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Current Alzheimer Research


ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Research Article

Astrocytic Expression of the Immunoreceptor CD300f Protects Hippocampal Neurons from Amyloid-β Oligomer Toxicity In Vitro

Author(s): Thiago Zaqueu Lima, Luis Roberto Sardinha, Joan Sayos, Luiz Eugenio Mello and Hugo Peluffo*

Volume 14, Issue 7, 2017

Page: [778 - 783] Pages: 6

DOI: 10.2174/1567205014666170202121709

Price: $65


Background: Astrocytes contribute to neuroinflammation that accompanies neurodegenerative disorders such as Alzheimer’s disease (AD). In this sense, the toxicity of these diseases might be attenuated through the modulation of astrocytic inflammatory responses. Recently, the CD300f immunoreceptor was described as a new member of the CD300 immunoreceptor family, showing promising modulatory properties.

Objective: Here, we investigated whether overexpression of hCD300f (the human isoform of CD300f) in astrocytes protects hippocampal neurons against the degeneration induced by amyloid-beta (Aβ) oligomer.

Method: Astrocyte monolayers were transfected with hCD300f before seeding the hippocampal neurons, and then the co-culture was exposed to Aβ1-42 oligomers (5 μM, 48h).

Results: hCD300f expression significantly abrogated the neuronal loss elicited by Aβ. This effect was dependent on neuron-astrocyte cell-cell interactions since no protection was observed using conditioned media from transfected astrocytes. Astrocyte modulation was dependent on the cytoplasmic signaling tail of hCD300f. Furthermore hCD300f expression did not affect the ability of astrocytes to uptake Aβ1- 42 oligomers by endocytosis, which discards the possibility that increased Aβ1-42 clearance could mediate neuroprotection by hCD300f.

Conclusion: These results suggest that the astrocyte-directed expression of the hCD300f immune receptor can be a neuroprotective strategy in AD disease.

Keywords: Alzheimer's disease, amyloid-beta, Astrocytes, CD300f, neuroprotection, endocytosis.

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