This archived news story is available only for your personal, non-commercial use. Information in the story may be outdated or superseded by additional information. Reading or replaying the story in its archived form does not constitute a republication of the story.
Knight Ridder Newspapers
OAKLAND, Calif. - Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.
A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.
It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.
Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.
The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.
Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.
As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's.
But so far nobody has been able to figure out exactly how the plaques do the killing.
"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."
Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.
Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.
Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.
But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.
But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.
This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.
Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.
"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.
The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.
"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.
Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.
Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.
The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.
"If you don't, your bank account will be less prepared down stream," Atamna said.
This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.
Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.
Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.
"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."
Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.
(C) 2004 Knight Ridder/Tribune News Service.. All Rights Reserved