News 14 april 2009
Increased symptoms lead mentally
disordered to become victims of violence
Contrary to common stereotypes, individuals
with major mental disorders are more likely to become victims of violent crimes when they
are experiencing an increase in symptoms than they are to commit crime, according to a new
study by Brent Teasdale, an assistant professor of criminal justice at Georgia State
University. Teasdale found that patients experiencing delusions, hallucinations and
worsening symptoms generally are most likely to become victims of violence. In addition,
individuals with mental disorders are particularly vulnerable for victimization during
times of homelessness and when suffering from alcohol abuse. "They actually have
higher rates of victimization than they have of violence commission, which I think is
counter to the stereotype that highly symptomatic, obviously delusional, visibly mentally
disordered people are dangerous, unpredictable and violent," Teasdale said.
"There's no one size fits all approach to these delusions, but the odds of
victimization are multiplied almost by a factor of two when a person experiences these
delusions." Teasdale analyzed data from the MacArthur Violence Risk Assessment
Study, a longitudinal study of psychiatric patients released from three psychiatric
hospitals in Pittsburgh, Pa., Kansas City, Mo., and Worchester, Mass. During the MacArthur
study, participants were interviewed every 10 weeks for one year about violence committed
against them, stress, symptoms and social relationships. When individuals with mental
disorders experience increases in delusions, symptom severity and alcohol problems they
may be more focused on their internal states and have fewer cognitive resources available
to devote to interactions with other people, Teasdale said. Other research suggests that
victimization happens because caretakers may be driven away, leaving the disordered
unprotected.
Biofuels Could Hasten Climate
Change
A new study finds that it will take more
than 75 years for the carbon emissions saved through the use of biofuels to compensate for
the carbon lost when biofuel plantations are established on forestlands. If the original
habitat was peatland, carbon balance would take more than 600 years. The study appears in
Conservation Biology. The oil palm, increasingly used as a source for biofuel, has
replaced soybean as the world’s most traded oilseed crop. Global production of palm
oil has increased exponentially over the past 40 years. In 2006, 85 percent of the global
palm-oil crop was produced in Indonesia and Malaysia, countries whose combined annual
tropical forest loss is around 20,000 square kilometers. Conversion of forest to oil palm
also results in significant impoverishment of both plant and animal communities. Other
tropical crops suitable for biofuel use, like soybean, sugar cane and jatropha, are all
likely to have similar impacts on climate and biodiversity.
Home Tooth Bleaching Slightly
Reduces Enamel Strength
New research shows that human teeth lost
some enamel hardness after the application of several different products used in the home
to whiten teeth. The study suggests that future generations of such products might be
reformulated in an effort to reduce these side effects. The researchers noted that teeth
typically can restore their previous hardness after losing small amounts of enamel
calcification. But this is the first study to show at a nanometer scale – measuring
in billionths of a meter – how human teeth are affected by the popular home
whiteners. “There is some significant reduction in nano-hardness of enamel, but we
are talking on a very minute scale. So even though it may not be visible to the human eye,
it’s important for research because that’s how we improve products,” said
Shereen Azer, assistant professor of restorative and prosthetic dentistry at Ohio State
University and lead author of the study.
Eat, drink and be merry?
Study says junk food makes kids fatter, but
happier. Fast food and soft drinks may be making children fatter but they also make them
happy. Programs aimed at tackling childhood obesity, by reducing children’s
consumption of unhealthy food and drink, are likely to be more effective if they also
actively seek to keep children happy in other ways, according to Professor Hung-Hao Chang
from National Taiwan University and Professor Rodolfo Nayga from the University of
Arkansas in the US. Their findings are published in Springer’s Journal of Happiness
Studies. Childhood obesity is a major public health issue worldwide. It is well accepted
that unhealthy eating patterns are partly responsible for the increase in childhood
obesity. However, very little is known about the relationship between fast food and soft
drink consumption and children’s happiness. For the first time, Chang and Nayga
looked at the relationship between unhealthy dietary habits and children’s
psychological health. In particular, they studied the effects of fast food and soft drink
consumption on children’s body weight and unhappiness. Using data from the National
Health Interview Survey in Taiwan - a nationwide survey carried out in 2001 – the
authors looked at the fast food and soft drink consumption, body weight and level of
happiness of 2,366 children aged between 2 and 12 years old. Fast food included French
fries, pizza and hamburgers; soft drinks included soda and other sugar-sweetened
beverages.
