In its latest attempt to kick-start lady libidos with a pill, Sprout Pharmaceuticals announced this week that it will resubmit its female sex drug, flibanserin, for FDA approval. If it gets the okay, the drug would be the first prescription of its kind for women in the United States: a treatment for female hypoactive sexual disorder, or a low sex drive. More…
SuperAgers, aged 80 and above — but with memories that are as sharp as those of healthy persons decades younger — have distinctly different looking brains than those of normal older people, according to new Northwestern Medicine research.
Understanding Superagers’ unique “brain signature” may enable scientists to decipher the genetic or molecular source and develop strategies to protect the memories of normal aging persons, as well as treat dementia.
Published Jan. 28 in the Journal of Neuroscience, the study is the first to quantify brain differences of SuperAgers and normal older people.
Cognitive SuperAgers were first identified in 2007 by scientists at Northwestern’s Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University Feinberg School of Medicine.
Discovery gives scientists hope of developing a therapy that could slowdown the progression of Alzheimer’s disease and other forms of dementia
People who carry a mutated gene linked to longer lifespan have extra tissue in part of the brain that seems to protect them against mental decline in old age.
The finding has shed light on a biological pathway that researchers now hope to turn into a therapy that slows the progression of Alzheimer’s disease and other forms of dementia.
Brain scans of more than 400 healthy men and women aged 53 and over found that those who carried a single copy of a particular gene variant had a larger brain region that deals with planning and decision making.
Further tests on the group found that those with an enlarged right dorsolateral prefrontal cortex (rDLPFC), as the brain region is known, fared better on a series of mental tasks.
About one in five people inherits a single copy of the gene variant, or allele, known as KL-VS, which improves heart and kidney function, and on average adds about three years to human lifespan, according to Dena Dubal, a neurologist at University of California, San Francisco.
Her latest work suggests that the same genetic mutation has broader effects on the brain. While having a larger rDLPFC accounted for only 12% of the improvement in people’s mental test scores, Dubal suspects the gene alters the brain in other ways, perhaps by improving the connections that form between neurons.
Scientists at the Stanford University School of Medicine have developed a new procedure that uses modified messenger RNA to quickly and efficiently increase the length of human telomeres, the protective caps on the ends of chromosomes that are associated with aging and disease.
Treated cells behave as if they are much younger than untreated cells, multiplying with abandon in the laboratory dish rather than stagnating or dying. Skin cells with telomeres lengthened by the procedure were able to divide up to 40 more times than untreated cells.
The procedure will improve the ability of researchers to generate large numbers of cells for study or drug development and may lead to preventing or treating diseases of aging, the scientists say.
Telomeres are the protective caps on the ends of chromosomes, which house our genomes. In young humans, telomeres are about 8,000–10,000 nucleotides long. They shorten with each cell division, however, and when they reach a critical length, the cell stops dividing or dies. This internal “clock” makes it difficult to keep most cells growing in a laboratory for more than a few cell doublings.
‘Turning back the internal clock’
“Now we have found a way to lengthen human telomeres by as much as 1,000 nucleotides, turning back the internal clock in these cells by the equivalent of many years of human life,” said Helen Blau, PhD, professor of microbiology and immunology at Stanford and director of the university’s Baxter Laboratory for Stem Cell Biology. “This greatly increases the number of cells available for studies such as drug testing or disease modeling.”
A paper describing the research was published in the FASEB Journal. Blau, who also holds the Donald E. and Delia B. Baxter Professorship, is the senior author. Postdoctoral scholar John Ramunas, PhD, of Stanford shares lead authorship with Eduard Yakubov, PhD, of the Houston Methodist Research Institute.
Is sugar making us sick? A team of scientists at the University of California in San Francisco believes so, and they're doing something about it. They launched an initiative to bring information on food and drink and added sugar to the public by reviewing more than 8,000 scientific papers that show ...
