Deposits of amyloid protein, which progressively damage brain tissue, are a cardinal feature of Alzheimer's disease. A molecule called "beta peptide" is a key component of these deposits and is responsible for initiating the damage.

Scientists have been looking at ways of blocking its action to prevent the buildup of amyloid deposits, and recent experimental research has shown that antibodies against beta peptide can clear them.

The preliminary research involved five patients with early Alzheimer's disease. Over a period of six months, they were given monthly intravenous injections of immunoglobulin containing antibodies against beta peptide. The patients' ages ranged from the mid-50s to the mid-60s.

Levels of the peptide in the cerebrospinal fluid, which bathes the brain and the spinal cord, were assessed at the beginning and end of the study. The patients' cognitive function also was tested.

At the end of the six months, levels of beta peptide in cerebrospinal fluid fell by 30 percent, and the level of beta peptide in the blood shot up 233 percent.

Although cognitive function improved only slightly in four patients, the authors note that this did not worsen, which would have been expected after six months.

Visual tasks, as assessed by a "mini-mental state exam," which usually fail early in the course of Alzheimer's disease, improved in three patients and stayed the same in the other two.

There were virtually no major side effects.

The authors are quick to point out that definitive conclusions cannot be drawn on the strength of a study of five patients, and much more work will need to be done. But they nevertheless conclude that their findings warrant further detailed investigation and add weight to the experimental evidence.

An accompanying editorial agrees, pointing out that intravenous immunoglobulin already has been used to treat several inflammatory conditions and immune disorders, including some neurological diseases. It may be that higher doses would be more effective, it suggests.