Model of Anorexia Created Using Stem Cells

Though often viewed as a non-biological disorder, new research suggests 50 to 75 percent of risk for AN may be heritable; with predisposition driven primarily by genetics and not, as sometimes presumed, by vanity, poor parenting or factors related to specific groups of individuals. NeuroscienceNews.com image is for illustrative purposes only.

Findings suggest a strong genetic factor could predispose people to anorexia and other eating disorders. Technique suggests novel gene may contribute to eating disorder.

An international research team, led by scientists at University of California San Diego School of Medicine, has created the first cellular model of anorexia nervosa (AN), reprogramming induced pluripotent stem cells (iPSCs) derived from adolescent females with the eating disorder.

Writing in the March 14th issue of Translational Psychiatry, the scientists said the resulting AN neurons — the disease in a dish — revealed a novel gene that appears to contribute to AN pathophysiology, buttressing the idea that AN has a strong genetic factor. The proof-of-concept approach, they said, provides a new tool to investigate the elusive and largely unknown molecular and cellular mechanisms underlying the disease.

“Anorexia is a very complicated, multifactorial neurodevelopmental disorder,” said Alysson Muotri, PhD, professor in the UC San Diego School of Medicine departments of Pediatrics and Cellular and Molecular Medicine, director of the UC San Diego Stem Cell Program and a member of the Sanford Consortium for Regenerative Medicine. “It has proved to be a very difficult disease to study, let alone treat. We don’t actually have good experimental models for eating disorders. In fact, there are no treatments to reverse AN symptoms.”



Primarily affecting young female adolescents between ages 15 and 19, AN is characterized by distorted body image and self-imposed food restriction to the point of emaciation or death. It has the highest mortality rate among psychiatric conditions. For females between 15 and 24 years old who suffer from AN, the mortality rate associated with the illness is 12 times higher than the death rate of all other causes of death.

Though often viewed as a non-biological disorder, new research suggests 50 to 75 percent of risk for AN may be heritable; with predisposition driven primarily by genetics and not, as sometimes presumed, by vanity, poor parenting or factors related to specific groups of individuals.

But little is actually known about the molecular, cellular or genetic elements or genesis of AN. In their study, Muotri and colleagues at UC San Diego and in Brazil, Australia and Thailand, took skin cells from four females with AN and four healthy controls, generated iPSCs (stem cells with the ability to become many types of cells) from these cells and induce these iPSCs to become neurons.



(Previously, Muotri and colleagues had created stem cell-derived neuronal models of autism and Williams syndrome, a rare genetic neurological condition.)

Then they performed unbiased comprehensive whole transcriptome and pathway analyses to determine not just which genes were being expressed or activated in AN neurons, but which genes or transcripts (bits of RNA used in cellular messaging) might be associated with causing or advancing the disease process.

No predicted differences in neurotransmitter levels were observed, the researchers said, but they did note disruption in the Tachykinin receptor 1 (TACR1) gene. Tachykinins are neuropeptides or proteins expressed throughout the nervous and immune systems, where they participate in many cellular and physiological processes and have been linked to multiple diseases, including chronic inflammation, cancer, infection and affective and addictive disorders.

The scientists posit that disruption of the tachykinin system may contribute to AN before other phenotypes or observed characteristics become obvious, but said further studies employing larger patient cohorts are necessary.



“But more to the point, this work helps make that possible,” said Muotri. “It’s a novel technological advance in the field of eating disorders, which impacts millions of people. These findings transform our ability to study how genetic variations alter brain molecular pathways and cellular networks to change risk of AN — and perhaps our ability to create new therapies.”
Source: NEUROSCIENCE NEWS

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

Poor Diet to Blame for almost Half of Cardio Vascular Deaths

Researchers say that a poor diet contributes to more than 415,000 deaths from CVD in the U.S.

It is well established that a poor diet can raise the risk of cardiovascular death. New research, however, sheds light on the leading dietary risk factors for death from cardiovascular disease, as well as how many cardiovascular deaths these risk factors equate to.

Cardiovascular disease (CVD) is an umbrella term for conditions that affect the heart and
blood vessels. These include heart attack, heart disease, heart failure, and stroke.

According to the World Health Organization (WHO), CVD is the leading cause of death across the globe. In 2012, CVD was the cause of around 17.5 million global deaths, accounting for around 31 percent of all deaths that year.

