Neural Regeneration Research ›› 2024, Vol. 19 ›› Issue (12): 2563-2564.doi: 10.4103/NRR.NRR-D-23-02002

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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.

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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.