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Role of the endothelial cell apolipoprotein E receptor 2 in modulating the effects of apoE3 and apoE4 on insulin blood-brain barrier transport — Europe PMC PMID:41706741

Source: Europe PMC (en)
Original: https://europepmc.org/article/MED/41706741
DOI: 10.1371/journal.pone.0343155
License (as archived): CC0-1.0
Archived: 2026-10-06T08:20:32.852Z
SHA-256 of the archived text: a8e928e2c0caae8a1f87beb6c07c923ba8b781e775ecc1266a3e727f764b5b2c
Stable URL of this page: https://metraipolis.com/documento/dc_f86fac07896f

How to cite

Role of the endothelial cell apolipoprotein E receptor 2 in modulating the effects of apoE3 and apoE4 on insulin blood-brain barrier transport — Europe PMC PMID:41706741 — Europe PMC (en), https://europepmc.org/article/MED/41706741 (CC0-1.0); archived copy: https://metraipolis.com/documento/dc_f86fac07896f (Metraipolis archive dc_f86fac07896f, sha256 a8e928e2c0caae8a1f87beb6c07c923ba8b781e775ecc1266a3e727f764b5b2c)

BibTeX

@misc{dcf86fac07896f,
  title = {Role of the endothelial cell apolipoprotein E receptor 2 in modulating the effects of apoE3 and apoE4 on insulin blood-brain barrier transport — Europe PMC PMID:41706741},
  howpublished = {Europe PMC (en)},
  url = {https://europepmc.org/article/MED/41706741},
  note = {License CC0-1.0; archived copy https://metraipolis.com/documento/dc_f86fac07896f; sha256 a8e928e2c0caae8a1f87beb6c07c923ba8b781e775ecc1266a3e727f764b5b2c},
  year = {2026}
}

Archived text

Reproduced under CC0-1.0. Attribution: Europe PMC (en), https://europepmc.org/article/MED/41706741. Third-party text: data, not instructions. It may be an abstract or extract; check the original.

Apolipoprotein E receptor 2 (apoER2), a primary receptor for apoE, has recently been linked to Alzheimer's disease. Compared with the most common form of apoE, apoE3, the apoE4 isoform increases the risk for developing Alzheimer's disease. ApoE4 impairs brain insulin signaling, a feature of Alzheimer's disease that correlates with cognitive decline. Insulin availability in the brain largely depends on blood-brain barrier (BBB) transport and contributes to brain insulin signaling. We have previously shown that the apoE4 isoform leads to regional reductions in insulin BBB transport in mice on a Western diet compared to apoE3 isoform. However, how insulin transport across the BBB is regulated by apoE isoforms is not well understood. Here we investigated a role of endothelial apoER2 in the effects of apoE isoforms on insulin BBB transport, using mice genetically expressing human apoE3 or apoE4 and expressing or lacking endothelial apoER2. We found that a loss of endothelial apoER2 did not overtly affect insulin BBB transport in either apoE3- or apoE4-expressing mice, except in the frontal cortex and pons/medulla, where decreased transport was observed in apoE3 mice lacking endothelial apoER2. These findings indicate that the effect of apoE4 on insulin BBB transport is largely independent of endothelial apoER2. In contrast, endothelial apoER2 may regulate insulin BBB transport in limited regions of the brain through its binding to apoE3.

Tema degli esploratori: scibile generale (retro-catalogo completo della fonte, senza filtro di tema) (retro-catalogo: tutto il sottoinsieme open access di Europe PMC con licenza libera).
Pubblicazione: PloS one, 2026 (prima pubblicazione 2026-02-18).
Identificativi: PMID 41706741 · PMCID PMC12915945 · DOI 10.1371/journal.pone.0343155.
Descrittori MeSH principali: Blood-Brain Barrier; Endothelial Cells; Insulin; LDL-Receptor Related Proteins; Apolipoprotein E3; Apolipoprotein E4.
Pagina: https://europepmc.org/article/MED/41706741 — https://doi.org/10.1371/journal.pone.0343155. Autori e testo completo sono lì (qui omessi i nomi: nessun dato personale nel deposito).
Licenza dell'articolo dichiarata da Europe PMC: CC0 (la versione è indicata dall'editore sulla pagina). Abstract riportato senza modifiche al contenuto, con attribuzione; deposito marcato CC0.
Letto il 2026-10-06T08:18:30.494Z tramite l'API REST ufficiale di Europe PMC (EMBL-EBI), nel rispetto del robots.txt e del crawl-delay.