(Credit: iStock) A systematic review of 37 randomized controlled trials showed promising evidence for the ability of yoga to improve cardiovascular and-
A systematic review of 37 randomized controlled trials showed promising evidence for the ability of yoga to improve cardiovascular and metabolic health, but found no significant difference in the effectiveness of yoga versus aerobic exercise.
Yoga showed significant improvement in body mass index, systolic blood pressure, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol; and significant changes in body weight, diastolic blood pressure, total cholesterol, triglycerides, and heart rate. ‘
“Despite the growing evidence on the health implications of yoga, the physiological mechanisms behind the observed clinical effects of yoga on cardiovascular risk remain unclear,” the researchers say, adding that “there’s a need for larger randomized controlled studies that meet explicit, high quality methodological standards to ascertain the effects of yoga” in improving modifiable risk factors of cardiovascular disease and metabolic syndrome.
Cardiovascular disease (CVD) and metabolic syndrome are major public health problems in the USA and worldwide. Metabolic syndrome is defined as having at least three metabolic risk factors — increased blood pressure, high blood sugar level, excess body fat, and abnormal cholesterol levels — and greatly increases chance of future cardiovascular problems. CVD and metabolic syndrome share many of the same modifiable risk factors, such as physical inactivity, the fourth leading risk factor of global mortality, the researchers note.
The study, by researchers at Erasmus MC, Harvard Medical School, and Harvard School of Public Health, was published (open-access) in the European Journal of Preventive Cardiology.
Some see ketamine as an effective drug for some patients, and others see it as a dangerous hallucinogen that has not been studied enough.
It is either the most exciting new treatment for depression in years or it is a hallucinogenic club drug that is wrongly being dispensed to desperate patients in a growing number of clinics around the country.
It is called ketamine — or Special K, in street parlance.
While it has been used as an anesthetic for decades, small studies at prestigious medical centers like Yale, Mount Sinai and the National Institute of Mental Health suggest it can relieve depression in many people who are not helped by widely used conventional antidepressants like Prozac or Lexapro.
And the depression seems to melt away within hours, rather than the weeks typically required for a conventional antidepressant.
But some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials, and they are alarmed that clinics are springing up to offer ketamine treatments, charging hundreds of dollars for sessions that must be repeated many times.
A promising new study suggests that a wireless, light-sensitive, and flexible film could potentially form part of a prosthetic device to replace damaged or defective retinas. The film both absorbs light and stimulates neurons without being connected to any wires or external power sources, standing it apart from silicon-based devices used for the same purpose. It has so far been tested only on light-insensitive retinas from embryonic chicks, but the researchers hope to see the pioneering work soon reach real-world human application.
Some neurons are genetically-predisposed to be sensitive to light. An emerging field called optogenetics uses light to stimulate and control those neurons, with applications not only in vision but also in gene therapy, brain mapping, reducing pain sensitivity, treatment of neurological disorders such as epilepsy and Parkinson's disease, and even mind control.
The researchers sought to develop an optogenetics approach to restoring vision. They combined semiconductor nanorods and carbon nanotube film and found that the resultant system stimulated neurons in light-insensitive embryonic chicks at day 14 of their development when illuminated with violet light for 100 ms.
In recent years, research has linked sleep problems to Alzheimer’s disease. This relationship involves a neurotransmitter called orexin that awakens the brain from sleep and has been shown to be heightened in moderate to severe sufferers of Alzheimer’s. New research conducted at Washington University in St Louis suggests that removing the orexin protein in mice enables them to sleep longer, which could serve to hinder development of the disease.
One of the ways that the orexin protein and sleep loss can lead to Alzheimer’s is through enabling the development of brain plaques. These build up before and during the onset of Alzheimer’s and correlate with the development of symptoms like memory loss and disorientation, leading scientists to believe that halting their buildup may go some way to combating the disease.
Putting this theory to the test, the researchers used mice that were genetically engineered to possess elevated amyloid beta, the protein that helps to make up brain plaques. By breeding these mice with other mice lacking the orexin protein, the researchers found the offspring had less sleep problems and developed around half as many plaques.
