Postsynaptic ProSAP/Shank scaffolds in the cross-hair of synaptopathies

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• 作者：Andreas M. Grabrucker¹ ;   ; ² ;   ; ^* ; Michael J. Schmeisser¹ ;   ; ^* ; Michael Schoen¹ ;   ; ^* ; Tobias M. Boeckers¹ ;   ; ^{tobias.boeckers@uni-ulm.de}
• 刊名：Trends in Cell Biology
• 出版年：2011
• 出版时间：October 2011
• 年：2011
• 卷：21
• 期：10
• 页码：594-603
• 全文大小：1343 K

文摘

Intact synaptic homeostasis is a fundamental prerequisite for a healthy brain. Thus, it is not surprising that altered synaptic morphology and function are involved in the molecular pathogenesis of so-called synaptopathies including autism, schizophrenia (SCZ) and Alzheimer's disease (AD). Intriguingly, various recent studies revealed a crucial role of postsynaptic ProSAP/Shank scaffold proteins in all of the aforementioned disorders. Considering these findings, we follow the hypothesis that ProSAP/Shank proteins are key regulators of synaptic development and plasticity with clear-cut isoform-specific roles. We thus propose a model where ProSAP/Shank proteins are in the center of a postsynaptic signaling pathway that is disrupted in several neuropsychiatric disorders.