Postsynaptic density protein PSD-95 expression in Alzheimer's disease and okadaic acid induced neuritic retraction

Neurobiology of Disease

Pascale Marin¹  Claude Walzer¹  Rudolf Kraftsik¹  Françoise Piotton²  Béatrice Carnal²  Geneviève Leuba²  Constantin Bouras³  Armand Savioz⁴  André Vernay⁴ 

[1] Service of Old Age Psychiatry, Department of Psychiatry, CHUV, Lausanne, Switzerland;Center for Psychiatric Neuroscience, Department of Psychiatry, CHUV, Lausanne, Switzerland;Department of Cell Biology and Morphology, Lausanne University, Lausanne, Switzerland;Department of Psychiatry, University Hospital Geneva, Geneva, Switzerland;

关键词: Alzheimer's disease;    Dendritic plasticity;    Synaptic proteins;    Entorhinal cortex;    PSD-95;    Synaptophysin;   

DOI  :  

来源: DOAJ

【 摘 要 】

In order to understand how plasticity is related to neurodegeneration, we studied synaptic proteins with quantitative immunohistochemistry in the entorhinal cortex from Alzheimer patients and age-matched controls. We observed a significant decrease in presynaptic synaptophysin and an increase in postsynaptic density protein PSD-95, positively correlated with β amyloid and phosphorylated Tau proteins in Alzheimer cases. Furthermore, Alzheimer-like neuritic retraction was generated in okadaic acid (OA) treated SH-SY5Y neuroblastoma cells with no decrease in PSD-95 expression. However, in a SH-SY5Y clone with decreased expression of transcription regulator LMO4 (as observed in Alzheimer's disease) and increased neuritic length, PSD-95 expression was enhanced but did not change with OA treatment. Therefore, increased PSD-95 immunoreactivity in the entorhinal cortex might result from compensatory mechanisms, as in the SH-SY5Y clone, whereas increased Alzheimer-like Tau phosphorylation is not related to PSD-95 expression, as suggested by the OA-treated cell models.

【 授权许可】

Unknown