News 3 april 2009
Childhood Asthma and Exposures at
Swimming Pools
Current evidence of an association between
childhood swimming and new-onset asthma is suggestive but not conclusive. Important data
gaps need to be filled, particularly in exposure assessment and characterization of asthma
in the very young. Participants recommended that additional evaluations using a
multidisciplinary approach are needed to determine whether a clear association exists.
Dioxin-like Compounds and Metabolic
Syndrome
Environmental exposure to some persistent
organic pollutants has been associated with metabolic syndrome in the United States.
Uemura et al. (p. 568) conducted a cross-sectional study during 2002–2006 to evaluate
associations between metabolic syndrome and body burden levels of dioxins and related
compounds in Japan. They measured lipid-adjusted concentrations of 10 polychlorinated
dibenzo-p-dioxins, 7 polychlorinated dibenzofurans, and 12 dioxin-like polychlorinated
biphenyls in fasting blood samples. Metabolic syndrome was assessed based on body mass
index, high-density lipoprotein cholesterol, triglyceride, and hemoglobin A1c
measurements, and measured or self-reported hypertension. The authors report that body
burden levels of dioxins and related compounds were associated with metabolic syndrome,
with high blood pressure, elevated triglycerides, and glucose intolerance most closely
associated with these pollutants.
Lead Exposure and Cognition in
Older Women
Chronic low-level exposure to lead has been
associated with accelerated declines in cognition in older age, but few studies have
included women, and none have reported results for women specifically. Weuve et al. (p.
574) examined tibia, patella, and blood lead levels in relation to performance on a
battery of cognitive tests among 587 women 47–74 years of age. Levels of all three
lead biomarkers were associated with worse cognitive performance for all tests combined,
with stronger associations estimated for tibia bone lead, a measure of cumulative exposure
over many years. Results suggest that a one-standard-deviation increase in tibia lead was
associated with a reduction in cognitive scores, which was similar to that associated with
a 3-year increase in age. The authors conclude that cumulative exposure to lead, even at
low levels experienced in community settings, may have adverse consequences for
women’s cognition in older age.
Exposure to BPA among Premature
Infants in NICUs
Premature infants in neonatal intesive care
units (NICUs) may be exposed to di(2-ethylhexyl) phthalate (DEHP), bisphenol A (BPA), and
other phenols in medical products, but data on potential exposures are limited. Calafat et
al. (p. 639) measured urinary levels of BPA, triclosan, benzophenone-3, methyl paraben,
and propyl paraben in 42 low-birth-weight infants from two NICUs in the Boston,
Massachusetts, area. They found that the geometric mean urinary concentration (30.3 µg/L)
of BPA among the study subjects was one order of magnitude higher than estimates for the
general population, and that intensity of DEHP-containing product use was associated with
total BPA concentration but not concentrations of any of the other phenols measured.
Conjugated species were the primary urinary metabolites of BPA, suggesting that premature
infants have some capacity to metabolize BPA. In addition, urinary BPA concentrations
differed substantially between the two institutions. The authors conclude that further
studies are needed to determine specific source(s) of exposure to BPA among premature
infants in NICUs.
Perfluorinated Chemicals and Fetal
Growth
Perfluorooctane sulfonate (PFOS) and
perfluorooctanoate (PFOA) are ubiquitous and persistent man-made contaminants in the
environment, wildlife, and humans. These chemicals have been reported to interfere with
fetal growth in humans, but results have been inconsistent. Washino et al. (p. 660)
conducted a hospital-based prospective cohort study to investigate the association between
relatively low levels of PFOS and PFOA in maternal serum and birth weight and birth size
among 428 women and infants in Sapporo, Japan. Characteristics of the mothers and infants
were obtained from self-administered questionnaires and medical records. The authors
report that in utero exposure to relatively low levels of PFOS was negatively correlated
with birth weight in the study population.
