Targeting Macroautophagy as a Therapeutic Opportunity to Treat Parkinson's Disease.

Macroautophagy, an evolutionary conserved catabolic process in the eukaryotic cell, regulates cellular homeostasis and plays a decisive role in self-engulfing proteins, protein aggregates, dysfunctional or damaged organelles, and invading pathogens. Growing evidence from and models shows that autophagy dysfunction plays decisive role in the pathogenesis of various neurodegenerative diseases, including Parkinson's disease (PD). PD is an incurable and second most common neurodegenerative disease characterised by neurological and motor dysfunction accompanied of non-motor symptoms that can also reduce the life quality of patients.

Burnout Syndrome in a Military Tertiary Hospital Staff during the COVID-19 Contingency.

(1) Background: Burnout syndrome (BOS) is defined as a psychological state of physical and mental fatigue associated with work. The COVID-19 pandemic greatly impacted the physical and mental wellbeing of health professionals. The objective of this work was to determine the impact on personnel, monitoring the frequency of BOS throughout the pandemic.

Intranasal dexamethasone: a new clinical trial for the control of inflammation and neuroinflammation in COVID-19 patients.

Background: By end December of 2021, COVID-19 has infected around 276 million individuals and caused over 5 million deaths worldwide. Infection results in dysregulated systemic inflammation, multi-organ dysfunction, and critical illness. Cells of the central nervous system are also affected, triggering an uncontrolled neuroinflammatory response.

Endophilin-B regulates autophagy during synapse development and neurodegeneration.

Synapses are critical for neuronal communication and brain function. To maintain neuronal homeostasis, synapses rely on autophagy. Autophagic alterations cause neurodegeneration and synaptic dysfunction is a feature in neurodegenerative diseases.

Macros to Quantify Exosome Release and Autophagy at the Neuromuscular Junction of .

Automatic quantification of image parameters is a powerful and necessary tool to explore and analyze crucial cell biological processes. This article describes two ImageJ/Fiji automated macros to approach the analysis of synaptic autophagy and exosome release from 2D confocal images. Emerging studies point out that exosome biogenesis and autophagy share molecular and organelle components.

Epidemiology of hospitalized patients with COVID-19 in a tertiary care hospital.

Introduction: COVID-19, caused by the betacoronavirus SARS-CoV-2, has overwhelmed the world's health systems.

Objective: To describe the epidemiological characteristics of patients treated in a tertiary care hospital.

Methods: A retrospective cohort study of patients diagnosed with or suspected of having COVID-19 from March 23 to July 31, 2020 was conducted.

The role of lipids in autophagy and its implication in neurodegeneration.

Neurodegenerative diseases are, at present, major socio-economic burdens without effective treatments and their increasing prevalence means that these diseases will be a challenge for future generations. Neurodegenerative diseases may differ in etiology and pathology but are often caused by the accumulation of dysfunctional and aggregation-prone proteins. Autophagy, a conserved cellular mechanism, deals with cellular stress and waste product build-up and has been shown to reduce the accumulation of dysfunctional proteins in animal models of neurodegenerative diseases.

A LRRK2-Dependent EndophilinA Phosphoswitch Is Critical for Macroautophagy at Presynaptic Terminals.

Synapses are often far from the soma and independently cope with proteopathic stress induced by intense neuronal activity. However, how presynaptic compartments turn over proteins is poorly understood. We show that the synapse-enriched protein EndophilinA, thus far studied for its role in endocytosis, induces macroautophagy at presynaptic terminals.

Torsins Are Essential Regulators of Cellular Lipid Metabolism.

Torsins are developmentally essential AAA+ proteins, and mutation of human torsinA causes the neurological disease DYT1 dystonia. They localize in the ER membranes, but their cellular function remains unclear. We now show that dTorsin is required in Drosophila adipose tissue, where it suppresses triglyceride levels, promotes cell growth, and elevates membrane lipid content.