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home:diseases:ocd [02.17.2019] – sallieqhome:diseases:ocd [09.14.2022] (current) – external edit 127.0.0.1
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-The identification of clinical features associated with PANDAS should assist in delineating risks for this subtype of obsessive-compulsive disorder/tics  (({{pubmed>long:21868033}}))+The identification of clinical features associated with PANDAS should assist in delineating risks for this subtype of obsessive-compulsive disorder/tics  (({{pmid>long:21868033}}))
    
  
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 This report provides phenotypic descriptions of three youth with PANDAS as well as their genetically identical siblings (in two cases of twins and one case of triplets). These cases highlight the potential for environmental influences for discordant presentations in genetically identical siblings.  This report provides phenotypic descriptions of three youth with PANDAS as well as their genetically identical siblings (in two cases of twins and one case of triplets). These cases highlight the potential for environmental influences for discordant presentations in genetically identical siblings. 
  
-Despite identical genetics, presentations showed marked variation across siblings (from a full PANDAS presentation to asymptomatic). Further research into environmentally driven influences such as postinfectious molecular mimicry and epigenetic factors that may influence the manifestation of these pediatric neuropsychiatric disorders will promote our understanding of their prevention and treatment.   (({{pubmed>long:21486169}}))+Despite identical genetics, presentations showed marked variation across siblings (from a full PANDAS presentation to asymptomatic). Further research into environmentally driven influences such as postinfectious molecular mimicry and epigenetic factors that may influence the manifestation of these pediatric neuropsychiatric disorders will promote our understanding of their prevention and treatment.   (({{pmid>long:21486169}}))
    
  
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 ===== Experience of Patients ===== ===== Experience of Patients =====
 +
 +<relatedarticle> [[home:symptoms:neurological:managing|Managing symptoms]] </article>
  
  
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 Interview with Julia Grier - sarcoidosis, OCD  Interview with Julia Grier - sarcoidosis, OCD 
-================================ 
  
-Phobias and OCD help available in the UK+  
 +__Phobias and OCD help__ available in the UK
  
 I think you've spoken to my twin sister Jean (also on the MP). I have been on the MP now for about 4 months.  I developed Obsessive Compulsive Disorder last July after my doctor gave me three antibiotics for CFS.  I could never have imagined the effect on my brain and the obsessive thoughts and handwashing rituals that resulted.  I would never have understood the link between bacteria and the brain if it weren't for the MP and information from my doctor.  It makes a lot of sense though. I think you've spoken to my twin sister Jean (also on the MP). I have been on the MP now for about 4 months.  I developed Obsessive Compulsive Disorder last July after my doctor gave me three antibiotics for CFS.  I could never have imagined the effect on my brain and the obsessive thoughts and handwashing rituals that resulted.  I would never have understood the link between bacteria and the brain if it weren't for the MP and information from my doctor.  It makes a lot of sense though.
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 In support of a humoral immune mechanism, clinical improvement often follows plasmapheresis or intravenous immunoglobulin. We recently described a PANDAS mouse model wherein repetitive behaviors correlate with peripheral anti-CNS antibodies and immune deposits in brain following streptococcal immunization. These antibodies are directed against group A beta-hemolytic streptococcus matrix (M) protein and cross-react with molecular targets complement C4 protein and alpha-2-macroglobulin in brain. Here we show additional deficits in motor coordination, learning/memory and social interaction in PANDAS mice, replicating more complex aspects of human disease.  In support of a humoral immune mechanism, clinical improvement often follows plasmapheresis or intravenous immunoglobulin. We recently described a PANDAS mouse model wherein repetitive behaviors correlate with peripheral anti-CNS antibodies and immune deposits in brain following streptococcal immunization. These antibodies are directed against group A beta-hemolytic streptococcus matrix (M) protein and cross-react with molecular targets complement C4 protein and alpha-2-macroglobulin in brain. Here we show additional deficits in motor coordination, learning/memory and social interaction in PANDAS mice, replicating more complex aspects of human disease. 
  
-Furthermore, we demonstrate for the first time that humoral immunity is necessary and sufficient to induce the syndrome through experiments wherein naive mice are transfused with immunoglobulin G (IgG) from PANDAS mice. Depletion of IgG from donor sera abrogates behavior changes. These functional disturbances link to the autoimmunity-related IgG1 subclass but are not attributable to differences in cytokine profiles. The mode of disrupting blood-brain barrier integrity differentially affects the ultimate CNS distribution of these antibodies and is shown to be an additional important determinant of neuropsychiatric outcomes. This work provides insights into PANDAS pathogenesis and may lead to new strategies for identification and treatment of children at risk for autoimmune brain disorders. (({{pubmed>long:19668249}}))+Furthermore, we demonstrate for the first time that humoral immunity is necessary and sufficient to induce the syndrome through experiments wherein naive mice are transfused with immunoglobulin G (IgG) from PANDAS mice. Depletion of IgG from donor sera abrogates behavior changes. These functional disturbances link to the autoimmunity-related IgG1 subclass but are not attributable to differences in cytokine profiles. The mode of disrupting blood-brain barrier integrity differentially affects the ultimate CNS distribution of these antibodies and is shown to be an additional important determinant of neuropsychiatric outcomes. This work provides insights into PANDAS pathogenesis and may lead to new strategies for identification and treatment of children at risk for autoimmune brain disorders. (({{pmid>long:19668249}}))
  
