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Study Links Brain Size to Alzheimer's
> 4/16/2008 12:38:29 PM

Though the cause of Alzheimer's disease (AD) remains unclear, research has indicated an association between AD and accumulations of amyloid-beta plaque and neurofibrillary tangles in the brain. While these abnormal brain changes have been viewed as a defining characteristic of AD, autopsies have shown that plaques and tangles can also be present in the brains of people who did not experience cognitive decline while alive. New research from the Oregon Health and Science University in Portland indicates that brain size may be involved in this discrepancy. The study, which was presented this week at the annual meeting of the American Academy of Neurology in Chicago, found that individuals with a large hippocampus were less likely to have symptoms of AD although plaques and tangles were present in their brains.

The hippocampus, which lies within the temporal lobe, plays an important role in memory formation, and the brain changes and cell death associated with AD first become apparent within this brain structure. The researchers examined the brains of 36 deceased individuals. While all of the individuals had similar amounts of plaques and tangles in their brains, only 24 had been diagnosed with AD while alive. The other 12 had not displayed symptoms of memory loss or cognitive decline. In analyzing the brains, the researchers found that the hippocampi of individuals who had not been diagnosed with AD were around 10 percent larger than the hippocampi of those who had received an AD diagnosis, and their overall brain volume was also larger. The researchers controlled for age and sex and found no socioeconomic or educational differences between the two groups.

Plaques and tangles are not always accompanied by mental decline, and the researchers provided some explanations for why this might be true. For individuals with larger brains, greater accumulations of plaques and tangles may be necessary before symptoms of AD become apparent. Still, there could be other factors that protect some individuals from the damage of these neural changes, and the researchers note that other biological mechanisms likely play an important role as well. Some studies have already illustrated the danger of spending too much focus only on plaques and tangles, including a recent trial of a vaccine that would allow the brain to destroy neural plaque. While the vaccine succeeded in this aim, the reduction in plaque did not lead to any significant change in cognitive ability.

The current study was small, but its results show the need for further research if we are to better understand the relationship between AD and plaques and tangles. The researchers stress that future studies should focus on other potential contributing factors. By looking beyond plaques and tangles, we may develop a new understanding of how AD develops and perhaps discover mechanisms that can be targeted by medication.

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