How does diet contribute to the burden of CVD death in the United States?
Dr. Ashkan Afshin, of the Institute for Health Metrics and Evaluation at the University of Washington, and colleagues sought to answer this question with their new study.



Results were recently presented at the American Heart Association's Epidemiology and Prevention/Lifestyle and Cardiometabolic Health 2017 Scientific Sessions, held in Portland, OR.

“Almost half of CVD deaths could be prevented with a healthful diet”

The researchers used data from a variety of global sources to reach their findings, including 1990-2012 data from the National Health and Nutrition Examination Survey and food availability data from the Food and Agriculture Organization of the United Nations.

The team then looked at the number of CVD deaths that occurred in the U.S. in 2015 and used a systematic approach to quantify how certain dietary factors contributed to these deaths.
The researchers calculated that both a lack of healthful foods and high intake of unhealthful foods contributed to more than 415,000 CVD deaths in the U.S. in 2015. Of these deaths, more than 222,000 occurred in men and more than 193,000 occurred in women.



The team found that low intake of nuts and seeds and a low intake of vegetables were the two leading dietary risk factors for CVD death, accounting for 11.6 percent and 11.5 percent of deaths, respectively.

A low intake of whole grains accounted for 10.4 percent of CVD deaths, while excess salt intake was responsible for around 9 percent of CVD deaths.

Dr. Afshin and colleagues say that their findings show that adopting a healthful diet could help to save tens of thousands of lives every year.

"Low intake of healthy foods such as nuts, vegetables, whole grains, and fruits combined with higher intake of unhealthy dietary components, such as salt and trans-fat, is a major contributor to deaths from cardiovascular disease in the United States.

Our results show that nearly half of cardiovascular disease deaths in the United States can be prevented by improving diet."
Source: Written by Honor Whiteman

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

Experimental Treatment for Parkinson’s Symptoms Shows Early Promise

Depicted is a reconstruction of bi-hemispheric DBS electrodes that have been surgically placed into the most common target structure for treatment of Parkinson Disease, the sub-thalamic nucleus (orange). Other subcortical structures include the red nucleus (green), the substantia ‘nigra’ (yellow), the internal (cyan) and external (blue) pallidum and the striatum (red). A stimulation volume is modeled by applying 2V (at 1000Ω impedance) to the second-uppermost contact of the left electrode. Structural ‘fibertracts’ traversing through this volume are visualized and cortical regions that they connect with the stimulation volume are selected from an automatic anatomical labeling atlas and visualized. NeuroscienceNews.com image is credited to Andreashorn and is for illustrative purposes only

DBS Plus, a new version of deep brain stimulation, shows promise in helping to relieve Parkinson’s symptoms.

About 14 years ago, Bill Crawford noticed a persistent twitching in one of his fingers that was interfering with his rehearsal time as the music pastor at Porter Memorial Church.
“It was driving me crazy,” said the 57-year-old Lexingtonian.

He’d noticed a few other things too, like weakness. He had mentioned it to his primary care physician, who ordered heart and lung function tests, but both were negative.

Finally, however, he was so weak that he could no longer ride his bike. “I just couldn’t seem to go,” he said. So he made an appointment with a neurologist.

After a few minutes with Crawford, the neurologist asked him to return on Monday – and bring his wife Lisa with him.

On that dreadful day, the neurologist told Bill that he had Parkinson’s disease. At the time, Bill was just 44 years old.

“Obviously not what you want to hear,” Crawford said. “But then I began to think of Michael J. Fox and all he had accomplished, and I thought I could do that too.”

Eventually, though, the medicines that helped Bill control his Parkinson’s symptoms began to lose their effectiveness.

“There is no cure for Parkinson’s, and treatments we currently have at our disposal can only reduce symptoms,” explained Dr. John T. Slevin, a specialist at UK HealthCare’s Kentucky Neuroscience Institute, who began treating Crawford in 2006. “The disease progression inevitably overcomes the drugs’ capacity to alleviate the rigidity and tremor that are hallmarks of Parkinson’s.”

That meant that Crawford would go into what he called “full body charley horses” – sudden, painful involuntary spasms that left him paralyzed and lying on the floor for as much as 45 minutes.

“It was the pits,” Crawford said. Sometimes at the last minute he would be unable to conduct
musical performances at church services, which was particularly disheartening. “I didn’t want to be a spectacle.”

