Takato yamamoto biography of mahatma
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Interviews / Studio Visit: Ryan Hewett
Previews: Ed Templeton Synthetic Suburbia @ Roberts Tilton
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Streets: El Mac “Ánimo Sin Fronteras” (El Paso)
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FMR1 genetically interacts with DISC1 to regulate glutamatergic synaptogenesis
Introduction
Schizophrenia is a severe mental disorder that impacts about 1% of the population1,2,3. Although the molecular and pathological mechanism of schizophrenia remains elusive, genome-wide and familial lineage studies of schizophrenia patients indicate multiple genetic risk factors contributing to the pathological condition. An increasing number of potential risk factor loci have been identified to date4,5,6,7,8,9,10,11,12,13,14,15. These studies also indicate that numerous genetic risk loci associated with schizophrenia are shared with other psychiatric disorders, including bipolar disorder, autism spectrum disorder, and intellectual disability16,17,18,19,20. Many of these shared risk loci encode genes for synaptic proteins, indicating a convergence in their biological functions toward pathways that regulate synaptic development and plasticity9,10,14,21,22,23. The molecular methods used to study schizophrenia have shown changes in a set of transcripts that control synaptic functions, which aligns well with the findings of genetic studies24,25,26. This further supports the synaptic hypothesis, suggesting that disrupted neuronal connectivity and signaling could be key causes