Air Pollution and Lung Injury in
Asthmatic Children
Air pollution has been associated with
adverse respiratory outcomes, but the influence of air pollution on lung injury is
unclear, in part because of a lack of appropriate noninvasive biomarkers of lung
inflammation. Liu et al. (p. 668) measured fractional exhaled nitric oxide (FeNO),
thiobarbituric acid reactive substances (TBARS), 8-isoprostane, and interleukin-6 in the
breath condensate of 182 asthmatic children to investigate acute effects of air pollution
on these markers of airway oxidative stress and inflammation. Interquartile-range
increases in 3-day average ambient sulfur dioxide (5.4 ppb), nitrogen dioxide (6.8 ppb),
and PM2.5 (particulate matter < 2.5 µm in aerodynamic diameter; 5.4 µg/m3) were
associated with increases in TBARS and decreases in pulmonary function, with stronger
associations estimated for children not taking corticosteroids. Results were consistent
with an increase in airway oxidative stress and a decrease in small airway function in
response to air pollution among asthmatic children. The authors conclude that TBARS in
breath condensate may be a useful tool to investigate air pollution-related oxidative
stress.
4 Promising Autism Treatments, From
Vitamin B12 to Alzheimer’s Drug Namenda
MIND researchers recently tested injections
of methyl B12 in a controlled trial on 30 children, since prior recent findings had shown
that some children with autism have altered biomarkers for oxidative stress. The results
weren’t statistically significant, but Hendren says nine of the children did improve
in language and socialization, and those children had changes in biomarkers for oxidative
stress. The institute will run a larger trial this summer with 50 children in an effort to
figure out if the treatment really does have a benefit.
Beverage Consumption a Bigger
Factor in Weight
When it comes to weight loss, what you
drink may be more important than what you eat, according to researchers at the Johns
Hopkins Bloomberg School of Public Health. Researchers examined the relationship between
beverage consumption among adults and weight change and found that weight loss was
positively associated with a reduction in liquid calorie consumption and liquid calorie
intake had a stronger impact on weight than solid calorie intake. The results are
published in the April 1, 2009, issue of the American Journal of Clinical Nutrition.
“Both liquid and solid calories were associated with weight change, however, only a
reduction in liquid calorie intake was shown to significantly affect weight loss during
the 6-month follow up,” said Benjamin Caballero MD, PhD, senior author of the study
and a professor with the Bloomberg School’s Department of International Health.
“A reduction in liquid calorie intake was associated with a weight loss of 0.25 kg at
6 months and 0.24 kg at 18 months. Among sugar-sweetened beverages, a reduction of 1
serving was associated with a weight loss of 0.5 kg at 6 months and 0.7 kg at 18 months.
Of the seven types of beverages examined, sugar-sweetened beverages were the only
beverages significantly associated with weight change.” Researchers conducted a
prospective study of 810 adults aged 25-79 years old participating in the PREMIER trial,
an 18-month randomized, controlled, behavioral intervention. Caballero along with
colleagues from the Johns Hopkins School of Medicine; the National Heart, Lung, and Blood
institute; Duke University; the Pennington Biomedical Research Center; the Kaiser
Permanente Center for Health Research; the University of Alabama; and Pennsylvania State
University measured participant’s weight and height using a calibrated scale and a
wall-mounted stadiometer at both 6 and 18 months. Dietary intake was measured by
conducting unannounced 24-hour dietary recall interviews by telephone. Researchers divided
beverages into several categories based on calorie content and nutritional composition:
sugar-sweetened beverages (regular soft drinks, fruit drinks, fruit punch, or high-calorie
beverages sweetened with sugar), diet drinks (diet soda and other “diet” drinks
sweetened with artificial sweeteners), milk (whole milk, 2 percent reduced-fat milk, 1
percent low-fat milk, and skim milk), 100 percent juice (100 percent fruit and vegetable
juice), coffee and tea with sugar, coffee and tea without sugar and alcoholic beverages.
They found that at 37 percent sugar-sweetened beverages were the leading source of liquid
calories.
New storage system design brings
hydrogen cars closer to reality
Researchers have developed a critical part
of a hydrogen storage system for cars that makes it possible to fill up a vehicle's fuel
tank within five minutes with enough hydrogen to drive 300 miles. The system uses a fine
powder called metal hydride to absorb hydrogen gas. The researchers have created the
system's heat exchanger, which circulates coolant through tubes and uses fins to remove
heat generated as the hydrogen is absorbed by the powder. The heat exchanger is critical
because the system stops absorbing hydrogen effectively if it overheats, said Issam
Mudawar, a professor of mechanical engineering who is leading the research.
Researchers reveal how the brain
processes important information
Researchers at UT Southwestern Medical
Center have shed light on how the neurotransmitter dopamine helps brain cells process
important information.