It was then that Slevin suggested a treatment called Deep Brain Stimulation and connected Crawford with UK HealthCare neurosurgeon Dr. Craig van Horne.

Deep Brain Stimulation (DBS) is a surgical procedure used to treat the problems associated with Parkinson’s disease. The procedure involves implanting electrodes into the brain that are connected to a small, pacemaker-like device implanted in the chest. These electrodes produce electrical signals that override the abnormal electrical impulses caused by the disease, which attacks and breaks down nerve cells in the brain.



The procedure isn’t suitable for everyone and requires thorough psychological testing and motion studies to ensure that a patient is ready for DBS. “I wasn’t sure I would qualify,” Crawford said. “But I knew this was my last chance.”

Crawford considers it a blessing that he was, in fact, qualified to receive DBS. But then came an additional surprise: after further testing, van Horne told Crawford that he was qualified to participate in a study for a new version of DBS called “DBS Plus.”

Van Horne explains that the central nervous system – which is comprised of the brain and spinal cord – is unable to heal itself after injury or disease. However, peripheral nerves from the rest of the body are able to regenerate.

“Our study is designed to test whether taking a small part of peripheral nerve tissue and putting it in the brain would prompt healing in the areas of the central nervous system damaged by Parkinson’s,” he said.

With DBS Plus, van Horne and his team (Greg Gerhard, PhD, and George Quintero, PhD,) take a small piece of nerve tissue from the patient’s ankle and implant it in their brain. Because the tissue is from a patient’s own body there are no concerns about rejection, and because the experimental treatment is applied during a procedure that was declared safe and effective by U.S. Food and Drug Administration (FDA) almost two decades ago, DBS Plus is considered relatively safe with only minimal additional risk.



Nonetheless, van Horne is cautious about the process of enrolling patients in the study.
“It’s more ethical, in my opinion, to wait until after a patient qualifies for the basic DBS before I tell them about my study,” he said. “I don’t want patients to elect to do DBS just because they want DBS Plus.”

And van Horne says he was thrilled that Crawford qualified for the study.
“When I met Bill for the first time, he was lying paralyzed on the floor in the treatment room,” van Horne recalled. “It was a startling and heart-breaking sight.”
Crawford received DBS Plus in August 2015. His family can’t get over the dramatic changes in his mobility.

“I’m climbing ladders now, I can plan our church’s worship time, I can lead the services, I can still lead others in worship,” he said.

The charley horses have gone away, and Crawford now takes just one or two pills a day, down from 12 before the surgery. A before and after video of Crawford walking the halls outside van Horne’s office is astonishing.

To date, 34 patients have participated in the DBS Plus study with encouraging results. Of the 17 patients that are 12 months out from their procedure, 65 percent of them have shown a clinically important improvement in motor performance as a result of the graft.



Van Horne is quick to point out that the study needs to be tested on a larger sample size at many other medical centers around the country before it can be deemed a viable treatment. Furthermore, he cautions, while 12-month results are promising, it’s important to evaluate effectiveness over a longer term. But assuming all goes as well as it has so far, DBS Plus shows promise as a means of slowing down the disease process.

Van Horne and his team garner no financial benefit from DBS Plus, which adds just a fraction of cost to the DBS surgery that is already covered by most insurance plans. “Our payback is the gratification we receive in seeing our patients do well,” van Horne said.

Crawford understands that DBS Plus isn’t a cure for his Parkinson’s, but is delighted to have a little more time to enjoy life.

“‘Feeling the beat’ is critical to my work as a musician, and my Parkinson’s had begun to take that away from me,” he said. “I couldn’t even snap my fingers with the music anymore.”
But, said Crawford, as he woke up from the surgery, he instinctively began to tap his fingers like a metronome. Two members of the team, Julie Gurwell, the PA responsible for programming the DBS equipment, and Ann Hanley, a Parkinson’s patient who personally accompanies patients through their surgeries, were sitting with him, and they asked him what he was doing.

“I was too emotional to explain but I managed to say ‘I can feel the beat.’ And they high-fived each other.”
Source: Laura Dawahare – University of Kentucky
NEUROSCIENCE NEWSJANUARY 6, 2017

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

Amazing breakthrough: Progress in World’s First Alzheimer’s Vaccine

Researchers have made a breakthrough discovery in the international quest to discover a new and potentially effective vaccine targeting the pathological proteins associated with Alzheimer’s disease.

