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By using antisense oligonucleotides to inhibit a mutated exon associated with Timothy syndrome mutation, researchers restored neuron function.
Source: the-scientist.com
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By using antisense oligonucleotides to inhibit a mutated exon associated with Timothy syndrome mutation, researchers restored neuron function.
Scientists have discovered that inhibiting the protein Mdm2 may help stop the decline of brain plasticity through the destruction of synapses and dendritic spines commonly seen in Alzheimer's disease.