Researchers found in a study of mouse cells that this neurotransmitter, one of the
molecules used by nerve cells to communicate with one another, causes certain brain cells
to become more flexible and changes brain-cell circuitry to process important information
differently than mundane information. “This can help one remember a new, important
episode as distinct from any other episode, such as remembering where you parked your car
today versus yesterday,” said Dr. Robert Greene, professor of psychiatry at UT
Southwestern and senior author of the study published in the March 11 issue of the Journal
of Neuroscience.“If we can one day manipulate the way that salient information is
processed, we might be able to not only improve learning, but also improve the learning
needed to extinguish severe fear responsiveness, such as when a soldier can’t forget
emotional war memories associated with post-traumatic stress disorder,” he said.Dr.
Greene said the research also could have implications for addictions and schizophrenia,
because those conditions are associated with alterations in dopamine in the brain.
Researchers have known that dopamine is released in the brain in association with
experiencing “important” events and remembering salient acts, such as learning
to avoid a hot stove or that a good grade is rewarded. The current research focused on how
dopamine operates on the cells associated with this type of memory formation.
Intestinal cancer in spite of
screening
Only every second patient with colorectal
carcinoma had taken part in an early detection program within the last ten years. This is
the result, at least for a group of 212 colorectal cancer patients whose screening
behavior is examined in the current edition of Deutsches Ärzteblatt International (Dtsch
Arztebl Int 2009; 106[12]: 195 ) by Konrad Schoppmeyer and his colleagues from Leipzig
University Hospital. The authors have performed a retrospective analysis of the data
on screening examinations for the ten years before the diagnosis of colorectal cancer. In
83% of patients, the colorectal carcinoma was discovered after symptoms had developed. In
17% of patients, the diagnosis was made during screening. In the 10 years before the
diagnosis, 51% of the colorectal cancer patients had used screening tests for early
recognition. The most frequent of these was the test for fecal occult blood—although
this was mostly not in accordance with the guidelines. 25 patients had undergone
colonoscopy, 20 of these within the five years before diagnosis. The most frequent reason
that screening tests were not used was that patients were unaware of what was available.
Schoppmeyer et al. therefore advocate that doctors should provide their patients with more
detailed advice. Moreover, procedures should be in accordance with the guidelines.
Can periodontal disease act as a
risk factor for HIV-1?
Today, during the 87th General Session of
the International Association for Dental Research, convening at the Miami Beach Convention
Center, a group of scientists from Nihon University (Tokyo, Japan) will present findings
suggesting that periodontal disease could act as a risk factor for reactivating latent
HIV-1 in affected individuals. Latently infected cells harbor HIV-1 proviral DNA genomes
integrated with heterochromatins, allowing for the persistence of transcriptionally silent
proviruses. Hypoacetylation of histone proteins by histone deacetylases (HDACs) is
primarily involved in the maintenance of HIV-1 latency by repressing transcription from
HIV-1 provirus. On the other hand, periodontal diseases, caused by infection with the
bacterium Porphyromonas gingivalis (P. gingivalis), are found worldwide and are among the
most prevalent microbial diseases of mankind. The investigators demonstrated the effects
of such periodontopathic bacteria on HIV-1 replication. They found that P. gingivalis
could strongly facilitate HIV-1 reactivation via chromatin modification. The bacteria
produced high concentrations of butyric acid, a potent inhibitor of HDACs, and induced
acetylation of histones, leading to reactivation of HIV-1 in latently infected cells.
These results suggest that periodontal disease could act as a risk-factor for HIV-1
reactivation in latently infected individuals, and might contribute to the systemic
dissemination of the virus causing clinical progression of acquired immunodeficiency
syndrome (AIDS). The findings emphasize the essential role of maintaining oral hygiene and
controlling oral diseases for the prevention of AIDS.
Pregnancy and tobacco a 'smoking
gun' for baby
Monash University researchers have shown
that babies born to a mother who smokes are more likely to be slower to wake or respond to
stimulation – and this may explain their increased risk of Sudden Infant Death
Syndrome (SIDS). Scientific director of the Ritchie Centre for Baby Health Research
Associate Professor Rosemary Horne and PhD student Heidi Richardson compared babies of
mothers who smoked both during the pregnancy and after the baby was born, with babies who
lived in a smoke-free environment. Professor Horne said the study suggested that maternal
smoking can impair a baby's ability to respond to external stimuli, which may explain
their increased risk of SIDS. "Those babies whose mothers smoked did not have as many
arousals overall and the progression of the arousal response through the brain was also
impaired. Mothers who smoked while pregnant and continued to smoke afterward significantly
increased their baby's chances of succumbing to SIDS," Professor Horne said.
