رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

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رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

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رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

طب يعني كده مفيش امل الا انهم يلاقو حل للموصلات العصبية

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

نريد طبيب يترجم لنا المقال

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

انا ابني طلع عنده تلف فيها لكن فسرت الدكتورة عبير ذلك ان الجراثيم والمواد السامه وصلت للمخ واتلفت هذه الماده .. فالسبب ليس وراثي بحت وانما هناك مشاكل في جهاز المناعه والجهاز الهضمي تؤدي لخلل في الجسم ويصل للمخ والاعصاب ... والله اعلم ..

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

ام ضفاف ياريت لو تضعى رابط الموضوع لو تفضلتى

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

عزيز تى انا حقا لا اعرف كيف افعل الرابط ولكن هذا هو العنوان بالمناسبة الموقع جميل جدا


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عندما تفتحين ادخلى صفحة التوحد. ارجو ان تستفيدى من الموقع

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

شكرا وجزاك الله خيرا

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

برك الله فيك اختي ام ضفاف

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

للامانه هذي المستشفى غير كل المستشفيات اللي عرفتها
ناس فاهمه لابعد حد وعارفين اش يعني طفل ولن تجدي عندهم الا العلم الصح

الموضع اختي الكريمه هوا صح 100% وهنا احب ابين ان اغلب الاطباء الكسالا او المغرورين يقولو على طول للتوحدي هذا تخلف عقلي وللاسف طلعت موضى الحين عشان يسوي نفسه الطبيب فاهم ومواكب التطور يقول على التخلف العقلي العكس انه توحدي

تلف الدماغ ماله علاج ببساطه لكن فيه نظريه روسيه قديمه تقول ان الدماغ بخلاياه مثل المرايه يعني ممكن الاستفاده من سطح المنطقه التالفه لتقليل حجم التلف كفائه وليس حجم فعلي ،، هذه النظريه دوبهم الامريكان يتكلمو عنها

احب اشيد بهذا الدكتور الرائع مصطفى شاهين ايام ولدي كان زائر وكان فاهم لحالته من نظره طبيب يكلف على نفسه ويحط لولدي ممرضه عندها طفل بنفس عمر ولدي معاه لاني جيت فيه لحالي هذا مو طبيب وبس هذا ملاك

الان باذنه تعالي اترجم لكم المقال كامل

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

ارجو قص ولصق المقال بالانجليزيه هنا واترجمه لكم بطريقه علميه

اي مقال بالنجليزيه او الفرنسيه لا تترددو حطوه بموضوع ولكم ترجمته

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

جزاكم الله كل خير الكاتب والمتلقي وربنا يبختنا في اطباء زي هذولاء والحمدلله على كل حال

والف حمد وسلامه لرجوعك المنتدى اخي ابو صالح

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

الس يد ابو التوحدي المحترم انا شاكرة جدا لتعاونك وهذا هو المقال
Evidence That Autism Is a Brain 'Connectivity' Disorder
ScienceDaily (Jan. 11, 2010) — Studying a rare disorder known as tuberous sclerosis complex (TSC), researchers at Children's Hospital Boston add to a growing body of evidence suggesting that autism spectrum disorders, which affect 25 to 50 percent of TSC patients, result from a miswiring of connections in the developing brain, leading to improper information flow. The finding may also help explain why many people with TSC have seizures and intellectual disabilities.

