Head Size, Genes Linked
to Alzheimer's Onset
Excerpt By Anthony J. Brown, MD, Reuters Health

NEW YORK (Reuters Health) - Having a small head along with a genetic predisposition to Alzheimer's disease may hasten the onset of the disease, researchers report.

The current findings lend support to the ``brain reserve'' theory of Alzheimer's disease, the researchers note.

Alzheimer's disease is characterized by the development of plaques and tangles in the brain. According to the brain reserve theory, once the accumulation of these abnormalities reaches a critical point, mental function is affected. But this critical point may vary among individuals, depending on how much ``brain reserve'' they have. Theoretically, smaller head size would result in a smaller brain reserve and an earlier onset of Alzheimer's symptoms.

To investigate, Dr. Amy Borenstein Graves from the University of South Florida in Tampa and colleagues measured the head size of 1,865 people aged 65 and older who had no signs of dementia. They were also able to check whether or not 1,111 of these individuals had a gene variation called APOE e4, which is known to increase Alzheimer's risk.

During the follow-up period, 59 people developed probable Alzheimer's disease. The researchers found that people with the APOE e4 gene were nearly five times more likely to develop Alzheimer's than those without this variation. And people with the APOE e4 gene whose head circumference was less than 21.4 inches were 14 times more likely to develop the disease.

But head circumference alone had no significant association with Alzheimer's risk, according to the report published in the October 23rd issue of Neurology.

People who developed Alzheimer's were also older, less educated, shorter, lighter and had lower estimated verbal IQ scores than people who did not develop the disease, the authors note.

``We don't think that head circumference is a risk factor for (Alzheimer's disease),'' Graves told Reuters Health. ''However, head circumference does seem to influence the age of clinical onset in individuals with pathologic changes,'' she said. ``Therefore, in people with APOE e4--a gene associated with rapid plaque accumulation--clinical disease onset is earlier in individuals with smaller head circumferences.''

Graves mentioned that her team is ``currently trying to understand why some people with the neuropathologic changes of Alzheimer's do not develop clinical manifestations in their lifetime.''

Once the factors that influence disease onset are understood, ``we may be able to develop therapeutic interventions that delay onset so that predisposed individuals actually die from other causes before Alzheimer's disease is clinically apparent,'' she said.

SOURCE: Neurology 2001;57:1453-1460.

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