Mice with no orexin slept for around an hour extra during twelve-hour observation periods, while mice with orexin were more lively. Conversely, when the researchers heightened orexin levels, the mice stayed awake for longer and grew more plaques. Another noteworthy finding was that manipulating orexin levels in a section of the brain unrelated to the mouse's ability to sleep had no bearing on levels of plaque.
In recent years, research has linked sleep problems to Alzheimer’s disease. New research shows that removing orexin in mice, a protein that regulates arousa...
For the last two years, the US$2.25 million Nokia Sensing X Challengehas lured entrants from around the globe to submit groundbreaking technologies that improve access to health care. A panel of experts have awarded this year's grand prize to Massachusetts-based DNA Medical Institute (DMI), whose hand-held device is capable of diagnosing ailments in minutes, using only a single drop of blood.
The DMI team were selected from 11 finalists. Among them were Swiss team Biovotion, whose wearable computer monitors vital signs such heart rate and breathing, along with the US-based Eigen Lifescience team, whose low-cost, portable device is capable of testing for Hepatitis B in less than 10 minutes. But it was DMI's Reusable Handheld Electrolyte and Lab Technology for Humans system (rHealth) that impressed the judges most.
"Our expert judging panel reviewed a very exciting group of sensing technologies, all with the potential to address a wide array of diagnostic and personal health needs,” said Dr. Peter H. Diamandis, chairman and CEO of X Prize, the foundation behind the competition. “DMI’s rHealth system embodies the original goal of the Nokia Sensing X Challenge, to advance sensor technology in a way that will enable faster diagnoses and easier, more sophisticated personal health monitoring.”
The user presses the bulb of the smartphone dongle, designed to fit in one hand, to initiate the fluid flow (credit: Tassaneewan Laksanasopin, Columbia-
A low-cost smartphone accessory that can detect three infectious disease markers from a finger prick of blood in just 15 minutes, performing all mechanical, optical, and electronic functions of a lab-based blood test.
That’s what team of researchers led by Samuel K. Sia, associate professor of biomedical engineering at Columbia Engineering, has developed.
It performs an enzyme-linked immunosorbent assay (ELISA) triplexed immunoassay not currently available in a single test format: HIV antibody, treponemal-specific antibody for syphilis, and non-treponemal antibody for active syphilis infection.
Sia’s innovative accessory (dongle), a small device that easily connects to a smartphone or computer, was recently piloted by health care workers in Rwanda. They tested whole blood obtained via a finger prick from 96 patients who were enrolling into prevention-of-mother-to-child-transmission clinics or voluntary counseling and testing centers.
A compound found in green tea can kill oral cancer cells without damaging healthy cells, and now scientists think they've figured out how it works.
Earlier studies showed the compound called epigallocatechin-3-gallate (EGCG) killed oral cancer cells, but researchers didn’t how it worked, says Joshua Lambert, associate professor of food science at Penn State University.
“EGCG is doing something to damage the mitochondria and that mitochondrial damage sets up a cycle causing more damage and it spirals out, until the cell undergoes programmed cell death.
“It looks like EGCG causes the formation of reactive oxygen species in cancer cells, which damages the mitochondria, and the mitochondria responds by making more reactive oxygen species.”
As this mitochondrial demise continues, the cancer cell also reduces the expression of antioxidant genes, further lowering its defenses.
“So, it’s turning off its mechanism of protection at the same time that EGCG is causing this oxidative stress,” Lambert says.
The compound did not cause the same reaction in normal cells—in fact it appeared to increase the protective capabilities of the cell, according to the study published online in the journal Molecular Nutrition and Food
Gladstone Institutes researchers have uncovered a new memory regulator in the brain that may offer a potential treatment to improve memory in Alzheimer’s disease using a drug that targets those receptors.
They found in their research* that decreasing the number of A2A adenosine receptors in astrocyte brain cells improved memory in healthy mice. It also prevented memory impairments in a mouse model of Alzheimer’s disease.
