Combating Iron In The Brain: Researchers Find Anti-aging Micromolecule

Mito

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The older we get, the more our brain ages. Cognitive abilities decline and the risk of developing neurodegenerative diseases like dementia, Alzheimer’s and Parkinson’s disease or having a stroke steadily increases. A possible cause is the accumulation of iron molecules within neurons, which seems to be valid for all vertebrates. In a collaborative research project, scientists found that this iron accumulation is linked to a microRNA called miR-29......We strongly believe that our results are relevant for humans as well," says Alessandro Cellerino, Professor of Physiology at SNS in Pisa and guest scientist at the FLI, who is one of the study's leaders. In fact, the link between an increased iron accumulation and neurodegenerative diseases or strokes in humans has been known for some time; there are also results showing a reduced concentration of miR-29 in these diseases. However, it is totally new that miR-29 acts as molecular switch that inhibits iron accumulation.....


https://www.sciencedaily.com/releases/2017/02/170214094040.htm


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Age-related damage accumulation is an inescapable condition that tends to change cellular homeostasis; on the other hand, cells tend to maintain their homeostasis inducing a progressive and adaptive response in order to counteract this inevitable process and preserve their physiological functions. Age-dependent up-regulation of miR-29 is part of this adaptive response and its deficiency leads to exacerbation of aging-induced damage (Fig. 7), partly due to impaired iron homeostasis.

MicroRNA miR-29 controls a compensatory response to limit neuronal iron accumulation during adult life and aging | BMC Biology | Full Text
 
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Iron Brain Menace: The Involvement of Ferroptosis in Parkinson Disease​

Abstract​

Parkinson disease (PD) is the second-most common neurodegenerative disease. The characteristic pathology of progressive dopaminergic neuronal loss in people with PD is associated with iron accumulation and is suggested to be driven in part by the novel cell death pathway, ferroptosis. A unique modality of cell death, ferroptosis is mediated by iron-dependent phospholipid peroxidation. The mechanisms of ferroptosis inhibitors enhance antioxidative capacity to counter the oxidative stress from lipid peroxidation, such as through the system xc-/glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis and the coenzyme Q10 (CoQ10)/FSP1 pathway. Another means to reduce ferroptosis is with iron chelators. To date, there is no disease-modifying therapy to cure or slow PD progression, and a recent topic of research seeks to intervene with the development of PD via regulation of ferroptosis. In this review, we provide a discussion of different cell death pathways, the molecular mechanisms of ferroptosis, the role of ferroptosis in blood-brain barrier damage, updates on PD studies in ferroptosis, and the latest progress of pharmacological agents targeting ferroptosis for the intervention of PD in clinical trials.
 

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