NEUROSCIENCE:
Cause Clarified for Alzheimer’s Dementia
Using extracts directly from human brain tissue, Dennis Selkoe (left), Gansesh
Shankar, and colleagues found that dimers of human amyloid-beta protein (Abeta)
can induce the synapse dysfunction and loss that are hallmarks of early-stage
Alzheimer’s
disease. These results, which support the hypothesis that excess Abeta initiates
Alzheimer’s,
are the first to analyze the toxic effects of human-brain extracts. This approach
is compelling because over the past decade much of the evidence supporting the
amyloid hypothesis has relied on synthesized forms of Abeta or Abeta produced
from cell cultures. The findings, published online June 22 in Nature Medicine, provide
insight into how the disease begins and how it might be treated.
BIOLOGY:
Stem Cells May Take Random Walk to Stable State
Stem cells appear to have minds of their own, so stubbornly do they resist
researchers’ efforts to make them differentiate. But it is unclear
how individual stem cells come to possess their proclivities. Sui Huang
(left), Hannah Chang, and colleagues separated stem cells into three
groups—those expressing low, medium, and high amounts of the protein
Sca-1. Each isolate reconstituted the original bell curve distribution
of low-, medium-, and high-expressing cells. The findings,
which appear in the May 22 Nature, suggest that stem cells share
a characteristic of even the most resolute of human minds: a tendency
to vacillate.
GENETICS:
Autism Genes Tied to Glitches in Early Learning
The genetic basis of autism seems to be as varied as the severity of symptoms,
which can range from oddities in social communication to severe mental retardation.
A study in the July 11 Science adds a handful of affected genes to the
list and finds a common biological link among several of them. The newfound mutations
may interfere with the brain’s ability to create the connections normally
sculpted by a child’s early experiences, report Eric Morrow (right), Christopher
Walsh, and colleagues.
METABOLISM:
Deleting Protein Cuts Fat in Liver
Researchers including Laurie Glimcher (left) and
Ann-Hwee Lee have found that XBP1, a transcription factor involved
in the ER stress response, plays a previously unknown role in hepatic
lipid synthesis. After conditionally deleting XBP1 in the liver of
adult mice, the team observed decreases in cholesterol, triglycerides,
and free fatty acids in the blood without any accompanying fat accumulation
in liver cells. The findings make XBP1 a promising therapeutic target
for simultaneously controlling high cholesterol and high triglyceride
levels in humans. The work appears in the June 13 Science.
Copyright 2008 by the President and Fellows of Harvard College