Protein fragments that comprise Alzheimer’s lesions have been implicated as a hallmark of the disease, but until now, why they accumulate or cause brain cells to die has not been understood.
Now, researchers have used giant X-ray centers – called synchrotrons – to investigate and have found that biological material may contribute to the build-up of toxic iron in the brain.
The researchers, who publish their results in the journal ACS Inorganic Chemistry, say they used the Diamond Light Source synchrotron in the UK, as well as other synchrotrons in Switzerland and the US to arrive at their findings.
The facility in the UK employed beams of light 10 billion times brighter than the sun to study the chemical and magnetic makeup of iron after it had interacted with beta-amyloid peptides, the fragments implicated in Alzheimer’s lesions.
Iron is naturally occurring in the human body and brain, and as a part of normal functioning, it converts between two chemical forms.
But when one of these forms – ferrous iron – is overproduced or builds up in tissues, the researchers say it can be highly toxic.
Though scientists have known that this toxic iron accumulates in the same place as brain lesions caused by Alzheimer’s disease, they have not understood how and why it occurs, or whether it is a cause or symptom of the brain cell damage in patients with the disease.
According to the Centers for Disease Control and Prevention (CDC), in the US in 2010, there were 83,494 deaths attributed to Alzheimer’s disease.
However, Medical News Today recently reported on a study that suggested the death toll for Alzheimer’s is larger than reported, possibly due to incorrect identification of the disease as the real cause of death.
Researchers from this latest study say by 2021 in the UK, there will be a million people with dementia. As this is a rising health issue in many parts of the world, the team investigated further.
Using the synchrotrons, the researchers were able to observe the predominant biological form of iron changing into the more toxic ferrous form.
- Cause of death rank in the US: 6 (though research suggests this rank is higher)
- Percent of US residents in assisted living with dementia: 41.8%
- Deaths per 100,000 population due to Alzheimer’s: 27.
In detail, they found that the beta-amyloid peptide is able to convert iron into its toxic form, which could then be causing brain cell damage.
The researchers say this means the lesions caused by the disease could actually be causing a slight disruption in how the brain manages iron, which in turn introduces a level of toxicity to brain cells that they are unable to manage.
“When findings showed increased levels of toxic iron within Alzheimer’s disease tissues, we realized that techniques we had used to study other iron based materials could be applied to understand where this toxic iron came from,” says Dr. Neil Telling, lead researcher from the University of Keele in the UK.
The team says their findings could pave the way for more research into treatments that could stop or manage the conversion of iron into its toxic form.
Additionally, it could lead to further development in using magnetic resonance imaging (MRI) to map altered patterns of iron in the brain, thus detecting early stages of the disease.
Dr. Telling says:
“Our observations suggest an origin for the toxic iron; that it may well be made toxic by the lesions themselves. This could open up new avenues of research into treatments to stop the build-up of this neurotoxic substance, potentially limiting the damage done by Alzheimer’s.”
“It’s at an early stage but these promising results seem to be another piece of the jigsaw to fully understand Alzheimer’s,” he adds.
Dr. Doug Brown, director of Research and Development at Alzheimer’s Society UK, says that there is a need for “more research aimed at unravelling the underlying causes of dementia to help us in our quest to find better treatments and ultimately a cure.”
Medical News Today recently reported on a study that suggested Alzheimer’s could be triggered by sleep disturbances.