Jonas J. Neher

TL;DR: Evidence suggesting that phagoptosis may contribute to neuronal loss during brain development, inflammation, ischaemia and neurodegeneration is discussed.

TL;DR: This work sequenced bacterial 16S rRNA from fecal samples of Aβ precursor protein (APP) transgenic mouse model and found a remarkable shift in the gut microbiota as compared to non-transgenic wild-type mice, indicating a microbial involvement in the development of Abeta amyloid pathology and suggesting that microbiota may contribute to the developed neurodegenerative diseases.

TL;DR: It is demonstrated that peripherally applied inflammatory stimuli induce acute immune training and tolerance in the brain and lead to differential epigenetic reprogramming of brain-resident macrophages (microglia) that persists for at least six months.

TL;DR: Microglial phagocytosis of stressed neurons may contribute to their loss, and activation of PHOX alone causes little or no death, but when combined with iNOS expression results in apparent apoptosis via peroxynitrite production.

TL;DR: It is reported that under inflammatory conditions in primary rat cultures of neurons and glia, phagocytosis actively induces neuronal death, indicating a novel form of inflammatory neurodegeneration, where inflammation can cause eat-me signal exposure by otherwise viable neurons, leading to their death through phagcytosis.