ealth & Science
Page 11
Tuesday • April 29, 1997
searchers find link
Alzheimer's disease
RINGTON (AP) — A defect
fnes that drive energy me-
i in cells may play a role in
|ier’s disease, new labora-
lies have found,
irchers say they have dis-
I a mutation in the mito-
la DNA of cells in
Iter’s patients that may
i" - ' : to a rise of a destructive
l 5 hical, called oxygen-free rad-
|ed fo'-B the brain,
tied*:IW. Davis Parker of the Uni-
5ume: tty of Virginia and senior au-
^ a study to be published
^ in the Proceedings of the
nl Academy of Sciences
[ findings suggest a link be-
jhe way brain cells process
md Alzheimer’s disease,
jn Khachaturian, a scientist
le Alzheimer’s Association,
| Saturi^F new finding “is a poten-
bjectedBry important new piece of
Tiental information” that
pead to diagnostic tests for
fease and a new under-
bg of how it develops,
ieimer’s is a disorder that
tin cells and causes a grad-
bline in memory, a change
lonality and behavior, and,
Sally, death. About 4 million
Americans, mostly elderly, have
been diagnosed with the disease.
There is no known cure.
In the new study, researchers
found that a mutation in cellular
DNA leads to a failure of glucose
processing in brain cells. This
breakdown causes a rise in oxygen
free radicals which could kill brain
cells, a characteristic of
Alzheimer’s disease.
Mitochondria are structures
that produce energy to make cells
function. The mitochondria have
their own DNA which is different
from the DNA in the genes of each
cell. The mitochondria DNA is
only inherited from the mother.
To find the gene defect, the
researchers removed mitochon
dria DNA from normal neuron
cells and inserted DNA from
Alzheimer’s disease patients.
The altered cells then func
tioned in cultures using the
transplanted DNA.
The researchers found that the
altered cells developed energy
processing failures, leading to the
excessive oxygen-free radicals.
They found the mutation was in a
mitochondria gene called cy-
tochromic oxidase.
Gene offers insight
to cause of shortness
► Researchers are
trying to determine
how a gene called
SHOX affects a
person's height
NEWYORK (AP) —Why are really
short people so short? It is largely a
mystery. But now scientists have dis
covered a gene that might cause
some cases.
Followup work might help scien
tists understand the biology of what
determines a person’s height and
lead to new drugs that could make
short children taller.
The study defined "short” as
belonging to the shortest 2.5 per
cent of the population. That’s a
standard cutoff. For American
men, that translates to about 5-
foot-4 and under; for American
women it’s just under 5 feet.
Nobody knows exactly why
most people in this group are so
short. Genes clearly play a role, but
few genes that stunt growth have
been identified. Other factors like
nutrition and environment also
clearly enter in.
Most of these people are healthy,
so medical conditions can explain
only a small percentage.
The newly found gene is called
SHOX. Researchers found it was
damaged in one person out of a
group of 91 healthy short people, or
about 1 percent.
The mutation did not show up in
300 DNA samples from people of
normal height.
The short person who showed
the mutation was a girl who stood
35 inches tall at age 4.
On average, girls in the United
States are about 40 inches tall on
their fourth birthdays.
The researchers looked at DNA
from several generations of the girl’s
family, which lived in Germany. They
found the SHOX gene flaw in all five
family members who met the criteria
for shortness, but not in three family
members who did not.
The SHOX gene is a “strong can
didate” for causing some cases of
shortness, researchers from Ger
many, the Netherlands and Japan
write in the May issue of the jour
nal Nature Genetics.
Dr. Judith Ross, a pediatric en
docrinologist at Thomas Jefferson
University in Philadelphia, called
the results provocative. But it
would take more work to prove
that a mutated SHOX gene really
makes people short, she said.
dentists say hormone burns fat inside cells
br lir
tesi—RINGTON (AP) — Leptin, a hormone
Jill be act s in the brain to suppress appetite, also
[eft ;sobesity by burning up fat within cells, re-
lionsliiBrs report.
jddresif Roger H. Unger of the University of Texas
Ipia; thwestern Medical Center at Dallas said
dres ratory rats that are genetically altered to
JteLe' jhigh levels of leptin lose all the fat in their
espithin days.
Jresearchers say a study to be published
la^ in the Proceedings of the National Acad-
ofSciences shows for the first time that leptin
i inside body cells and not just in the brain,
bre is a huge effect in cells on the metabo-
i of fatty acids,” Unger said. “The fat never
llhe cells. It is burned up inside.”
Fat was depleted in cells that normally store fat
and in muscle, liver and pancreas cells, he said.
“Within seven days, there is no fat detectable in
the body at all,” Unger said.
Earlier studies of leptin had shown that the hor
mone acts in the brain to repress appetite. Rats
with high levels of leptin were found to eat about
half the food of normal rats.
Unger and his associates transferred genes that
boosted the leptin levels in laboratory rats to about
20 times normal.
The animals’ appetite and feeding habits were
then carefully monitored.
For comparison, normal rats were fed ex
actly the amount of food as the high-leptin rats,
Unger said.
Later, tissue of all of the rats was examined for
fat content.
Unger said the normal rats lost fat, but only
about one-half the amount shed by the leptin
rodents. Also, the normal rats retained fat in
their muscle cells.
The study suggested that leptin may be use
ful in the control of Type II diabetes, the form
of the disease that often develops in older,
overweight people. He said the rat study
showed that by burning up fat in the cells, the
excess leptin also lowered blood sugar and
made the cells more sensitive to insulin, the
hormone that controls sugar levels. Diabetes
develops when the body stops making or be
comes insensitive to insulin.
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