With more than 7.5 million new cases of Alzheimer’s disease a year, the race to find a vaccine and effective treatment for dementia is growing by the day.

Now researchers in the US and Australia have make a breakthrough discovery in the international quest to discover a new and potentially effective vaccine targeting the pathological proteins associated with Alzheimer’s disease (AD), the most common cause of dementia in the elderly.

In research findings just released in Nature’s Scientific Reports journal, Flinders University experts as part of a high-level US research team at the Institute of Molecular Medicine (IMM) and University of California, Irvine (UCI) have made a successful vaccine formulation that targets the abnormal beta-amyloid and tau proteins that signal Alzheimer’s disease.



With more than 48 million dementia cases in 2015, Alzheimer’s is emerging as one of the biggest cost to the world’s health-care systems, especially in mature economies in western countries.

The World Health Organization has projected the total global societal cost of dementia-related illnesses and care at more than $US600 billion a year.

“If we are successful in pre-clinical trials, in three to five years we could be well on the way to one of the most important developments in recent medical history,” says Flinders University School of Medicine Professor Nikolai Petrovsky, who also is director of South Australian vaccine research company Vaxine Pty Ltd.



“Along with our rapidly ageing populations, we now know that the explosion in type 2 diabetes in the West is likely to further dramatically fuel the projected rise in the number of cases of dementia globally, with diabetes being the major risk factor for Alzheimer’s disease,” Professor Petrovsky says.

The scale of the dementia problem has seen the US Congress commit a further $US350 million to the National Institutes of Health (NIH) for research into Alzheimer’s disease, taking research funding in the US to more than $US1.3 billion this year.

With NIH and Alzheimer’s Association funding, the US researchers say they have developed an “exceptional” universal vaccine platform, called MultiTEP, to target the hallmark proteins, aberrant forms of AB and tau proteins.

β-amyloid (AB) is a protein found to be prominent in driving Alzheimer’s disease, but the accumulation of pathological tau also correlates with the formation of dementia in Alzheimer’s patients.



Using a combination of anti-amyloid-beta and anti-tau vaccines with powerful and safe adjuvant technology called Advax™ developed by Vaxine Pty Ltd “shows promise for both preventive and therapeutic approaches in AD,” Professor David Cribbs from the UCI Institute for Memory Impairments and Neurological Disorders (UCI MIND) told Bloomberg news agency in the US.
Professor Michael Agadjanyan, head of IMM Department of Molecular Immunology, says the MultiTEP platform-based vaccines “do not induce potentially harmful auto-reactive cellular immune responses, while still generating antibodies that bind strongly to the amyloid and tau pathological molecules in brain tissue from AD patients”.

Co-author of the latest paper, IMM Department of Molecular Immunology, Associate Professor Anahit Ghochikyan, says: “This study suggests that we can immunize patients at the early stages of AD, or even healthy people at risk for AD, using our anti-amyloid-beta vaccine, and, if the disease progresses, then vaccinate with another anti-tau vaccine to increase effectiveness.”



She says the cooperative studies with National Institute of Aging IMM scientists and collaborators from UCI and the University of Southern California are working with experts from four companies to conduct non-clinical safety-toxicology studies to fulfil US Government safety standards for the Investigational New Drug application.

After completion of these pre-clinical studies, they plan to test the immunogenicity and efficacy of the new vaccines in human trials.



Source: Flinders University
Neuroscience News

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

Scientist warn of more US “Superbug” cases this Summer

After two confirmed U.S. cases of “A Superbug” that thwarts a last-resort antibiotic, infectious disease experts say they expect more cases in coming months because the bacterial gene behind it is likely far more widespread than previously believed.

Army scientists in May reported finding E. coli bacteria that harbor a gene which renders the antibiotic colistin useless. The gene, called mcr-1, was found in a urine sample of a Pennsylvania woman being treated for a urinary tract infection.

On Monday, researchers confirmed preliminary findings that E. coli carrying the same mcr-1 gene were found in a stored bacterial sample of a New York patient who had been treated for an infection last year, as well as in patient samples from nine other countries.



The report came from a global effort called the SENTRY Antimicrobial Surveillance Program, led by Mariana Castanheira of JMI Laboratories based in North Liberty, Iowa.

The mcr-1 superbug has been identified over the past six months in farm animals and people in about 20 countries, including China, Germany and Italy.

