Thursday, January 27, 2022

Taming ApoE Via the LDL Receptor Calms Microglia, Slows Degeneration


The APOE gene exacerbates pathology not only of the amyloid variety, but tau, as well. Previous research has tied ApoE’s effect on tau to microglial activation, but how does ApoE trigger microglia? In the June 10 Neuron online, scientists led by David Holtzman at Washington University, St. Louis, implicate the low-density lipoprotein receptor (LDLR), one of two ApoE receptors. In a tauopathy mouse model, overexpressing LDLR lowered ApoE and calmed microglia. This, in turn, slowed tau pathology and neurodegeneration. Curiously, excess LDLR was also a good thing for other glia. It dampened astrocyte reactivity and boosted the number of oligodendrocyte precursor cells (OPCs), bolstering myelination.

  • In tauopathy mice, increased LDLR dramatically lowered ApoE in the brain.
  • This shifted microglia from a DAM into protein clearance/neuron support…
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