Excess levels of a mineral responsible for healthy blood and brain function may raise the risk of Parkinson’s disease and dementia, a study suggests.
Iron is an essential mineral that helps make hemoglobin, a protein in red blood cells that carries oxygen from the lungs to the rest of the body’s vital tissues.
The body cannot produce iron on its own, and it instead comes from animal proteins such as lean red meat, clams and oysters, along with plant-based foods like spinach, lentils, tofu and white beans.
Iron deficiency, which affects one in seven Americans, or 36 million people, has also been linked to developmental issues and cognitive decline, as the mineral also supports energy and neurotransmitter production.
But researchers at the Salk Institute in California have found that excess iron can slowly accumulate inside neurons. While this has little effect early in life, for older adults, it may cause nerve cells to die.
They believe this is because excess iron lowers cells’ defenses, which makes them more vulnerable to stressors.
Cell death in areas of the brain responsible for memories and cognitive function, such as the hippocampus and cerebral cortex, can lead to dementia, which affects about 7 million Americans.
And striking 1 million Americans, Parkinson’s disease is caused by the loss of neurons responsible for producing dopamine, which coordinates movement, so the death of these cells could contribute to the disease.
A new study found an accumulation of iron may lead to cell changes associated with dementia and Parkinson’s disease
The researchers noted that evaluating iron levels could be a key tool in preventing neurodegenerative diseases like dementia and Parkinson’s.
‘Resilience has become a huge topic of discussion when it comes to Alzheimer’s disease and other neurodegenerative disorders, trying to make the brain more resilient in the face of stressors that contribute to neurodegeneration,’ Dr Pam Maher, senior and co-corresponding study author and research professor at the Salk Institute, said.
‘Our study reveals that cells lose resilience when iron hits a certain level, making neurons more susceptible to stressors that damage or even kill them.’
The findings come as both dementia and Parkinson’s disease are on the rise in the US.
Experts estimate dementia diagnoses are expected to double by 2050.
The Parkinson’s Foundation estimates 1.2million Americans will be diagnosed with Parkinson’s by 2030, and 90,000 are struck by the disease every year.
This is an increase from the previously estimated rate of 60,000 a decade ago, the foundation estimates.
Recent research suggests environmental exposures like pollution and pesticides, along with growing rates of chronic conditions like obesity and diabetes, may be to blame, but scientists are still unraveling the causes.
Michael J Fox (pictured above at the 32nd Annual Actor Awards in March) was diagnosed with Parkinson’s disease in 1991, revealing his diagnosis in 1998. In 2000, he founded the Michael J Fox Foundation to help fund Parkinson’s research
The new study, published in the journal Cell Death Discovery, used human neural cells from the nervous system cancer neuroblastoma to compare the effects of acute and chronic iron exposure. Acute exposure lasted between six and eight hours, while chronic was about nine days.
Chronic exposure was meant to mimic slow accumulation that would be seen during aging.
Using the cell models, the researchers coined the new pathway chronoferroptosis. Ferroptosis is a well-studied phenomenon in which cell death is caused by a process called lipid peroxidation.
This occurs when harmful molecules called free radicals steal electrons from the lipids in cell membranes, resulting in cell damage.
In chronoferroptosis, however, that pathway doesn’t end in cell death.
Instead, neurons chronically exposed to iron saw long-term functional changes rather than immediate death. Acutely exposed neurons could handle the stress, but those with chronic exposure became vulnerable to neurodegenerative diseases.
‘We think these coordinated alterations in iron-handling and antioxidant defense proteins make chronically exposed neurons vulnerable to neurodegenerative pathology,’ Dr Nawab John Dar, co-corresponding study author and postdoctoral researcher in Maher’s lab, said.
‘Entering this state of chronoferroptosis may set neurons up for age-related failure.’
Iron cannot be produced by the body on its own, but it is rich in animal proteins like lean meat, fish and beef liver
Dar noted that by using the progressive model, the team found it’s ‘not the amount of iron that seals the fate of these cells, it’s the amount of time they spend under stress.’
‘It’s one of the most important minerals in the body,’ he added. ‘So, it isn’t the iron itself that is a problem with age. It is this accumulation of iron over time that is the problem.’
The researchers were able to treat the iron toxicity with Ferrostatin-1, a synthetic antioxidant that inhibits chronoferroptosis and blocks cell stress and death.
There were several limitations to the research, including not specifying an exact amount of iron that leads to chronoferroptosis and looking at cell models rather than humans.