The bacteria can be transmitted by fecal contact and poor hygiene, which suggests a far wider likely presence than the documented cases so far, according to leading infectious disease experts.
Health officials fear the mcr-1 gene, carried by a highly mobile piece of DNA called a plasmid, will soon be found in bacteria already resistant to all or virtually all other types of antibiotics, potentially making infections untreatable.

"You can be sure (mcr-1) is already in the guts of people throughout the United States and will continue to spread," said Dr. Brad Spellberg, professor of medicine at the University of Southern California.

Dr. David Van Duin, an infectious disease expert at the University of North Carolina in Chapel Hill, said he expects more documented U.S. cases of mcr-1 in coming months because it is already here and will spread from abroad. "We will see a lot more of this gene."



Colistin causes kidney damage, but doctors have opted for it as other antibiotics increasingly fail. Its overuse, especially in overseas farm animals, has allowed bacteria to develop resistance to it.
To track the mcr-1 gene, U.S. hospitals are working together with state and federal agencies to test bacteria samples of patients that have recently been treated for infections. Many of the largest research hospitals are examining samples of antibiotic-resistant bacteria that have long been stored in their freezers.

Gautam Dantas, associate professor of pathology at Washington University Medical Center in St. Louis, has tested hundreds of U.S. samples of archived bacteria in recent months and has not yet detected mcr-1. But he expects dozens of confirmed cases of the gene will be documented by next year in the country, mostly among current patients.



The concern of many disease experts is that mcr-1 could soon show up in bacteria also resistant to carbapenems, one of the few remaining dependable classes of antibiotics. In that event, with colistin no longer a last-ditch option, some patients would have to rely on their immune systems to fight off infection.

"Within the next two to three years, it's going to be fairly routine for infections to occur in the United States for which we have no (effective) drugs available," Dantas said.

Castanheira also believes mcr-1 will find its way into carbapenem-resistant bacteria, formally known as carbapenem-resistant enterobacteriaceae (CRE).

In an interview, she said the resulting virtually impervious bacterium would likely spread slowly inside the United States because CRE themselves are not yet widespread in the country, giving drugmakers some time to create new antibiotics.

Beginning in August, the U.S. Centers for Disease Control and Prevention will use $21 million to expand surveillance at laboratories operated by all 50 state health departments and seven larger regional labs. The federal funding will help pay for more-sensitive equipment to test for antibiotic resistance in bacteria samples provided by hospitals.



Source: Fox News Health

YOUR INPUT IS MUCH APPRECIATED! LEAVE YOUR COMMENT BELOW.

Can Alzheimer's disease be prevented?

New clinical studies are showing a dramatic breakthrough in the fight against Alzheimer's disease. In a model of studies, using animals that mimicked the human trials, researchers at the University of California (UC), and the School of Medicine in San Diego, reported a treatment, long-term, using a drug compound of small molecules that reduces the activity of the brain circuits stress, also significantly reduces the neuropathology of Alzheimer's disease (AD) and prevents the occurrence of cognitive impairment. These tests on neurodegenerative disease were developed using a mouse as a model.
The results are described in the publication, on internet, Alzheimer and Dementia magazine, published by: The Journal of the Alzheimer's Association.
“Alzheimer’s is a progressive brain disease that causes problems with memory, reasoning, behavior and motor skills. Symptoms of Alzheimer’s slowly worsen over time, and the disease is ultimately fatal.

Alzheimer’s is the most common form of dementia, which is defined as a loss of cognitive functioning and behavioral abilities that interferes with daily life. Other forms of dementia include vascular dementia, dementia with Lewy bodies, and frontotemporal dementia. Each of these diseases has its own set of specific symptoms.”



