In the April 2, 1994, issue of the Lancet, a study was published that found Alzheimer's disease to be correlated with pathological changes in the brain that had not been known about before. Using a CT scan, the researchers discovered loss of neurons (nerve cells) in a part of the brain called the medial temporal lobe. They found that the average rate of atrophy or deterioration of the medial temporal lobe was 15% per year in patients with Alzheimer's disease. Because the medial temporal lobe in normal control subjects of the same age shrank at only one-tenth this rate, it was concluded that Alzheimer's disease cannot be the result of an acceleration of normal aging, but must be the consequence of a disease process.
In a study in the April 2, 2002, Proceedings of the National Academy of Sciences, Rachael I. Scahill and colleagues confirmed and extended this study. Using magnetic resonance imaging, they found increasing brain atrophy to be occurring with advancing Alzheimer's disease, and they found this atrophy to be occurring before the onset of symptoms of the disease.
Two questions naturally arise from these findings: First, what causes this deterioration of the brain to begin? Second, what can be done to prevent it?
The Homocysteine Connection
By the age of 85 virtually everyone will have some neurofibrillary tangles (the hallmark of Alzheimer's disease) in their brain, but not everyone will develop Alzheimer's disease. What is different about those who do and those who don't? Well, many things, but one of them is that people with Alzheimer's disease have higher levels of homocysteine in their blood than people without Alzheimer's disease. Homocysteine is an amino acid that is a normal by-product of protein metabolism. It is toxic, and the body disposes of it quickly through three different pathways if everything is working right. When it is not, homocysteine can accumulate in the body and initiate disease. It has been implicated as a risk factor in cardiovascular disease, stroke, osteoporosis and, since the mid-nineties, Alzheimer's disease. Evidence that homocysteine can cause the brain atrophy seen in Alzheimer's disease can be found in three studies.
In the November 1998 issue of the Archives of Neurology, a study published by Robert Clark and colleagues found that Alzheimer's patients with elevated homocysteine levels had more rapid atrophy of the medial temporal lobe during 3 years of follow-up than those with lower homocysteine levels. The medial temporal lobe contains the center for smell, some areas for memory and learning, and a region where choice is made of thoughts to express. A study in the January 2002 issue of the journal, Brain, found that in people without Alzheimer's, those with higher plasma homocysteine had more atrophy of the cortex and the hippocampus, both areas of the brain important for memory, than those with lower levels of homocysteine. And finally, in a study published in the journal, Age Ageing, in November 2002, lead author J. H. Williams and colleagues found that the width of the hippocampus shrank as the level of homocysteine rose in healthy older people. They concluded that reducing homocysteine levels in healthy older people may help prevent Alzheimer's disease. Fortunately, this is not difficult and can be done through natural means rather than drugs.
This will be the subject of next week's column.
Mary Lou Williams, M. Ed., is a writer in the field of nutrition. She welcomes inquiries. She can be reached at 267-6480.