Which brain parts are damaged in Alzheimer’s?
Some of the most severe brain damage can be seen in people with the progressive form of Alzheimer’s disease, or P.E.D., which affects the way neurons communicate and function.
The National Institutes of Health estimates that one in every 10,000 people in the U.S. is at least one-fifth of an older person.
That’s about the same as the number of Americans with heart disease and strokes.
The condition is more common in men than women, with an estimated 4.4 million Americans older than 65 living with it, according to the Alzheimer’s Association.
In the past, doctors have thought brain damage might be the result of damage to the brain’s connections to the rest of the body.
But the damage can occur in areas other than the brain itself.
Researchers are now studying the connections between the brain stem, the part of the brain that controls breathing and movement, and the spinal cord, the long nerve connecting the legs and feet to the head.
They are looking for ways to reduce the damage.
Researchers at Duke University School of Medicine and at Johns Hopkins University in Baltimore recently reported finding signs of reduced function in the spinal cords of mice that had been treated with a chemical that blocks a protein called N-methyl-D-aspartate, or NMDA, which can cause damage to nerve cells in the brain.
The researchers also found signs of increased damage to synapses, the connections in the body between neurons that act like synapses.
That finding led them to think the chemical might have some effect on the brain cells that control movement, or the parts of the spinal tract that connect the spinal column to the legs.
The study, published online in the journal Nature Neuroscience, is a follow-up to previous research that showed N-acetylcysteine, or CEA, was a promising candidate for treating the disease.
Researchers found the NMDA-blocking drug could protect neurons that control breathing and reduce damage to neurons that are critical for learning and memory.
It was also effective at restoring the ability of neurons to communicate with each other, and to fire when they are stimulated.
“This is the first evidence of NMDA’s ability to reverse damage in brainstem-associated neurodegeneration,” lead researcher Matthew Grosnick, a neurologist at Duke and a professor of neurobiology and molecular medicine at Johns’ Johns Hopkins School of Advanced International Studies, said in a statement.
“We are working with colleagues in the pharmaceutical industry to identify potential ways to make NMDA safer.”
Grosnick and his colleagues used an antibody to treat neurons in the mouse brains of patients with the disease, and found it had a similar effect as N-Acetylcysteinyl-CoA, a type of creatine that is a common supplement.
N-Acetoacetic acid, also known as NAC, has been used for decades in the treatment of muscle cramps and depression.
But because it is also found in a number of foods, including some high-protein foods such as chicken and eggs, it has been considered a possible anti-aging agent.
Grosnell said the study is the latest to suggest that NMDA could work as an anti-cancer agent.
Researchers also found that NAC can prevent the development of brain tumors, but it did not protect cells that make up the nervous system, which controls movement.
The findings have important implications for how NMDA is used therapeutically, said lead researcher Richard Wahlgren, a neuroscientist at Harvard University.
He is also the director of the Mapping of Neurodegenerative Disorders Program in the Department of Neurology at Harvard Medical School.
“When we are looking at the potential therapeutic benefit, NMDA has the potential to be a very important agent because of the potential for long-term protection of the neurons that make the spinal reflexes, the movements that control our muscles,” he said.
“I think it would be a really interesting study if we could find ways to use NMDA as a way to protect these neurons.”
Scientists are also looking at a new type of drug called AM251, which blocks a group of amino acids that are present in nerve cells.
These amino acids are known to cause damage when they bind to DNA and cause a chemical reaction called methylation.
The NMDA inhibitor, called AM281, also blocks this enzyme, but researchers are not sure whether it would prevent damage to neuronal cells.
This new type is much safer than NAC because it blocks the enzyme and doesn’t affect the proteins in the cell, but still, it’s still unclear whether it could protect the cells from damage.
Wahlgren said researchers are still figuring out the exact way the NMMA inhibitors work, but he said they may be able to stop the damage to certain parts of cells that might be damaged by NAC.
The new finding may also help explain how N-Ascisylcystatin, or NA