At this point is important to mention that the results highlight the complexity and diversity of AD, the causes appear to be a combination of genetic, lifestyle and environmental factors. Previous research has shown a link between stress modulating pathways in the brain and AD. Specifically, the release of a hormone "stress-confrontation" called Corticotropin-Releasing Factor (CRF), which is largely located in the brain and acts as a neurotransmitter / neuromodulator. This molecule is dysregulated in AD and is associated with impaired cognition and detrimental changes in the tau protein, and increases the production of fragments of amyloid beta in proteins, which are grouped and trigger neurodegenerative actions in AD.
“Our work and that of our colleagues on stress and CRF have been mechanistically implicated in Alzheimer’s disease, but agents that impact CRF signaling have not been carefully tested for therapeutic efficacy or long-term safety in animal models,” said the study’s principal investigator and corresponding author Robert Rissman, PhD, assistant professor in the Department of Neurosciences and Biomarker Core Director for the Alzheimer’s Disease Cooperative Study (ADCS).
“The novelty of this study is two-fold: We used a preclinical prevention paradigm of a CRF-antagonist (a drug that blocks the CRF receptor in brain cells) called R121919 in a well-established AD model – and we did so in a way that draws upon our experience in human trials. We found that R121919 antagonism of CRF-receptor-1 prevented onset of cognitive impairment and synaptic/dendritic loss in AD mice.”



In other words, the researchers determined that modulating the mouse brain’s stress circuitry (without actually changing the normal response) mitigated generation and accumulation of amyloid plaques widely attributed with causing neuronal damage and death. As a consequence, behavioral indicators of AD were prevented and cellular damage was reduced. The mice began treatment at 30-days-old – before any pathological or cognitive signs of AD were present – and continued until six months of age.
One particular challenge, Rissman noted, is limiting exposure of the drug to the brain so that it does not impact the body’s ability to response to stress. “This can be accomplished because one advantage of these types of small molecule drugs is that they readily cross the blood-brain barrier and actually prefer to act in the brain,” Rissman said. Drugs like R121919 were originally designed to treat generalized anxiety disorder, irritable bowel syndrome and other diseases, but failed to be effective in treating those disorders.
“Rissman’s prior work demonstrated that CRF and its receptors are integrally involved in changes in another AD hallmark, tau phosphorylation,” said William Mobley, MD, PhD, chair of the Department of Neurosciences and interim co-director of the Alzheimer’s Disease Cooperative Study at UC San Diego. “This new study extends those original mechanistic findings to the amyloid pathway and preservation of cellular and synaptic connections. Work like this is an excellent example of UC San Diego’s bench-to-bedside legacy, whereby we can quickly move our basic science findings into the clinic for testing,” said Mobley.
Rissman said R121919 was well-tolerated by AD mice (no significant adverse effects) and deemed safe, suggesting CRF-antagonism is a viable, disease-modifying therapy for AD. Rissman noted that repurposing R121919 for human use was likely not possible at this point. He and colleagues are collaborating with the Sanford Burnham Prebys Medical Discovery Institute to design new assays to discover the next generation of CRF receptor-1 antagonists for testing in early phase human safety trials.



“More work remains to be done, but this is the kind of basic research that is fundamental to ultimately finding a way to cure – or even prevent – Alzheimer’s disease,” said David Brenner, MD, vice chancellor, UC San Diego Health Sciences and dean of UC San Diego School of Medicine. “These findings by Dr. Rissman and his colleagues at UC San Diego and at collaborating institutions on the Mesa suggest we are on the cusp of creating truly effective therapies.”

Trinity Researchers Report Major breakthrough in understanding Alzheimer’s Disease

Scientists at Trinity College Dublin have shed light on a fundamental mechanism underlying the development of Alzheimer's disease, which could lead to new forms of therapy for those living with the condition.

Alzheimer's is the most common form of dementia globally and affects up to 4.5 people in USA as today. It is the fourth leading cause of death in individuals over the age of 65 and it is the only cause of death among
the top ten that cannot be prevented, cured or even slowed down.
The condition is classically associated with memory loss. However, other symptoms and warning signs include difficulty performing familiar tasks, problems with language such as forgetting phrases or words, and changes
in mood, behavior and personality.
The research, published this week in leading international journal, Science Advances, was supported by Science Foundation Ireland (SFI) and the US-based charity, Brightfocus Foundation.
Alzheimer's disease is characterized, in part, by the build-up of a small protein ('amyloid-beta') in the brains of patients. Impaired clearance of this protein appears to be a major factor in the build-up of plaques, and then
in the disease process itself. While the mode by which amyloid-beta is cleared remains unclear, it is evident that it needs to be removed from the brain via the bloodstream.
Unlike blood vessels anywhere else in the body, those in the brain have properties that strictly regulate what gets in and out of the delicate tissue - this is what is known as the blood-brain barrier (BBB). The BBB functions
as a tightly regulated site of energy and metabolite exchange between the brain tissue and the bloodstream.
"We have shown that distinct components of these blood vessels termed tight junctions are altered in Alzheimer's disease. We think that this alteration could be an entrained mechanism to allow for the clearance of toxic
amyloid-beta from the brain in those living with Alzheimer's disease," said postdoctoral researcher in Trinity's School of Genetics and Microbiology, Dr James Keaney, who spearheaded the study.
Working with the Dublin Brain Bank, which is based in Beaumont Hospital, the researchers from Trinity examined brain tissues of individuals who were affected by Alzheimer's disease during their lifetime and then compared
results to those observed in model systems in the laboratory.
Research Assistant Professor in Genetics at Trinity, Dr Matthew Campbell, added: "Our recent findings have highlighted the importance of understanding diseases at the molecular level. The concept of periodic clearance of
brain amyloid-beta across the BBB could hold tremendous potential for Alzheimer's patients in the future. The next steps are to consider how this might be achieved.
"Given the recent advances in clinical trials of anti-amyloid beta antibodies, we hope our findings may lead to improved and adjunctive forms of therapy for this devastating condition."
Source: Trinity College, Dublin