Although the exact cause of SIDS is unknown, research suggests that an impairment of the
arousal process from sleep in response to a life-threatening situation is involved.
Autopsies of SIDS victims have revealed brainstem abnormalities in key areas that are
required for arousal and cardio respiratory control. The study involved 12 healthy,
full-term infants born to mothers who smoked an average of 15 cigarettes per day. Their
arousal responses during daytime sleep were monitored and compared with that of healthy
infants who were born to non-smoking mothers. The study was performed on each child on
three occasions: at two to four weeks, two to three months and five to six months.
Arousals were induced without compromising the infants' natural sleep cycles by delivering
a pulsatile air-jet for five seconds at the infants' nostrils through a hand-held cannula.
Naturally fluorescent molecules may
serve as cancer biomarker
Excess amounts of a naturally fluorescent
molecule found in all living cells could serve as a natural biomarker for cancer,
according to bioengineers. NADH, or nicotinamide adenine dinucleotide, is a key coenzyme
-- a non-protein molecule necessary for the functioning of an enzyme -- found mostly in
the inner membrane of a cell's power plant, or mitochondria. It fuels a series of
biochemical reactions that involve various enzymes to produce ATP, the major energy source
in cells. In the event of disease or a metabolic disorder, these enzymes and their related
reactions can become disabled, causing a buildup of unused NADH. "Dysfunctional
enzymes in the mitochondria are known to be associated with serious health problems such
as cancer and neurodegenerative diseases," said Ahmed Heikal, associate professor of
bioengineering, Penn State. "By detecting the level of NADH and its distribution
inside living cells, we should be able to monitor the mitochondrial activity and thus the
integrity of any given cell, without adding potentially toxic dyes or actually destroying
the cell." According to Heikal, one of the main challenges in cancer diagnosis is the
ability to differentiate cancer cells from normal ones at the early stages of tumor
progression. To tease apart the critical difference between normal and cancerous cells,
the researchers used the fluorescence of natural NADH. Using a combination of
state-of-the-art spectroscopy and microscopy techniques, the researchers were able to
convert such fluorescence into an accurate measure of NADH concentration in live cells.
Heikal and Yu, graduate student, bioengineering, have found that the average concentration
of NADH in breast cancer cells is about twice that in normal breast cells.
JHU researcher discovers brain
cells have 'memory'
As we look at the world around us, images
flicker into our brains like so many disparate pixels on a computer screen that change
every time our eyes move, which is several times a second. Yet we don't perceive the world
as a constantly flashing computer display. Why not? Neuroscientists at The Johns Hopkins
University think that part of the answer lies in a special region of the brain's visual
cortex which is in charge of distinguishing between background and foreground images.
Writing in a recent issue of the journal Neuron, the team demonstrates that nerve cells in
this region (called V2) are able to "grab onto" figure-ground information from
visual images for several seconds, even after the images themselves are removed from our
sight. "Recent studies have hotly debated whether the visual system uses a buffer to
store image information and if so, the duration of that storage," said Rudiger von
der Heydt, a professor in Johns Hopkins' Zanvyl Krieger Mind-Brain Institute, and
co-author on the paper. "We found that the answer is 'yes,' the brain in fact stores
the last image seen for up to two seconds."
The image that the brain grabs and holds onto momentarily is not detailed; it's more like
a rough sketch of the layout of objects in the scene, von der Heydt explains. This may
elucidate, at least in part, how the brain creates for us a stable visual world when the
information coming in through our eyes changes at a rapid-fire pace: up to four times in a
single second. The study was based on recordings of activity in nerve cells in the V2
region of the brains of macaques, whose visual systems closely resemble that of humans.
Located at the very back of the brain, V2 is roughly the size of a wristwatch strap.
Lead in the blood increases women's
mortality
Lead concentrations in the blood are
associated with an increased risk of death from coronary heart diseases (CHD). A study of
533 American women, published in BioMed Central's open access journal Environmental
Health, has shown that those with blood lead concentrations above 8?g/dL were three times
more likely to die of CHD.
