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New Study to Assess Very Premature Infants. Associate Professor Linda Fetters of the department of physical therapy at Sargent College is studying the motor development of premature, very low-birth-weight infants with a team of researchers from Children's Hospital and the Harvard Medical School. The team, which includes experts in neonatology, radiology, and psychology, received a four-year $1.1 million award from the National Institute of Neurological Diseases and Stroke. They will study infants born between 26 and 30 weeks of gestational age (40 weeks is full term) and under 1,500 grams (about three pounds).

Team members are particularly interested in infants with white matter disease (WMD), diagnosed with high resolution ultrasound during the newborn period. White matter supports and improves the function of the brain's gray matter, which is integral to the functioning of the central nervous system. WMD infants have damaged or underdeveloped white matter.

"Infants with WMD have a higher incidence of motor disorders and cerebral palsy, although the incidence continues to be very low, even in this group," notes Fetters. "We will study 40 infants with WMD, 40 infants without the disease, and 20 full-term infants. I will evaluate kinematic measures as a possible early predictor of motor disorder and cerebral palsy."

Hormone May Limit Stroke's Damage. A School of Medicine researcher has discovered that 17 beta-estradiol, a common hormone used in estrogen replacement therapy, has a protective effect on neuron survival. According to Professor David Farb, chair of the department of pharmacology, the discovery may imply further beneficial effects of estrogen replacement therapy. "Beta-estradiol can't prevent strokes, but it can limit the damage that strokes have on the brain's functions," he says. The study was published in the July issue of Brain Research.

According to Farb, neurons (one of the two basic brain cells) can die when exposed to excess amounts of a substance called glutamate. One key way in which glutamate is produced occurs when a special molecule known as an NMDA-receptor is activated. "When a person has a stroke, even a small one, neurons will die from a lack of oxygen supply," he says. "But in dying, neurons release excess glutamate, which activates the NMDA-receptors of neighboring cells, killing them, and those cells in turn produce more glutamate and kill even more cells. So there's a secondary damage. But the beta-estradiol prevents the glutamate from causing damage upon reaching its target." Thus, a woman on estrogen replacement therapy with a higher level of beta-estradiol in her bloodstream might still have the same risk of stroke as a woman not on estrogen, but suffer from less secondary damage. This leads to a lowered overall risk of dementia, which can be caused by dozens of mini-strokes over a period of years.

Farb's work may explain why other studies have found that the risk and severity of dementia are decreased in women who have received estrogen replacement therapy. "We've shown a new way in which beta-estradiol protects against NMDA-induced neuronal death," Farb says. "This study contributes to the discussion about advantages and disadvantages of hormone replacement, but women need to consider all the risks before deciding to undergo that course of treatment."

Understanding Alzheimer's. Alzheimer's disease strikes about a quarter of all people who reach their eighties and affects millions of patients and their families.

Although the cause of the disease remains a mystery, it is known that the brains of Alzheimer's victims contain structures -- senile plaques and neurofibrillary tangles -- that aren't present in normal brains.

A team of physicists at the Center for Polymer Studies, working with neurologists at Massachusetts General Hospital, has been able to gain a clearer picture of the structure of these plaques, and has proposed a new theory about how they develop in the brain. Led by Physics Professor H. Eugene Stanley, the BU team, Sergey Buldyrev, Luis Cruz, Shlomo Havlin, and Brigita Urbanc, worked from digitized images of extremely thin sections of plaques produced by the MGH team. Using a Silicon Graphics Onyx2 supercomputer, the BU team reconstructed the plaques in three dimensions and found that contrary to previous belief, the plaques are not solid but have porous cores that become progressively less dense moving from the center toward the outer surface. The scientists then developed a computer simulation to "grow" the plaques, molecule by molecule, in an effort to demonstrate that the porosity could be caused by a simultaneous building up and wearing down of the amyloid protein (amyloid beta) that makes up the plaque.

Another aspect of the research, mapping the topography of normal brains and comparing them with those of people who have died of Alzheimer's, has resulted in the discovery of a column-like structure of neurons between the layers of the brain, which is less pronounced in Alzheimer's victims. Work is also under way to better understand how neurofibrillary tangles are formed and how they affect the neurons of the brain.

The research was funded in part by a five-year .2 million National Institutes of Health grant and a more recent one- year 0,000 grant from an anonymous foundation.

"Research Briefs" is written by Joan Schwartz in the Office of the Provost. To read more about BU research, visit


15 May 2003
Boston University
Office of University Relations