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Relationship between beta-AP peptide aggregation and microglial activation.

Carme Casal·Joan Serratosa·Josep M Tusell
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Abstract

We compared the relationship between the state of aggregation of two peptides (beta-AP 25-35 and beta-AP 1-42) and microglial activation. After 7 days at 37 degrees C beta-AP 25-35 was in an amorphous state and did not activate microglial cells. In the same conditions, aggregated beta-AP 1-42 activated these cells and caused changes in microglial ramification, increasing the proliferation index and inducing tumor necrosis factor alpha (TNF alpha) release. Neither peptide induced a release of nitric oxide (NO). As the toxicity of beta-AP peptides in cell culture is associated with the formation of amyloid fibrils, we also examined the toxicity of both peptides in microglial cell cultures and in PC 12 cell cultures. The results suggest that the two beta-AP fragments studied have similar neurotoxic effects but different pro-inflammatory activities.

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Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCell DifferentiationCell DivisionCell SizeEncephalitisGliosisMicrogliaNeuronsNitric OxideNitric Oxide SynthasePC12 CellsPeptide FragmentsPlaque, AmyloidRatsRats, WistarTumor Necrosis Factor-alphaComparative StudyJournal ArticleResearch Support, Non-U.S. Gov't

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Carme Casal, Joan Serratosa, Josep M Tusell. 2002-02-22. Relationship between beta-AP peptide aggregation and microglial activation.. https://doi.org/10.1016/s0006-8993(01)03362-5

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