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    Israeli researchers develop treatment to prevent retardation, autism

    Source: Xinhua| 2018-11-15 23:44:32|Editor: Mu Xuequan
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    JERUSALEM, Nov. 15 (Xinhua) -- Israeli researchers have developed a treatment that may prevent developmental retardation and autism, a report published by Tel Aviv University said Thursday.

    The researchers found that early therapy with the peptide NAP (nucleosome assembly protein) normalizes the development of mice in a model of ADNP (activity-dependent neuroprotective protein) syndrome in children.

    This genetic mutation is one of the major causes of developmental delay and autism in children.

    The ADNP gene plays a role in the development of cognition. Embryos with partial ADNP deficiency will suffer from mental retardation and, in most cases, autism.

    In recent years, with the development of genetic sequencing technology, autistic children with mental retardation had random mutations in the ADNP gene, which appear to occur during pregnancy.

    The resulting protein is shorter than usual, and as a result, children suffer from incomplete ADNP (which is ADNP syndrome).

    The researchers found that mice with ADNP produced only about half the number of synapses (the link points between nerve cells) compared to healthy mice - especially in the brain areas responsible for cognitive activity, according to the report.

    These mice showed developmental delay, social difficulty, and sensitivity, like children with mental retardation and autism.

    At the next stage, the NAP peptide was injected daily into the affected mice from the moment of birth, followed by nasal spray to mice weaned from breastfeeding.

    The results were very impressive: the treated mice, unlike those untreated, developed normally. They made voices to call their mothers, walked, had proper memory, were able to distinguish between familiar and unfamiliar mice, and developed strength in their muscles.

    It also turned out that the brains of these mice began to produce a proper number of synapses.

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