Systematic review and meta-analysis of mass spectrometry proteomics applied to ocular fluids to assess potential biomarkers of age-related macular degeneration.

Background: Age-related macular degeneration (AMD) is a significant cause of severe vision loss. The main purpose of this study was to identify mass spectrometry proteomics-based potential biomarkers of AMD that contribute to understanding the mechanisms of disease and aiding in early diagnosis.

Methods: This study retrieved studies that aim to detect differences relate to proteomics in AMD patients and healthy control groups by mass spectrometry (MS) proteomics approaches.

Brain-specific loss of Abcg1 disturbs cholesterol metabolism and aggravates pyroptosis and neurological deficits after traumatic brain injury.

Based on accumulating evidence, cholesterol metabolism dysfunction has been suggested to contribute to the pathophysiological process of traumatic brain injury (TBI) and lead to neurological deficits. As a key transporter of cholesterol that efflux from cells, the ATP-binding cassette (ABC) transporter family exerts many beneficial effects on central nervous system (CNS) diseases. However, there is no study regarding the effects and mechanisms of ABCG1 on TBI.

The Neurobiological Links between Stress and Traumatic Brain Injury: A Review of Research to Date.

Neurological dysfunctions commonly occur after mild or moderate traumatic brain injury (TBI). Although most TBI patients recover from such a dysfunction in a short period of time, some present with persistent neurological deficits. Stress is a potential factor that is involved in recovery from neurological dysfunction after TBI.

Mechanism of Ferroptosis and Its Relationships with Other Types of Programmed Cell Death: Insights for Potential Therapeutic Benefits in Traumatic Brain Injury.

Traumatic brain injury (TBI) is a serious health issue with a high incidence, high morbidity, and high mortality that poses a large burden on society. Further understanding of the pathophysiology and cell death models induced by TBI may support targeted therapies for TBI patients. Ferroptosis, a model of programmed cell death first defined in 2012, is characterized by iron dyshomeostasis, lipid peroxidation, and glutathione (GSH) depletion.

Neurobiological Links between Stress, Brain Injury, and Disease.

Stress, which refers to a combination of physiological, neuroendocrine, behavioral, and emotional responses to novel or threatening stimuli, is essentially a defensive adaptation under physiological conditions. However, strong and long-lasting stress can lead to psychological and pathological damage. Growing evidence suggests that patients suffering from mild and moderate brain injuries and diseases often show severe neurological dysfunction and experience severe and persistent stressful events or environmental stimuli, whether in the acute, subacute, or recovery stage.

Restraint Stress Delays the Recovery of Neurological Impairments and Exacerbates Brain Damages through Activating Endoplasmic Reticulum Stress-mediated Neurodegeneration/Autophagy/Apopotosis post Moderate Traumatic Brain Injury.

Based on accumulating evidence, patients recovering from mild and moderate traumatic brain injury (TBI) often experience increased sensitivity to stressful events. However, few studies have assessed on the effects and pathophysiological mechanisms of stress on TBI. In the current study, using a mouse model of moderate TBI, we investigated whether restraint stress (RS) regulates secondary neurodegeneration and neuronal cell death, which are commonly associated with neurological dysfunctions.