New Theory Links Early-Onset Alzheimer’s to How Cells Store Iron

A team of scientists has proposed a new theory suggesting that the way our cells handle iron could be linked to the development of early-onset Alzheimer’s disease. Their findings are published in the journal Frontiers in Neuroscience.

Researchers from the University of Adelaide in Australia led a new study investigating the potential link between iron in our cells and the rare gene mutations that cause Alzheimer’s disease. If proven, the theory could assist in finding new ways to prevent the debilitating disease.

The scientists caution against making choices about diet or supplements based on this idea, however, as the theory only relates to how our cells handle iron, not how much iron is in our diet.

“For 20 years, most scientists have believed that a small protein fragment, amyloid beta, causes Alzheimer’s disease,” said Associate Professor Michael Lardelli from the School of Biological Sciences at the University of Adelaide.

“Clearing out amyloid beta from the brains of people who are developing Alzheimer’s disease can slow their rate of cognitive decline. But, so far, nothing has been able to stop the relentless progression of the disease,” he said.

A chance conversation between Lardelli, Dr. Amanda Lumsden from South Australian Health and Medical Research Institute (SAHMRI) and Flinders University, and Dr. Morgan Newman from the University of Adelaide was the inspiration for the new theory of how mutations might cause Alzheimer’s disease.

Lumsden has a background in the biology of how cells use iron, while the Adelaide researchers study the genes that cause Alzheimer’s disease when mutated.

They ran their ideas past additional experts, such as Associate Professor Jack Rogers at Harvard Medical School and Dr. Shohreh Majd of Flinders University in Australia. Now, the research team has published a paper suggesting their new theory for how mutations might cause the rare but devastating early-onset form of Alzheimer’s disease that afflicts some families.

The researchers say that the abnormalities seen in inherited Alzheimer’s disease could result from problems in how neurons handle iron.

“Cells need iron to survive. In particular, iron is essential for the tiny powerhouses of all cells, the mitochondria, to generate most of the energy that keeps cells functioning,” Lardelli says.

“The genes mutated in inherited Alzheimer’s disease seem likely to affect how iron enters neurons, how it is recycled within neurons, and how it is exported from neurons. Since neurons have such huge energy needs, disturbing the way they handle iron can have serious, long-term consequences.

“Furthermore, iron is a key player in inflammation and in the production of damaging molecules named ‘reactive oxygen species,’ and both occur at high levels in brains with Alzheimer’s disease.”

Although the researchers observe compelling links between iron and Alzheimer’s disease, more investigation is required to understand how mutations that cause the disease impact cellular iron.

Source: University of Adelaide


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