In defence of ferroptosis.

Rampant phospholipid peroxidation initiated by iron causes ferroptosis unless this is restrained by cellular defences. Ferroptosis is increasingly implicated in a host of diseases, and unlike other cell death programs the physiological initiation of ferroptosis is conceived to occur not by an endogenous executioner, but by the withdrawal of cellular guardians that otherwise constantly oppose ferroptosis induction. Here, we profile key ferroptotic defence strategies including iron regulation, phospholipid modulation and enzymes and metabolite systems: glutathione reductase (GR), Ferroptosis suppressor protein 1 (FSP1), NAD(P)H Quinone Dehydrogenase 1 (NQO1), Dihydrofolate reductase (DHFR), retinal reductases and retinal dehydrogenases (RDH) and thioredoxin reductases (TR).

Quantitative susceptibility mapping of the fear circuit: Associations with silent symptoms in relapsing-remitting multiple sclerosis.

Multiple sclerosis (MS) is a long-term autoimmune inflammatory disorder that affects the central nervous system leading to neurodegeneration, and can involve a variety of symptoms. These symptoms can include fatigue, anxiety, depression, and cognitive decline, which may be silent. The objective of this study was to explore changes in brain iron deposition in people with relapsing-remitting MS (pw-RRMS) compared to healthy controls (HCs), with a particular focus on regions of fear circuit.

Deferiprone in Alzheimer Disease: A Randomized Clinical Trial.

Importance: Interventions that substantially slow neurodegeneration are needed to address the growing burden of Alzheimer disease (AD) to societies worldwide. Elevated brain iron observed in AD has been associated with accelerated cognitive decline and may be a tractable drug target.

Objective: To investigate whether the brain-permeable iron chelator deferiprone slows cognitive decline in people with AD.

The link between amyloid β and ferroptosis pathway in Alzheimer's disease progression.

Alzheimer's disease (AD) affects millions of people worldwide and represents the most prevalent form of dementia. Treatment strategies aiming to interfere with the formation of amyloid β (Aβ) plaques and neurofibrillary tangles (NFTs), the two major AD hallmarks, have shown modest or no effect. Recent evidence suggests that ferroptosis, a type of programmed cell death caused by iron accumulation and lipid peroxidation, contributes to AD pathogenesis.