study.

    "It's too early to tell whether the abnormal behaviour we observed in these mutated mice can be directly connected with human disease."

    Erratic behaviour

    The genes under study were NPAS1 and NPAS3. The researchers mated mice that were genetically engineered to lack copies of the gene and watched their offspring's behaviour.

    Those that lacked a working copy of NPAS3 were especially erratic, the researchers reported.

    Normally, caged mice climb over and sniff one another, but the mice with the genetic mutations didn't socialise. One small group of the mutant mice darted around wildly, avoiding their siblings.

    Normally, NPAS genes are expressed, or active, in brain cells called inhibitory interneurons. They control transcription factors, which are proteins that can activate or deactivate other genes. Just which genes they may control is unclear, McKnight said.

    McKnight's team said when they examined the brains of the psychotic mice, they found abnormally low levels of a protein called reelin.

    Reelin is important in the embryonic development of the brain and later in life to brain cell signaling.

    Other studies of people who died with schizophrenia have found reduced levels of reelin in their brains.

    .

  4. #4
    Senior Member Vetinari's Avatar
    Join Date
    Oct 2003
    Last Online
    Friday, June 15th, 2012 @ 04:40 AM
    Subrace
    Other
    Country
    United States United States
    Gender
    Politics
    Nationalist
    Religion
    Lovecraftian
    Posts
    244
    Thanks Thanks Given 
    0
    Thanks Thanks Received 
    1
    Thanked in
    1 Post

    Post Re: Genes unravel mystery of schizophrenia

    Quote Originally Posted by Johannes de León
    Genes unravel mystery of schizophrenia
    Reuters

    Psychotic mice that flee other mice may offer insights into diseases such as schizophrenia, U.S. researchers say.[/center]
    Schizophrenia 'helped the ascent of man'

    Scientist says gene mutation is key to genius and despair

    Robin McKie, science editor

    Observer

    Sunday March 18, 2001


    Tiny mutations in our ancestors' brain cells triggered mankind's takeover of the world 100,000 years ago. But these changes also cursed our species to suffer from schizophrenia and depression.

    This is the controversial claim by biochemist David Horrobin in a new book, The Madness of Adam & Eve: How schizophrenia shaped humanity, to be published by Bantam Press next month.

    Horrobin - who is medical adviser to the Schizophrenia Association of Great Britain - argues that the changes which propelled humanity to its current global ascendancy were the same as those which have left us vulnerable to mental disease.

    'We became human because of small genetic changes in the chemistry of the fat in our skulls,' he says. 'These changes injected into our ancestors both the seeds of the illness of schizophrenia and the extraordinary minds which made us human.'

    Horrobin's theory also provides support for observations that have linked the most intelligent, imaginative members of our species with mental disease, in particular schizophrenia - an association supported by studies in Iceland, Finland, New York and London. These show that 'families with schizophrenic members seem to have a greater variety of skills and abilities, and a greater likelihood of producing high achievers,' he states. As examples, Horrobin points out that Einstein had a son who was schizophrenic, as was James Joyce's daughter and Carl Jung's mother.

    In addition, Horrobin points to a long list of geniuses whose personalities and temperaments have be-trayed schizoid tendencies or signs of mental instability. These include Schumann, Strindberg, Poe, Kafka, Wittgenstein and Newton. Controversially, Horrobin also includes individuals such as Darwin and Faraday, generally thought to have displayed mental stability.

    Nevertheless, psychologists agree that it is possible to make a link between mental illness and creativity. 'Great minds are marked by their ability to make connections between unexpected events or trends,' said Professor Til Wykes, of the Institute of Psychiatry, London. 'By the same token, those suffering from mental illness often make unexpected or inappropriate connections between day-to-day events.'

    According to Horrobin, schizophrenia and human genius began to manifest themselves as a result of evolutionary pressures that triggered genetic changes in our brain cells, allowing us to make unexpected links with different events, an ability that lifted our species to a new intellectual plane. Early manifestations of this creative change include the 30,000-year-old cave paintings found in France and Spain.

    The mutation Horrobin proposes involves changes to the fat content of brain cells. 'Sixty per cent of the non-aqueous material of the brain is fat. Humans have bigger heads than chimpanzees because their heads are full of fat.' By adding fat to our brain cells, we were able to control the flow of electrical signals more carefully and make more complex connections within our cortexes.

    Our 'schizophrenia inheritance' was 'the single most important event in human history' and marked the break 'between our large-brained, possibly pleasant but unimaginative ancestors, and the restless, creative creatures we are today,' he adds.

    This idea was last week described as 'a reasonable hypothesis' by palaeontologist Professor Chris Stringer, of the Natural History Museum, London. 'It is well known there have been key brain cell mutations in our species in our recent past. It is also likely there would have been undesirable side-effects.'

    Horrobin points out that schizophrenia is found in every racial group, at a frequency of between 0.7 and 1.0 per cent. However, mankind would initially have been largely unaffected by the disease because our hunter-gatherer forebears ate meat and other fat-rich foods.

    These supplied our brain with the chemicals needed to maintain proper mental operation. With the invention of agriculture our diets changed and the fat content of our food altered - making us more vulnerable to mental diseases, says Horrobin.

    Many scientists remain sceptical about the ideas of Horrobin, former managing director of Scotia Pharmaceuticals, which made evening primrose oil and other chemicals until it fell into insolvency this year.

    Professor Tim Crow of Oxford University agreed genetic changes may have made us vulnerable to schizophrenia. 'The trouble is Horrobin's mechanism does not explain why so very few of us ever develop the disease.'

    http://www.guardian.co.uk/Archive/Ar...154224,00.html

Similar Threads

  1. Schizophrenia Amongst Negroes
    By SaxonPagan in forum Psychology, Behavior, & Neuroscience
    Replies: 5
    Last Post: Wednesday, March 15th, 2017, 09:57 AM
  2. Replies: 0
    Last Post: Sunday, February 26th, 2012, 03:18 PM
  3. Genes Drive Behaviour, But Culture Can Select Genes: Study
    By Nachtengel in forum Medical & Behavioral Genetics
    Replies: 3
    Last Post: Saturday, October 31st, 2009, 06:48 AM
  4. Scientists Unravel Mystery of Ancient Greek Machine
    By Blutwölfin in forum Ancient
    Replies: 0
    Last Post: Wednesday, November 29th, 2006, 06:20 PM
  5. How Did Recessive Genes (Light Skin & Eyes, Blonde Hair, etc) Replace Dominant Genes?
    By Tryggvi in forum Bio-Anthropology & Human Variation
    Replies: 12
    Last Post: Sunday, August 22nd, 2004, 02:44 AM

Bookmarks

Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts
  •