Signals from stroking have direct
route to brain
Nerve signals that tell the brain that we
are being slowly stroked on the skin have their own specialised nerve fibres in the skin.
This is shown by a new study from the Sahlgrenska Academy. The discovery may explain why
touching the skin can relieve pain. The specialised nerve fibres in the skin are called CT
nerves (C-tactile) and they travel directly to the areas in the brain that are important
in the emergence of feelings. ”Basically the signals that tell the brain that we are
being stroked on the skin have their own direct route to the brain, and are not blocked
even if the brain is receiving pain impulses from the same area. In fact it’s more
the opposite, that the stroking impulses are able to deaden the pain impulses,” says
Line Löken, postgraduate student in neurophysiology at the Sahlgrenska Academy. The
results are being published in the distinguished scientific journal, Nature Neuroscience.
The research group examined a group of healthy subjects using a technique called
microneurography. “By inserting a thin electrode into a nerve in the forearm we can
listen in on the nerve and pick up signals from one of the thousands of nerve fibres that
make up a nerve,” explains Associate Professor Håkan Olausson, who is leading the
research group behind the discovery, together with Johan Wessberg.
Colon cancer shuts down receptor
that could shut it down
Though a high-fiber diet has long been
considered good for you and beneficial in staving off colon cancer, Medical College of
Georgia researchers have discovered a reason why: roughage activates a receptor with
cancer-killing potential. Researchers report in the April issue of Cancer Research that
the GPR109A receptor is activated by butyrate, a metabolite produced by fiber-eating
bacteria in the colon. The receptor puts a double-whammy on cancer by sending signals that
trigger cell death, or apoptosis, and shutting down a protein that causes inflammation, a
precursor to cancer. "We know the receptor is silenced in cancer but it's not like
the gene goes away," says Dr. Vadivel Ganapathy, corresponding author and chair of
the Department of Biochemistry and Molecular Biology in the MCG School of Medicine. Cancer
shuts down the receptor by chemically modifying its gene through a process called DNA
methylation. It's a typical MO for cancer to turn genes off to suit its purpose which is
why DNA methylation inhibitors already are under study for a variety of cancers.
Aspirin and similar drugs may be
associated with brain microbleeds in older adults
Individuals who take aspirin or other
medications that prevent blood clotting by inhibiting the accumulation of platelets appear
more likely to have tiny, asymptomatic areas of bleeding in the brain, according to a
report posted online today that will appear in the June print issue of Archives of
Neurology, one of the JAMA/Archives journals. Cerebral microbleeds—small deposits of
the iron-storing protein hemosiderin in the brain—may be a sign of cerebral
small-vessel disease, according to background information in the article. This condition,
common among older adults, occurs when the walls of blood vessels in the brain become
weakened. When microbleeds occur in certain brain areas, they may indicate a type of small
vessel disease known as cerebral amyloid angiopathy, in which the accumulation of amyloid
(a protein often related to Alzheimer's disease) causes degeneration of smooth muscle
cells and increases the susceptibility of blood vessels to ruptures and hemorrhages. Meike
W. Vernooij, M.D., and colleagues at Erasmus MC University Medical Center, Rotterdam, the
Netherlands, investigated the relationship between cerebral microbleeds and the use of
anti-clotting medications in 1,062 individuals without dementia involved in the Rotterdam
Scan Study. Participants (average age 69.6) underwent magnetic resonance imaging
examinations in 2005 and 2006. Pharmacy records were used to assess whether any of the
individuals took anti-clotting drugs. These included aspirin and carbasalate
calcium—called platelet aggregation inhibitors because they prevent the accumulation
of platelets that form blood clots. In the years before MRI, 363 (34.2 percent) of the
participants had used any anti-clotting drugs, including 245 (23.1 percent) who took
platelet aggregation inhibitors (67 taking aspirin and 141 taking carbasalate calcium).
