α-Synuclein disrupts microglial autophagy through STAT1-dependent suppression of Ulk1 transcription.

Background: Autophagy dysfunction in glial cells is implicated in the pathogenesis of Parkinson's disease (PD). The previous study reported that α-synuclein (α-Syn) disrupted autophagy in cultured microglia. However, the mechanism of microglial autophagy dysregulation is poorly understood.

Dying to Defend: Neutrophil Death Pathways and their Implications in Immunity.

Neutrophils, accounting for ≈70% of human peripheral leukocytes, are key cells countering bacterial and fungal infections. Neutrophil homeostasis involves a balance between cell maturation, migration, aging, and eventual death. Neutrophils undergo different death pathways depending on their interactions with microbes and external environmental cues.

Lipid metabolism and neutrophil function.

Neutrophils are an essential part of the innate immune system, playing a critical role in the control of infectious diseases, maintenance of tissue homeostasis and regulation of tumorigenesis. However, their functional importance has often been overlooked due to the conception that they are short-lived and unable to proliferate. Recent studies indicate that the functions of neutrophils are diverse and can be influenced by cellular metabolisms, including that governing lipid homeostasis.

α-synuclein suppresses microglial autophagy and promotes neurodegeneration in a mouse model of Parkinson's disease.

The cell-to-cell transfer of α-synuclein (α-Syn) greatly contributes to Parkinson's disease (PD) pathogenesis and underlies the spread of α-Syn pathology. During this process, extracellular α-Syn can activate microglia and neuroinflammation, which plays an important role in PD. However, the effect of extracellular α-Syn on microglia autophagy is poorly understood.

AMPK S-sulfuration contributes to HS donors-induced AMPK phosphorylation and autophagy activation in dopaminergic cells.

Hydrogen sulfide (HS) serves as a neuromodulator and regulator of neuroinflammation. It is reported to be therapeutic for Parkinson's disease (PD) animal and cellular models. However, whether it affects α-synuclein accumulation in dopaminergic cells, the key pathological feature in PD, is poorly understood.

Expression of autophagy related genes in peripheral blood cells in Parkinson's disease.

Parkinson's disease (PD) is the second most common neurodegenerative disorder and affects dopaminergic neurons. Autophagy often shows a circadian rhythm pattern under physiological conditions across 24 h. Abnormal autophagy and circadian dysfunction are two characteristics of PD.