Lipocalin 2 modulates the cellular response to amyloid beta

S. D. Mesquita, A. C. Ferreira, A. M. Falcao, J. C. Sousa, T. G. Oliveira, M. Correia-Neves, N. Sousa, F. Marques, J. A. Palha

Research output: Contribution to journalArticlepeer-review


The production, accumulation and aggregation of amyloid beta (Aβ) peptides in Alzheimer's disease (AD) are influenced by different modulators. Among these are iron and iron-related proteins, given their ability to modulate the expression of the amyloid precursor protein and to drive Aβ aggregation. Herein, we describe that lipocalin 2 (LCN2), a mammalian acute-phase protein involved in iron homeostasis, is highly produced in response to Aβ 1-42 by choroid plexus epithelial cells and astrocytes, but not by microglia or neurons. Although Aβ 1-42 stimulation decreases the dehydrogenase activity and survival of wild-type astrocytes, astrocytes lacking the expression of Lcn2 are not affected. This protection results from a lower expression of the proapoptotic gene Bim and a decreased inflammatory response. Altogether, these findings show that Aβ toxicity to astrocytes requires LCN2, which represents a novel mechanism to target when addressing AD.

Original languageEnglish (US)
Pages (from-to)1588-1599
Number of pages12
JournalCell Death and Differentiation
Issue number10
StatePublished - Oct 1 2014

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


Dive into the research topics of 'Lipocalin 2 modulates the cellular response to amyloid beta'. Together they form a unique fingerprint.

Cite this