Compared with patients who did not use anti-clotting drugs, those who took aspirin or
carbasalate calcium were more likely to have cerebral microbleeds visible on MRI. This
association was particularly strong among individuals taking these drugs at higher doses,
typically used to treat or prevent heart disease. Microbleeds in the frontal lobe were
more common among aspirin users than carbasalate calcium users. There was no association
between other types of anti-clotting drugs and cerebral microbleeds. "There is
currently major interest in bleeding risks with the use of antithrombotic or thrombolytic
treatment in persons who have microbleeds that are apparent on MRI because this may affect
treatment in patients with cardiovascular or cerebrovascular disease," the authors
write. "The cross-sectional design of our analyses prohibited an investigation of
whether persons with cerebral microbleeds are at increased risk for symptomatic hemorrhage
[excessive bleeding] when using platelet aggregation inhibitors." The beneficial
effects of anti-clotting drugs for individuals at risk for heart attack and stroke
typically outweigh any risks of bleeding, they note. "Nevertheless, it may be that in
selected persons (e.g., those with signs of cerebral amyloid angiopathy), this
risk-benefit ratio may differ for certain drugs (e.g., aspirin), thus influencing
treatment decision," they conclude.
Use of Pancreatic Islets Show
Promise in Diabetes Research, Treatments
The use of pancreatic islets
(hormone-producing cells) is increasing in diabetes research and may play an important
role in future treatments, according to an article in the April 15 issue of JAMA, a theme
issue on diabetes. John S. Kaddis, B.S., of the City of Hope National Medical Center,
Duarte, Calif., presented the findings of the article at a JAMA media briefing at the
National Press Club in Washington, D.C. "The primary objective of islet-based
research is to cure diabetes. Perhaps the most prominent clinical application of this
research is currently in the form of cell replacement therapy. With the exception of 1
report in a type 2 diabetic cohort, islet transplantation has been used exclusively for a
subset of individuals with type 1 diabetes mellitus and was shown, at least temporarily,
to improve glucose control and, in a few cases, to lead to insulin independence,"
writes Mr. Kaddis and colleagues. With this procedure, pancreatic islets are transplanted
from a donated pancreas to a person with diabetes as a means of restoring beta-cell
function. The destruction of beta cells in the pancreas is the cause of type 1 diabetes.
"Although islet transplantation has been shown to offer both protection against
long-term complications of the disease and significant improvement in quality of life,
several obstacles remain, such as limited engraftment [acceptance of the islets within the
recipient], chronic immunosuppression, and inconsistent supply of human islets. These
issues must be addressed if the procedure is to be used as a standard of care for
qualified individuals," they write.
Omega-3 Fatty Acids May Benefit
Cancer Patients Undergoing Major Operations
New research from Trinity College Dublin
published in this month’s Annals of Surgery points to a potentially significant
advance in the treatment of patients undergoing major cancer surgery. The study was
carried out by the oesophageal research group at Trinity College Dublin and St
James’s Hospital. A randomised controlled trial showed omega-3 fatty acids given as
part of an oral nutritional supplement resulted in the preservation of muscle mass in
patients undergoing surgery for oesopahageal cancer, a procedure normally associated with
significant weight loss and quality of life issues. The trial was designed by Professor
John V Reynolds, Professor of Surgery at Trinity College Dublin and St James’s
Hospital, Dublin, and Dr Aoife Ryan PhD, a research dietitian at St James’s Hospital,
Dublin*. Omega 3 fats are essential fats found naturally in oily fish, with highest
concentrations in salmon, herring, mackerel, and sardines. Recently food manufacturers
have begun to add omega 3 to foods such as yogurt, milk, juice, eggs and infant formula in
light of a body of scientific evidence which suggests that they reduce cardiovascular
disease risk, blood pressure, clot formations, and certain types of fat in the blood.
Study Reports Success in Treating a
Rare Retinal Disorder
Patients with a rare, blinding eye disease
saw their vision improve after treatment with drugs to suppress their immune systems,
according to researchers at the University of Michigan Kellogg Eye Center. Because
autoimmune retinopathy (AIR) is difficult to diagnose, the biggest challenge now is to
find biologic markers that identify patients who can benefit from treatment. In a review
of 30 patients with autoimmune retinopathy, 21 individuals showed improvement after
receiving treatment with immunosuppression therapy. The study, reported in the April issue
of Archives of Ophthalmology, is the largest review of AIR cases to date. Improvement was
defined by several measures, including the ability to read a minimum of two additional
lines on the standard eye chart or expansion of at least 25% in visual field size.