-See also Orbitofrontal-Cortex-Lesioned Rats: Possible Involvement of the Serotonergic System.   (({{pubmed>long:20072118}}))   +See also Orbitofrontal-Cortex-Lesioned Rats: Possible Involvement of the Serotonergic System.   (({{pmid>long:20072118}}))   
  
  
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 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
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-  * **Obsessive compulsive disorder and childhood infections like strep** – A 2010 team of researchers developed a new animal model to show how exposure to strep affects the brain and leads to a number of physical and mental ailments. According to one of the collaborators, Daphna Joel, "It's almost impossible to show how strep can lead to OCD in humans ― almost all of us, even very young children, have been exposed to the bacterium at one time or another. But childhood seems to provide a distinct window of opportunity for the disorder to take root through strep infection. This work was presented at a [[http://www.sciencedaily.com/releases/2010/10/101020131712.htm|2010 meeting]] and is expected to be published at the beginning of 2011.+  * **Obsessive compulsive disorder and childhood infections like strep** – A 2010 team of researchers developed a new animal model to show how exposure to strep affects the brain and leads to a number of physical and mental ailments. According to one of the collaborators, Daphna Joel, "It's almost impossible to show how strep can lead to OCD in humans ― almost all of us, even very young children, have been exposed to the bacterium at one time or another. But childhood seems to provide a distinct window of opportunity for the disorder to take root through strep infection. This work was presented at a [[https://www.sciencedaily.com/releases/2010/10/101020131712.htm|2010 meeting]] and is expected to be published at the beginning of 2011.
  
  
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   * legacy content   * legacy content
-  * http://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=54060#p54060 s64+  * https://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=54060#p54060 s64
  
  
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 School of Psychological Sciences, Tel Aviv University, Tel Aviv, Israel. School of Psychological Sciences, Tel Aviv University, Tel Aviv, Israel.
 Abstract Abstract
-Group A streptococcal (GAS) infections and autoimmunity are associated with the onset of a spectrum of neuropsychiatric disorders in children, with the prototypical disorder being Sydenham chorea (SC). Our aim was to develop an animal model that resembled the behavioral, pharmacological, and immunological abnormalities of SC and other streptococcal-related neuropsychiatric disorders. Male Lewis rats exposed to GAS antigen exhibited motor symptoms (impaired food manipulation and beam walking) and compulsive behavior (increased induced-grooming). These symptoms were alleviated by the D2 blocker haloperidol and the selective serotonin reuptake inhibitor paroxetine, respectively, drugs that are used to treat motor symptoms and compulsions in streptococcal-related neuropsychiatric disorders. Streptococcal exposure resulted in antibody deposition in the striatum, thalamus, and frontal cortex, and concomitant alterations in dopamine and glutamate levels in cortex and basal ganglia, consistent with the known pathophysiology of SC and related neuropsychiatric disorders. Autoantibodies (IgG) of GAS rats reacted with tubulin and caused elevated calcium/calmodulin-dependent protein kinase II signaling in SK-N-SH neuronal cells, as previously found with sera from SC and related neuropsychiatric disorders. Our new animal model translates directly to human disease and led us to discover autoantibodies targeted against dopamine D1 and D2 receptors in the rat model as well as in SC and other streptococcal-related neuropsychiatric disorders.   (({{pubmed>long:22534626}}))+Group A streptococcal (GAS) infections and autoimmunity are associated with the onset of a spectrum of neuropsychiatric disorders in children, with the prototypical disorder being Sydenham chorea (SC). Our aim was to develop an animal model that resembled the behavioral, pharmacological, and immunological abnormalities of SC and other streptococcal-related neuropsychiatric disorders. Male Lewis rats exposed to GAS antigen exhibited motor symptoms (impaired food manipulation and beam walking) and compulsive behavior (increased induced-grooming). These symptoms were alleviated by the D2 blocker haloperidol and the selective serotonin reuptake inhibitor paroxetine, respectively, drugs that are used to treat motor symptoms and compulsions in streptococcal-related neuropsychiatric disorders. Streptococcal exposure resulted in antibody deposition in the striatum, thalamus, and frontal cortex, and concomitant alterations in dopamine and glutamate levels in cortex and basal ganglia, consistent with the known pathophysiology of SC and related neuropsychiatric disorders. Autoantibodies (IgG) of GAS rats reacted with tubulin and caused elevated calcium/calmodulin-dependent protein kinase II signaling in SK-N-SH neuronal cells, as previously found with sera from SC and related neuropsychiatric disorders. Our new animal model translates directly to human disease and led us to discover autoantibodies targeted against dopamine D1 and D2 receptors in the rat model as well as in SC and other streptococcal-related neuropsychiatric disorders.   (({{pmid>long:22534626}}))
  
 </blockquote> </blockquote>
  
  
-===== References =====+===== References =====</nodisp> 
home/diseases/ocd.txt · Last modified: 09.14.2022 by 127.0.0.1
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