Naila Khalil worked with a team of researchers from the University of Pittsburgh and the
University of Maryland to study the effects of lead on the mortality of a group of 65-87
year old women who had joined an earlier study between 1986 and 1988. These women have
been followed ever since and their causes of death recorded. Khalil said, "Despite
population-wide declines in blood lead concentrations during the past 30 years,
environmental lead exposure continues to be a public health concern. Lead is a toxic
metal, and our results add to the existing evidence of adverse affects of lead on health
as seen in an older cohort who experienced greater historic environmental lead
exposure".
The average population blood lead concentration in the most recent US National Health and
Nutrition Examination Survey (2001-2002) had declined to 1.45?g/dL. The women studied in
Dr. Khalil's research, however, were alive while lead was still used in paints, water
systems and as a gasoline additive. They had an average blood concentration of 5.3?g/dL,
with some women showing levels as high as 21?g/dL. According to Khalil, "Women with a
blood lead concentration above 8?g/dL had a 73% increased risk of dying. In particular,
blood lead was associated with almost three-fold risk in CHD mortality". This study
shows that environmental toxicants, such as lead, may account for some of the burden of
cardiovascular disease, which is the leading cause of mortality worldwide. It kills nearly
half a million women in the United States every year, more than the next five causes of
death combined and nearly twice as many as all forms of cancer, including breast cancer.
The authors conclude, "While the damage may already have been done for some older
people, it is important that we recognize the harm that environmental exposure to lead can
cause. We must remain vigilant and ensure that lead pollution is minimized for the sake of
future generations' health".
Alzheimer's disease linked to
mitochondrial damage
Investigators at Burnham Institute for
Medical Research (Burnham) have demonstrated that attacks on the mitochondrial protein
Drp1 by the free radical nitric oxide—which causes a chemical reaction called
S-nitrosylation—mediates neurodegeneration associated with Alzheimer's disease. Prior
to this study, the mechanism by which beta-amyloid protein caused synaptic damage to
neurons in Alzheimer's disease was unknown. These findings suggest that preventing
S-nitrosylation of Drp1 may reduce or even prevent neurodegeneration in Alzheimer's
patients. The paper was published in the April 3 issue of the journal Science. The team of
scientists, led by neuroscientist and clinical neurologist Stuart A. Lipton, M.D., Ph.D.,
director of the Del E. Webb Center for Neuroscience, Aging and Stem Cell Research, showed
that S-nitrosylated Drp1 (SNO-Drp1) facilitates mitochondrial fragmentation, damaging
regions of nerve cell communication called synapses. Mitochondria are the energy
storehouses of the cell, and their compromise by excessive fragmentation causes synaptic
injury and eventual nerve cell death. Synapses are critical for learning and memory and
their impairment leads to the dementia seen in Alzheimer's patients. "We now have a
better understanding of the mechanism by which beta-amyloid protein causes
neurodegeneration in Alzheimer's disease," said Dr. Lipton. "We found that
beta-amyloid can generate nitric oxide that reacts with Drp1. By identifying Drp1 as the
protein responsible for synaptic injury, we now have a new target for developing drugs
that may slow or stop the progression of Alzheimer's." Drp1 is an enzyme that
mediates fission or fragmentation of mitochondria. The Burnham researchers showed that
excessive production of nitric oxide caused S-nitrosylation of Drp1 and induced excessive
fragmentation of mitochondria in cultured nerve cells or neurons. The scientists also
showed that beta-amyloid protein multimers, which had been previously implicated in
Alzheimer's disease, induced formation of SNO-Drp1. Importantly, elevated SNO-Drp1 levels
were also found in human brains of Alzheimer's patients, but not in those with Parkinson's
disease or controls who didn't have neurodegenerative diseases.
Molecular modeling performed by the team suggested that S-nitrosylation of Drp1 causes
dimerization of the protein and activation of enzymatic activity that induces
mitochondrial fragmentation. To confirm this hypothesis, the scientists showed that RNA
interference to knock down Drp1 or a mutation that prevented Drp1 activity inhibited
excess mitochondrial fragmentation and protected the neurons. Finally, the researchers
showed that a mutated Drp1, lacking the nitrosylation site, did not induce mitochondrial
fragmentation and also prevented neuronal damage. Taken together, these findings suggest
that multimers of beta-amyloid protein induce generation of nitric oxide, which reacts
with Drp1 to cause excessive mitochondrial fragmentation and in turn neuronal damage.