Reversing effects of altered enzyme
may fight brain tumor growth
An international team of scientists from
the Moores Cancer Center at the University of California, San Diego, the University of
North Carolina and several institutions in China have explained how a gene alteration can
lead to the development of a type of brain cancer, and they have identified a compound
that could staunch the cancer's growth. The researchers, led by Kun-Liang Guan, PhD,
professor of pharmacology at the UC San Diego School of Medicine, have shown that when a
mutated enzyme fails to do its job, the development of tumor-feeding blood vessels
increases, allowing more nutrients and oxygen to fuel cancer growth. They have also shown
in the laboratory that they could reverse the mutant enzyme's effects, effectively
blocking this process, called angiogenesis, and provide a potential future treatment
strategy against some types of brain tumors. They reported their findings in the current
issue of the journal Science. According to Guan, researchers have known that a mutation in
the gene encoding the enzyme, isocitrate dehydrogenase (IDH1), contributed to certain
brain tumors called low grade gliomas and secondary glioblastomas, but no one understood
how. Guan, Yue Xiong, PhD, at the University of North Carolina and their co-investigators
have now shown that this is because alterations in a specific gene, IDH1, impairs the
body's ability to keep a tumor growth-promoting protein, HIF-1 alpha, in check. The IDH1
enzyme works to produce a compound called alpha-KG, which is required for HIF-1 breakdown.
Without that control, HIF-1 can run amok, promoting angiogenesis and tumor growth. The
team was able to reverse this HIF-1 alpha effect by adding a modified form of alpha-KG to
brain tumor cells in culture. "This suggests a direction to exploit cell permeable
alpha-KG for potential treatment of brain cancer patients with an IDH1 mutation,"
Guan said.
University of Toronto chemists
uncover green catalysts
A University of Toronto research team from
the Department of Chemistry has discovered useful "green" catalysts made from
iron that might replace the much more expensive and toxic platinum metals typically used
in industrial chemical processes to produce drugs, fragrances and flavours. The synthesis
of drugs usually relies on the use of catalysts and the expense of the catalysts
influences the ultimate cost of the drug. If the catalyst is toxic, as it usually is when
platinum-metals such as ruthenium, rhodium and palladium are used, then it must be removed
completely from the synthesized product using costly purification techniques. "With a
cheaper and less toxic catalyst, like iron, these drawbacks are avoided," says
Professor Robert Morris. The study appeared online in Chemistry - A European Journal on
April 9. The successful use of iron as a catalyst in place of the more commonly used
ruthenium is surprising since iron has been considered to be a "base metal" of
low catalytic activity. The successful trick was to prepare a complex of iron with a
structure similar to the most active ruthenium catalyst, says Morris. Chemical catalysts
are generally known for their ability to speed up a reaction but they can also influence
the structure of the chemical that is produced in that reaction, says Morris. Catalysts
used in the synthesis of a chemical used as a drug or fragrance are most valuable when
they cause the production of the chemical in one structural form and not the mirror image
of that form (i.e. producing a left-handed form and not the right-handed one).
Poor nutrition in the womb causes
permanent genetic changes in the offspring
The new science of epigenetics explains how
genes can be modified by the environment, and a prime result of epigenetic inquiry has
just been published online in The FASEB Journal (http://www.fasebj.org): You are what your
mother did not eat during pregnancy. In the research report, scientists from the
University of Utah show that rat fetuses receiving poor nutrition in the womb become
genetically primed to be born into an environment lacking proper nutrition. As a result of
this genetic adaptation, the rats were likely to grow to smaller sizes than their normal
counterparts. At the same time, they were also at higher risk for a host of health
problems throughout their lives, such as diabetes, growth retardation, cardiovascular
disease, obesity, and neurodevelopmental delays, among others. Although the study involved
rats, the genes and cellular mechanisms involved are the same as those in humans.
"Our study emphasizes that maternal–fetal health influences multiple healthcare
issues across generations," said Robert Lane, professor of pediatric neonatology at
the University of Utah, and one of the senior researchers involved in the study. "To
reduce adult diseases such as diabetes, obesity, and cardiovascular disease, we need to
understand how the maternal–fetal environment influences the health of
offspring." The scientists made this discovery through experiments involving two
groups of rats. The first group was normal. The second group had the delivery of nutrients
from their mothers' placentas restricted in a way that is equivalent to preeclampsia. The
rats were examined right after birth and again at 21 days (21 days is essentially a
preadolescent rat) to measure the amount of a protein, called IGF-1, that promotes normal
development and growth in rats and humans. They found that the lack of nutrients caused
the gene responsible for IGF-1 to significantly reduce the amount of IGF-1 produced in the
body before and after birth.