Findings were published online in Nature Neuroscience on January 10.
TSC causes benign tumors throughout the body, including the brain. But patients with TSC may have autism, epilepsy or intellectual disabilities even in the absence of these growths. Now, researchers led by Mustafa Sahin, MD, PhD, of Children's Department of Neurology, provide evidence that mutations in one of the TSC's causative genes, known as TSC2, prevent growing nerve fibers (axons) from finding their proper destinations in the developing brain.
Studying a well-characterized axon route -- between the eye's retina and the visual area of the brain -- Sahin and colleagues showed that when mouse neurons were deficient in TSC2, their axons failed to land in the right places. Further investigation showed that the axons' tips, known as "growth cones," did not respond to navigation cues from a group of molecules called ephrins. "Normally ephrins cause growth cones to collapse in neurons, but in tuberous sclerosis the axons don't heed these repulsive cues, so keep growing," says Sahin, the study's senior investigator.
Additional experiments indicated that the loss of responsiveness to ephrin signals resulted from activation of a molecular pathway called mTOR, whose activity increased when neurons were deficient in TSC2. Axon tracing in the mice showed that many axons originating in the retina were not mapping to the expected part of the brain.
Although the study looked only at retinal connections to the brain, the researchers believe their findings may have general relevance for the organization of the developing brain. Scientists speculate that in autism, wiring may be abnormal in the areas of the brain involved in social cognition.
"People have started to look at autism as a developmental disconnection syndrome -- there are either too many connections or too few connections between different parts of the brain," says Sahin. "In the mouse models, we're seeing an exuberance of connections, consistent with the idea that autism may involve a sensory overload, and/or a lack of filtering of information."
Sahin hopes that the brain's miswiring miswiring can be corrected by drugs targeting the molecular pathways that cause it. The mTOR pathway is emerging as central to various kinds of axon abnormalities, and drugs inhibiting mTOR has already been approved by the FDA. For example, one mTOR inhibitor, rapamycin, is currently used mainly to prevent organ rejection in transplant patients, and Sahin plans to launch a clinical trial of a rapamycin-like drug in approximately 50 patients with TSC later this year, to see if the drug improves neurocognition, autism and seizures.
In 2008, Sahin and colleagues published related research in Genes & Development showing that when TSC1 and TSC2 are inactivated, brain cells grow more than one axon -- an abnormal configuration that exacerbates abnormal brain connectivity. The mTOR pathway was, again, shown to be involved, and when it was inhibited with rapamycin, neurons grew normally, sprouting just one axon.
Supporting the mouse data, a study by Sahin and his colleague Simon Warfield, PhD, in the Computational Radiology Laboratory at Children's, examined the brains of 10 patients with TSC, 7 of whom also had autism or developmental delay, and 6 unaffected controls. Using an advanced kind of MRI imaging called diffusion tensor imaging, they documented disorganized and structurally abnormal tracts of axons in the TSC group, particularly in the visual and social cognition areas of the brain (see image). The axons also were poorly myelinated -- their fatty coating, which helps axons conduct electrical signals, was compromised. (In other studies, done in collaboration with David Kwiatkowski at Brigham and Women's Hospital, giving rapamycin normalized myelination in mice.)
Sahin has also been studying additional genes previously found to be deleted or duplicated in patients with autism, and finding that deletion of some of them causes neurons to produce multiple axons -- an abnormality that, again, appears to be reversed with rapamycin.
"Many of the genes implicated in autism may possibly converge on a few common pathways controlling the wiring of nerve cells," says Sahin. "Rare genetic disorders like TSC are providing us with vital clues about brain mechanisms leading to autism spectrum disorders. Understanding the neurobiology of these disorders is likely to lead to new treatment options not only for TSC patients, but also for patients with other neurodevelopmental diseases caused by defective myelination and connectivity, such as autism, epilepsy and intellectual disability
The current study was funded by grants from the National Institutes of Health, the John Merck Scholars Fund, Tuberous Sclerosis Alliance, the Manton Foundation, the Children's Hospital Boston Translational Research Program, and the Children's Hospital Boston Mental Retardation and Developmental Disabilities Research Center.
Duyu Nie was first author on the paper. Coauthors were Duyu Nie, Alessia Di Nardo, Juliette M Han, Hasani Baharanyi, Ioannis Kramvis, and ThanhThao Huynh, all of the F.M. Kirby Neurobiology Center and Department of Neurology, Children's Hospital Boston; Sandra Dabora of Brigham and Women's Hospital; Simone Codeluppi and Elena B Pasquale of the Burnham Institute for Medical Research, and University of California San Diego; and Pier Paolo Pandolfi of Beth Israel Deaconess Cancer Center وشكرا لك مقدما

رد: مزيدا من الادلة على ان التوحد هواضطراب في موصلات الدماغ

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