The findings were published Monday (Jan. 26) in Nature Neuroscience.
In the largest collaborative study of the brain to date, about 300 researchers in a global consortium of 190 institutions identified eight common genetic mutations that appear to age the brain an average of three years.
The discovery could lead to targeted therapies and interventions for Alzheimer’s disease, autism, and other neurological conditions.
Led by the Keck School of Medicine of the University of Southern California (USC), an international team known as the Enhancing Neuro Imaging Genetics through Meta Analysis (ENIGMA) Network, pooled brain scans and genetic data worldwide to pinpoint genes that enhance or break down key brain regions in people from 33 countries.
This is the first high-profile study since the National Institutes of Health (NIH) launched its Big Data to Knowledge (BD2K) centers of excellence in 2014. The research was published Wednesday, Jan. 21, in the peer-reviewed journal Nature.
“Our global team discovered eight genes that may erode or boost brain tissue in people worldwide,” said Paul Thompson, Ph.D., Keck School of Medicine of USC professor and principal investigator of ENIGMA. ” Any change in those genes appears to alter your mental bank account or brain reserve by 2 or 3 percent. The discovery will guide research into more personalized medical treatments for Alzheimer’s, autism, depression and other disorders.”
When you first put on the ice vest, you will feel cold. Not intolerably cold, but cold enough to make you think, What am I doing with my life? Or, at least, as numbness spreads across your shoulders and down your back, There must be better ways to lose weight. And there are. But as an adjunct to those better ways, the vest carries some unlikely promise.
The sturdy Han Solo–style garment is loaded with ice packs, and it’s inspired by a theory gathering momentum among scientists: namely, that environmental thermodynamics can be harnessed in pursuit of weight loss. The basic idea is that because your body uses energy to maintain a normal body temperature, exposure to cold expends calories. The vest’s inventor, Wayne B. Hayes, an associate professor at the University of California at Irvine, claims that wearing it for an hour burns up to 250 calories, though his data are very rough. A little more than a year ago, he began selling the vest, which he calls the Cold Shoulder, out of his Pasadena apartment. Name notwithstanding, people won’t ignore you when you wear it.
Ken K. Liu, a principal at a hedge fund in Los Angeles, has been wearing the vest under his suit jacket on and off for about a year. He told me that some people’s first reaction to the unwieldy getup is “What the hell are you doing?” As soon as Liu explains the concept, though, many of them say it sounds like a good idea. Others still think it’s “stupid”—as did my colleagues, when I wore one—but Liu has not been deterred. Each morning while his coffee is brewing, he takes his vest out of the freezer and dons it without shame. Liu was never “fat,” by his estimation, but he says he did carry a few extra pounds that he had trouble dropping, despite exercise and attention to diet. The Cold Shoulder closed that gap.
Eating a Mediterranean diet might be a recipe for a long life because it appears to keep us genetically younger, say researchers.
Following a Mediterranean diet might be a recipe for a long life because it appears to keep people genetically younger, say US researchers.
Its mix of vegetables, olive oil, fresh fish and fruits may stop our DNA code from scrambling as we age, according to a study in the British Medical Journal.
Nurses who adhered to the diet had fewer signs of ageing in their cells.
The researchers from Boston followed the health of nearly 5,000 nurses over more than a decade.
The Mediterranean diet has been repeatedly linked to health gains, such as cutting the risk of heart disease.
Although it's not clear exactly what makes it so good, its key components - an abundance of fresh fruit and vegetables as well as poultry and fish, rather than lots of red meat, butter and animal fats - all have well documented beneficial effects on the body.
Foods rich in vitamins appear to provide a buffer against stress and damage of tissues and cells. And it appears from this latest study that a Mediterranean diet helps protect our DNA.
The researchers looked at tiny structures called telomeres that safeguard the ends of our chromosomes, which store our DNA code.
These protective caps prevent the loss of genetic information during cell division.
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