中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (12): 2563-2564.doi: 10.4103/NRR.NRR-D-23-02002

• 观点:退行性病与再生 • 上一篇    下一篇

Aper2/Lrp8:突触稳态的卧底警察

  

  • 出版日期:2024-12-15 发布日期:2024-03-30

Apoer2/Lrp8: the undercover cop of synaptic homeostasis

Gordon C. Werthmann*, Joachim Herz*   

  1. Department of Molecular Genetics and Center for Translational Neurodegeneration Research, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA (Werthmann GC, Herz J) 
    Department of Neuroscience; Department of Neurology; University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA (Herz J)
  • Online:2024-12-15 Published:2024-03-30
  • Contact: Gordon C. Werthmann, PhD, Chandler.Werthmann@utsouthwestern.edu; Joachim Herz, MD, Joachim.Herz@utsouthwestern.edu.
  • Supported by:
    This work was supported by NIH grants NS093382, NS108115, AG053391, HL063762 (to JH). JH was further supported by Blue Field Project to Cure FTD, BrightFocus Foundation (A20135245  and A2016396S), Harrington Discovery Institute, the Alzheimer’s Association, and a Circle of Friends Pilot Synergy Award. JH is a cofounder of Reelin Therapeutics, Inc.

摘要: https://orcid.org/0000-0001-7370-3928 (Gordon C. Werthmann)
https://orcid.org/0000-0002-8506-3400 (Joachim Herz)

Abstract: Apolipoprotein E receptor 2 (ApoER2) is a receptor for the protein ApoE, the most common genetic risk factor for late-onset Alzheimer’s disease (AD). It is also a key modulator of synaptic homeostasis, in part through its effect on the expression of neuronal genes including those implicated in AD and other neuropsychiatric disorders. In this perspective, we highlight several genes affected by ApoER2 and its alternatively spliced forms and how aberrant expression can be rescued by the reintroduction of the ApoER2 intracellular domain in the mouse hippocampus.