Source-
BBC News
3/28/03
Gene Therapy for
Alzheimer Disease
Scientists from The Salk Institute, UCSD, the
University of Kentucky, and Columbia University in New York City have
developed a gene therapy method that can be used to attach protein which
clumps together into plaques in the brains of Alzheimer's patients. They
also identified brain cells which could prevent the build up of plagues in
the brain.
The researchers used a modified version of the HIV
virus to transfer a neprilysin gene to neurons of genetically modified
mice. The genetically modified mice carry the human beta-amyloid gene.
The plaques that are near neprilysin injection
site were smaller and more compact than in other parts of the brain. The
plaques were reduced to less than half the size to those found in the
untreated areas of the brain. This treatment eliminated damage produced by
the build-up of beta amyloid.
The second study identified astrocytes that can
attack beta-amyloid plaques. Astrocytes are cells found near Alzheimer
plaques. They nourish and protect neurons in the brain.
Studies in mice showed that plaques were reduced
by 40% after they are exposed to astrocytes.
Scientists are hopeful that the two approaches
will be good candidates for therapy against Alzheimer's Disease.
Source-
HealthScoutNews
3/19/03
Mouse Testing Can Be
Misleading
American scientists have reported a genetic heart
mutation that is fatal in humans but does little damage in mice.
The researchers Evangelia G. Kranias and her
colleagues at the
University
of
Cincinnati
knocked out a gene for phospholamban (PLN), a protein that plays an
important role in heart function in mice. The mice seemed normal. The
experiments were published in the March 14 issue of the Journal of
Clinical Investigation.
Another study on two human families showed that a mutation in the
PLN gene, leading to loss of the protein, damages the heart.
Dr. David MacLennan of the University of Toronto School of Medicine
explains a reason for this discrepancy may be in the cardiac reserve
between mice and humans. Humans have cardiac reserve to draw on during
exercise. But in mice, the heart already uses most of its cardiac reserve,
and therefore the absence of PLN is not all that damaging.
Although mouse studies have produced a lot of
useful information, these experiments show that mouse studies may not
always be appropriate for early evaluation of treatments and other
features of human disease.
Source-
BBC
News 
3/15/03
Correcting
RNA Mutations
Scientists in the
UK
announced that they can reverse gene mutations using a genetic process,
known as “sticky-tape”.
Spinal Muscular Atrophy (SMA) is a fatal spinal
cord disease that affects muscles important for walking, head and neck
control and swallowing. It affects 1 in 10,000 people and 1 in 50 is a
carrier of the defective gene.
RNA transcription involves a process called
splicing. Unwanted RNA pieces are spliced first before the coding regions
are connected together. When splicing does not work properly, mutations
occur. Researchers were able to stick the right pieces of the RNA back
together using oligos (short pieces of RNA)- “sticky tape”. The oligos
ensured that the splicing mechanism works.
The method was tested on cells taken from a
patient with SMA. The expression of the defective genes was restored.
Source-
Nature
Online
3/6/03
Chloroplast
DNA in Genetically Modified Plants
Major
concern with GM (genetically modified plants) was the ability of
foreign genes introduced into plants may end up in their wild relatives
via pollen transfer. To remedy this situation, researchers have inserted
foreign DNA into the chloroplast instead of nuclear DNA since only nuclear
DNA is incorporated into pollen during cell division. However, recent
studies have shown that antibiotic resistance marker gene inserted in the
chloroplasts of tobacco plants was later detected in a plants' seedling.
The ratio was 1 in 16,000 of the plants' seedlings. The antibiotic
resistance gene had jumped from chloroplast to the nucleus, and was later
passed to the offspring.
According
to the researchers,
the rate of passage of functional genes from chloroplasts to nuclei is
likely to be several orders of magnitude less than 1 in 16,000. More
experiments are needed to determine these conclusions.
Source-
BBC
News .gif)
2/28/03
Gene
Linked to Heart Disease
Scientists at the Howard Hughes Medical Institute
in Maryland have shown that a defective gene may trigger dilated
cardiomyopathy (DCM).
DCM occurs when the heart is enlarged and fails to
pump blood efficiently. The disease affects 35 out of 100,000 people.
The gene is important in regulating the flow of
calcium through the heart. The heart muscle contracts and relaxes when
calcium is released into the muscle cell and then pumped back.
The researchers tested the defective mice and
found that they suffered severe damage to the heart. People with this
defect suffer chronic malfunction of calcium regulation in their heart
muscle which could lead to heart failure.
