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Symmetric Bihemispheric Postmortem Brain Cutting to Study Healthy and Pathological Brain Conditions in Humans
Published on: December 18, 2016
Contribution of analytical microscopies to human neurodegenerative diseases research (PSP and AD)
1Instituto Microelectronica de Madrid, Parque Tecnologici de Madrid, 8 Isaac Newton, 28760 Tres Cantos, Madrid, Spain. carmen@imm.cnm.csic.es
Abstract:
Using analytical microscopies we have observed an increase of Fe(2+) iron-induced oxidative stress inside pathological ferritin (Ft). This finding, together with the presence of Ft in myelinated axons associated with oligodendrocyte processes and myelin sheet fraying, suggests that a dysfunction of ferritin (a ferritinopathy) may be the non-specific aging-dependent pathogenic event responsible for neurodegenerative disease.
Insights
Pathological ferritin (Ft) accumulates excess iron, causing oxidative stress and myelin damage. This suggests a ferritinopathy, or ferritin dysfunction, may underlie age-dependent neurodegenerative diseases.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Ferritin (Ft) is crucial for iron regulation.
- Dysfunctional iron metabolism is implicated in neurodegeneration.
- Aging is a risk factor for neurodegenerative diseases.
Purpose of the Study:
- To investigate the role of ferritin in neurodegeneration.
- To explore the link between iron, oxidative stress, and myelin damage.
Main Methods:
- Analytical microscopy was employed.
- Observed ferritin within pathological contexts.
Main Results:
- Increased Fe(2+) iron-induced oxidative stress was detected within pathological ferritin.
- Pathological ferritin was found in myelinated axons.
- Evidence of oligodendrocyte process and myelin sheath fraying was observed.
Conclusions:
- Ferritin dysfunction (ferritinopathy) may be a key pathogenic event.
- This dysfunction is linked to aging and neurodegenerative diseases.
- Oxidative stress and myelin damage are consequences of pathological ferritin.