Protein protects neurons in brain
from damage due to inflammation
A research team from the University of
California, San Diego School of Medicine and the Salk Institute for Biological Studies in
La Jolla has identified a protein in the brain of mice that protects neurons from
excessive inflammation, which can lead to neurodegenerative disorders such as Parkinson's
disease. Their study, which identifies the protective function of a protein called Nurr1
and defines the pathway by which it works, will be published in the April 3 edition of the
journal Cell. Nurr1 is a transcription factor that has been known for some time to play an
essential role in the generation and maintenance of dopaminergic neurons in the brain.
Rare mutations in Nurr1 are associated with familial Parkinson's disease, and the loss of
dopaminergic neurons – which are the main source of dopamine in the central nervous
system – is associated with the disease. Dopamine helps control multiple brain
functions such as movement, attention, pleasure, emotion and motivation. The new findings
have uncovered a second and previously unexpected role of the Nurr1 protein in two other
cell types in the brain – microglia and astrocytes. The brain's microglia are
macrophage-like cells that are active components of the immune defense in the central
nervous system, while astrocytes are large star-shaped cells that normally play important
support functions in the brain. Working in mice, researchers in the Laboratory of Genetics
headed by Fred H. Gage, PhD, professor at the Salk Institute, reduced the expression of
Nurr1 in the brain to see how it affected the inflammatory stimulus when the brain was
infused with either bacterial lipolysaccharide (LPS) – a potent activator of
microglia – or with a mutant form of alpha synuclein that is associated with an early
form of familial Parkinson's disease. They found that, in the absence of Nurr1,
inflammation was increased in the region where dopaminergic neurons are found, resulting
in a toxic effect on those neurons. "LPS won't normally kill neurons, but the neurons
died when Nurr1 was removed, so we realized that another cell type in the brain must be
responding to LPS to cause this toxic effect," Gage said.
Sleep may help clear the brain for
new learning
A new theory about sleep's benefits for the
brain gets a boost from fruit flies in this week's Science. Researchers at Washington
University School of Medicine in St. Louis found evidence that sleep, already recognized
as a promoter of long-term memories, also helps clear room in the brain for new
learning.The critical question - How many synapses, or junctures where nerve cells
communicate with each other, are modified by sleep? Neurologists believe creation of new
synapses is one key way the brain encodes memories and learning, but this cannot continue
unabated and may be where sleep comes in."There are a number of reasons why the brain
can't indefinitely add synapses, including the finite spatial constraints of the
skull," says senior author Paul Shaw, Ph.D., assistant professor of neurobiology at
Washington University School of Medicine in St. Louis. "We were able to track the
creation of new synapses in fruit flies during learning experiences, and to show that
sleep pushed that number back down." Scientists don't yet know how the synapses are
eliminated. According to theory, only the less important connections are trimmed back,
while connections encoding important memories are maintained. Many aspects of fly sleep
are similar to human sleep; for example, flies and humans deprived of sleep one day will
try to make up for the loss by sleeping more the next day. Because the human brain is much
more complex, Shaw uses the flies as models for answering questions about sleep and
memory. Sleep is a recognized promoter of learning, but three years ago Shaw turned that
association around and revealed that learning increases the need for sleep in the fruit
fly. In a 2006 paper in Science, he and his colleagues found that two separate scenarios,
each of which gave the fruit fly's brain a workout, increased the need for sleep. The
first scenario was inspired by human research linking an enriched environment to improved
memory and other brain functions. Scientists found that flies raised in an enhanced social
environment—a test tube full of other flies—slept approximately 2-3 hours longer
than flies raised in isolation. Researchers also gave male fruit flies their first
exposure to female fruit flies, but with a catch—the females were either already
mated or were actually male flies altered to emit female pheromones. Either fly rebuffed
the test fly's attempts to mate. The test flies were then kept in isolation for two days
and exposed to receptive female flies. Test flies that remembered their prior failures
didn't try to mate again; they also slept more. Researchers concluded that these flies had
encoded memories of their prior experience, more directly proving the connection between
sleep and new memories. Scientists repeated these tests for the new study, but this time
they used flies genetically altered to make it possible to track the development of new
synapses, the junctures at which brain cells communicate. "The biggest surprise was
that out of 200,000 fly brain cells, only 16 were required for the formation of new
memories, " says first author Jeffrey Donlea, a graduate student. "These sixteen
are lateral ventral neurons, which are part of the circadian circuitry that let the fly
brain perform certain behaviors at particular times of day."