The discovery of the defect paves the way to new
treatments for the condition, and a better understanding of heart failure.
Source-
Reuters
2/10/03
Genetically
Modified Human Stem Cells
Scientists at the
University
of
Wisconsin
were able to delete a disease gene from human embryonic stem cells using
the method of homologous recombination. This method has been used to
remove genes from mice in order to study the functions of those genes.
Now, scientists will be able to genetically manipulate the cells to direct
them to become targeted tissues such as brain, heart, or pancreatic cells.
The experiments were conducted by Dr. Thomas Zwaka and his
colleagues, with the help of Dr. James Thomson. Thomson's lab was the
first in the world to produce human embryonic stem cells. The work is
published in the journal Nature Biotechnology.
The scientists hope that these cells can be used
to replace the brain cells that are destroyed in Parkinson's disease,
type-1 diabetes, or damaged spinal cords.
Dr. Zwaka said that the method could also be used
to create "universal" donor cell lines, of cells. The genes that
cause the body's immune system to reject foreign tissue would be
removed in these cells.
Dr. Zwaka was asked if this method could be used
to make designer babies. He answered that it would be impossible to do
with this technology.
Source-
Yahoo
Science News. Cell 2003; 112:257-269. 
1/28/03
Genetic
Link to Forgetfulness
Researchers have found a variant of the
gene BDNF ( makes brain-derived neurotrophic factor) that contributes to
impaired memory of past event. BDNF plays a role in memory formation.
In a study at the National Institute of
Mental Health in Maryland, 600 adults were asked to recall story events.
Those individuals with the variant metBDNF performed worse than those with
normal BDNF.
About 15-20% of the population carries
the variant metBDNF.
In another study, researchers injected
the normal and variant proteins of BDNF into rodent hippocampal cells in
the laboratory. The normal BDNF spread throughout the cells, in contrast
to the metBDNF which formed a clump inside the cells.
Source-
Reuters
and Nature 421:231-237, 268-272, 220-221; 2003 
1/16/03
Fat
Storage Genes in the Worm
Scientists have discovered that a worm
carries 417 genes that help control fat storage in its body. Many of them
are similar to humans.
The species of worm studied is
Caenorhabditis elegans, or C. elegans. Its entire genome has been decoded.
The worm carries about 20,000 genes..
Pinpointing specific genes that help
regulate body fat storage will help scientists have a better understanding
of obesity in humans.
The method used to discover the genes
involved in obesity in the worm, was through 'knocking out' a particular
gene by the worm's engineered food. The food also contained dye that
colored all body fat. Since the worm is transparent, it was easy for
scientists to detect and determine the percent fat in its body.
According to Ruvkun who is the lead
scientist for the study, approximately 10 proteins in humans will be
linked to fat absorption within the next few years.
Source-
SiliconValley.com
1/06/03
Excerpts
from interview with the Director of the Human Genome Project
Mercury News reporter Paul Jacobs
interviewed Dr. Francis S. Collins, director of the National Human Genome
Research Institute and head of the public Human Genome Project. The
following are some excerpts from the interview:
On plans to
celebrate the completion of the sequencing of the human genetic code next
April:
Essentially
in April of 2003 all of the original goals of the Human Genome Project as
outlined in 1990 will have been accomplished. Plus a bunch of other things
that were not anticipated could be done in that timetable like what we've
done to characterize human variation , which is I think a critical part of
understanding the genome, not one we contemplated being able to tackle
until 2005 or so.
So we're
having this internal discussion about whether we should say the Human
Genome Project is over: Hurray, let's have a big party and celebrate the
accomplishment ahead of schedule under budget of all these incredibly
ambitious goals. Or do we redefine the Human Genome Project in an ongoing
way allowing new and exciting scientific components to be defined that we
hadn't previously imagined that we could get to?
We haven't
completely decided but I think the majority view is we would do the
project a service by not redefining it every time it suits our purposes
but by saying, ``It's done. We did it. Hurray.''
Now we're
moving into a new phase where what we're now about is applying the genome
to health. And that is a natural follow-on, building on the foundation of
the Human Genome Project but with more explicit medical connections.
On how much
will still be unfinished:
The
definition of finishing all of the human DNA that can be reliably
sequenced in existing systems, that will be done. So the only things we
are not sequencing are the things that nobody knows how to. . .It's in the
neighborhood of 2 or 3 percent.
``Finished''
has a very vigorous definition, albeit it would not be the definition that
most people assume on the nature of the word. And maybe we need a better
word, like ``essentially finished'' or something like that.
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