Many clinicians unaware of
federally funded research on alternative therapies
Approximately one in four practicing
clinicians appear to be aware of two major federally funded clinical trials of alternative
therapies, and many do not express confidence in their ability to interpret research
results, according to a report in the April 13 issue of Archives of Internal Medicine, one
of the JAMA/Archives journals. Complementary and alternative (CAM) therapies are widely
used, but until recently few rigorous studies of their safety and effectiveness have been
conducted, according to background information in the article. The National Institutes of
Health (NIH) has invested more than $2 billion into this type of scientific research in
the past decade. "For this investment to achieve its anticipated social value,
clinical research must be translated into improvements in clinical and public health
practice—a process fraught with obstacles," the authors write. "For
evidence from clinical research to have an impact on medical practice, health care
professionals must first be aware of the research. Once aware, health care professionals
must be able to interpret these findings, judging both their validity and their
implications. Finally, they must apply the scientific evidence to their own
practices," they continue. To assess this translation process surrounding CAM
research, Jon C. Tilburt, M.D., M.P.H., of the NIH, Bethesda, Md., and Mayo Clinic,
Rochester, Minn., and colleagues surveyed 2,400 practicing acupuncturists, naturopaths,
internists and rheumatologists about their awareness of and attitudes toward CAM research.
A total of 1,561 clinicians (65 percent) completed the survey. Of those, 59 percent were
aware of at least one of two major clinical trials recently published on CAM therapies for
osteoarthritis of the knee (on assessing acupuncture and the other about the supplement
glucosamine); only 23 percent were aware of both trials. Acupuncturists (46 percent) and
rheumatologists (49 percent) were more likely to be aware of the acupuncture study than
naturopaths (30 percent) and general internists (22 percent), whereas for the glucosamine
trial, internists (59 percent) and rheumatologists (88 percent) were more aware than
acupuncturists (20 percent) and naturopaths (39 percent). A minority of clinicians in all
groups said they were "very confident" in their ability to critically interpret
research literature (20 percent of acupuncturists, 25 percent of naturopaths, 17 percent
of internists and 33 percent of rheumatologists); more described themselves as
"moderately confident" (59 percent of acupuncturists, 64 percent of naturopaths,
67 percent of internists and 59 percent of rheumatologists) "Compared with those who
were not aware of CAM trials, clinicians who were aware of CAM trials were much more
likely to be rheumatologists, to be practicing in an institutional or academic setting, to
have some research experience, to express greater ability to interpret evidence and to
report greater acceptance of evidence," the authors write. The results suggest that
the translation of CAM trial results into clinical practice may vary widely based on the
training, attitudes and experiences of the clinicians who might apply them, they continue.
"For clinical research in CAM (and conventional medicine) to achieve its potential
social value, concerted efforts must be undertaken that more deliberately train clinicians
in critical appraisal, biostatistics and use of evidence-based resources, as well as
expanded research opportunities, dedicated training experiences and improved dissemination
of research results," the authors conclude.
Researchers identify how PCBs may
alter in utero, neonatal brain development
In three new studies — including one
appearing online today in the Public Library of Science - Biology (PLoS - Biology) —
UC Davis researchers provide compelling evidence of how low levels of polychlorinated
biphenyls (PCBs) alter the way brain cells develop. The findings could explain at last
— some 30 years after the toxic chemicals were banned in the United States — the
associations between exposure of the developing nervous system to PCBs and behavioral
deficits in children. "We've never really understood the mechanism by which PCBs
produce neurobehavioral problems in children," said Isaac N. Pessah, professor of
molecular biosciences, director of the UC Davis Center for Children's Environmental Health
and co-author of all three studies. "With these studies we have now shown — from
the whole animal level to the molecular level — how PCBs alter the development and
excitability of brain cells. And that could explain why PCBs are associated with higher
rates of neurodevelopmental and behavioral disorders," said Pessah, who is also a
researcher with the UC Davis M.I.N.D. Institute. Together, the studies — published
within one month of each other — make a compelling case for the mechanism behind
PCBs' harmful effects on human neurological development.
