Iron buildup in the brain can trigger Alzheimer’s disease

2023-09-22 05:48:12

The exact causes of Alzheimer’s disease remain enigmatic. However, researchers have discovered a potential link between iron accumulation in the brain and the onset of this pathology, leading to a specific form of cell death called ferroptosis. This discovery opens new perspectives in the understanding and treatment of Alzheimer’s disease.

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Alzheimer’s disease affects millions of people worldwide. With the aging of the population, it is becoming more and more common. It is the most common form of neurodegenerative dementia in older adults. The underlying mechanisms of this pathologypathology are still little known. We know that the disease is characterized by the accumulation of amyloid plaquesamyloid plaques and neurofibrillary tangles in the brain. These anomaliesanomalies lead to a inflammationinflammationdisrupt neuronal communication and cause the death of neuronesneurones. A recent study from the University of Oregon Health and Science revealed an unexpected mechanism in triggering Alzheimer’s diseaseAlzheimer’s disease : the accumulation of ferfer in the brain leads to ferroptosis, a specific form of cell death, and the destruction of microgliesmicroglies, essential for brain function. The results were published in the journal Annals of Neurology.

Microglies and ferroptose

Microglia play an essential role in the brain as the first line of immune defense. They strive to eliminate wastewaste cells, including debris from myelinmyelin damaged. However, the act of removing this myelin has a downside: the release of iron. The authors observed microglia degeneration in post-mortem brain tissue samples. Iron from degraded myelin, when in excess, causes ferroptosis, thus endangering these microglia. Ferroptosis is a specific form of programmed cell death that is distinct from apoptosis, necrosis, and other cell death mechanisms. It is characterized by the accumulation of intracellular iron and the concomitant loss of antioxidants such as glutathione, leading to lipid oxidative damage and, ultimately, cell death.

Therapeutic implications

Researchers suggest that this cascade of degeneration originates from repeated episodes of reduced blood flow and oxygen supplies to the brain. Events such as AVCAVC or chronic illnesses likehypertensionhypertension and diabetes might be partly responsible. Treating this type of illness is one way to prevent Alzheimer’s disease. In therapeutic terms, this discovery suggests directing treatment research towards iron regulation and myelin protection. In addition, this new data might prove valuable for other demyelinating diseases, such as multiple sclerosis or the disorder of spectrespectre neuromyelitis optica.

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