New alternative to biopsy detects
subtle changes in cancer cells, Stanford study shows
A drop of blood or a chunk of tissue
smaller than the period at the end of this sentence may one day be all that is necessary
to diagnose cancers and assess their response to treatment, say researchers at the
Stanford University School of Medicine. In a study to be published April 12 in the online
version of Nature Medicine, the scientists used a specialized machine capable of analyzing
whether individual cancer-associated proteins were present in the tiny samples and even
whether modifications of the proteins varied in response to cancer treatments. Although
the study focuses on blood cancers, the hope is that the technique might also provide a
faster, less invasive way to track solid tumors. "Currently we don't know what's
going on in a patient's actual tumor cells when a treatment is given," said
oncologist Alice Fan, MD, a clinical instructor in the division of oncology at the medical
school. "The standard way we measure if a treatment is working is to wait several
weeks to see if the tumor mass shrinks. It would really be a leap forward if we could
detect what is happening at a cellular level." Fan, the lead author of the study,
performed the research in the laboratory of senior author Dean Felsher, MD, PhD, associate
professor of medicine and of pathology and the leader of the Stanford Molecular
Therapeutics Program. "This technology allows us to analyze cancer-associated
proteins on a very small scale," said Felsher, a member of Stanford's Cancer Center,
who studies how cancer genes called oncogenes initiate and influence tumor progression in
many types of cancers. "Not only can we detect picogram levels — one-trillionth
of a gram — of protein, but we can also see very subtle changes in the ways the
protein is modified." Variations in the way a protein is modified, or phosphorylated,
can affect how it functions in tumor progression. Cancer cells often evade common
therapies by rejiggering their levels of protein expression and degrees of
phosphorylation. Analyzing repeated small samples from a tumor undergoing treatment may
allow doctors to head off rogue cells at the pass before they have a chance to proliferate
into a more resistant tumor or to identify patients likely to fail standard approaches to
treatment. Fan and Felsher collaborated with researchers from Palo Alto-based Cell
Biosciences, which makes the machine used in this study, to separate cancer-associated
proteins in narrow capillary tubes based on their charge, which varies according to
modifications on the proteins' surface. Two versions of the same protein — one
phosphorylated and one not — can be easily distinguished because they travel
different distances in the tube. The researchers then used antibodies to identify the
relative amounts and positions of the various proteins.
Mount Sinai researchers discover
novel mechanisms that might causally link type 2 diabetes to Alzheimer's disease
A recent study by Mount Sinai faculty
suggests that a gene associated with onset of type-2 diabetes also decreases in
Alzheimer's disease dementia cases. The research, led by Dr. Giulio Maria Pasinetti, MD,
Ph.D., The Aidekman Family Professor in Neurology, and Professor of Psychiatry and
Geriatrics and Adult Development at Mount Sinai School of Medicine, was published this
week in the scientific journal, Archives of Neurology. "This new evidence is of
extreme interest," Dr. Pasinetti tells us, "especially because of the evidence
that approximately 60% of Alzheimer's disease dementia cases have at least one serious
medical condition primarily associated with type-2 diabetes, a chronic condition which
includes high blood glucose content (hyperglycemia) and reduced sensitivity to insulin,
among other conditions." "The relationship between type-2 diabetes and
Alzheimer's disease is elusive," says Dr. Pasinetti. Not all subjects with type-2
diabetes are affected by Alzheimer's disease, and similarly, not all Alzheimer's disease
cases are diabetic. However, in the last few years, epidemiological evidence indicates
that, relative to healthy elderly subjects, people of the same age affected by type-2
diabetes are twice as likely to develop Alzheimer's disease dementia. The reason is not
known. The new study from Dr. Pasinetti, reported in this week's issue of Archives of
Neurology, provides insight into a potential mechanism that might explain the relationship
between type-2 diabetes and Alzheimer's disease onset and progression. Dr. Pasinetti and
colleagues found that a gene known as proliferator-activated receptor coactivator 1 -
(PGC-1 ), a key regulator of glucose content currently investigated as a potential
therapeutic target for type-2 diabetes, is also decreased in Alzheimer' disease dementia
cases. Most importantly, Dr. Pasinetti reports that PGC-1 decreased in Alzheimer' disease
dementia cases with progression of the clinical disease and positively correlates with
brain accumulation of ?-amyloid, an abnormal protein highly linked to Alzheimer' disease
dementia and brain degeneration. This evidence is of high interest to the field and
suggests, for the first time, a strong relationship between decreased content of a gene
responsible for type-2 diabetes in Alzheimer's disease dementia cases, says Dr. Pasinetti.