Fast Food Fast Disease

Back in August, my son and his friends went to enjoy a baseball game between the NY Mets and the Pittsburgh Pirates. Being a big fan for the sport, it was my intention to speak with my son about his experience at the game as soon as he had gotten back. However, the conversation took a slightly different course than I had expected. My son did not begin the conversation by mentioning any highlights about the game or most importantly, who had won the game; instead he began to describe his observations of the fans who attended the baseball game.
One of many problems that is ubiquitous in the United States, is obesity, and sports events certainly contribute towards worsening the problem. My son vividly described the ways that the baseball fans were merely interested in consuming "junk foods” such as hot dogs, pizzas, hamburgers, etc; and beverages such as beer, soda, and other unhealthy products.The amount of consumption that took place was disturbing, and worst of all, the biggest problem was that these "junk foods" were the only type of foods that vendors sold. Now not only was it the only type of food being sold, but it was also accessible in large quantities, which makes it the perfect ambience for food conditioning.
The next day really had me in awe, as the conversation between my son and I raised questions and elucidated the perception of the food system of our society. Why is it that the diet in the most "powerful country in the world" consists primarily of cheap foods, with high levels of harmful elements for our health? The number of overweight/obese people is reaching intolerable levels and has become a systemic issue that is prevalent in our country. Precautionary actions must be taken with urgency to avoid the consequences that will not only affect us, but future generations as well. And it all begins with education.
Our children are receiving minimal education about the correct nutritional system to be followed. Yes they may comprehend the rudimentary levels of health and nutrition, however, most children are not adamant about eating healthy. Now what kind of message are we sending to our children? That such substantial consumption of unhealthy foods is acceptable? Being overweight increases the risk of high cholesterol, which can eventually become a major risk for cardiovascular disease; and not to mention the psychological effects that unhealthy eating causes as well.
What is happening to us? Why are we consciously destroying ourselves? Why are these large corporations with its majestic and sophisticated advertising systems encouraging us to eat these "junk foods" that have such detrimental effects to our bodies? Why are we not putting up a better effort to fight obesity? Why hasn't our society yet to make a vast effort to prevent people of permanent or chronic illnesses? Why not raise the concept of what is lawful to what is morally permissible? And please do not let your response be that at the end of the day; "business is business".
At whatever level you want to look at it, the United States has terribly failed in developing a comprehensive system that provides our citizens with the proper education about health and nutrition. From elementary through high school levels, the system is not only weak and ineffective, but also immature and primitive.
In 2015, we live in a fast society where work consumes most of our day, and consequently, our decisions as to what food we consume suffer as they take an inferior role.
Now when those decisions take an inferior role, we tend to act on emotion rather than logic. That creates opportunities for large corporations to sway in to induce individuals to eat unhealthy foods that are polluting our dietary preferences and are doing the same to our schools, neighborhoods, and workplaces. Large corporations, in a strategic way, geographically allocate their restaurants all around us to coincide with their extremely sophisticated sales strategies. Large corporations, such as Burger King, McDonalds, Taco Bell, Pizza Hut, Kentucky Fried Chicken, Domino's Pizza, among many others, use complex neuro-advertising systems and include chemicals additives in their products that constantly saturate our minds and stomachs with the famous poisonous condition that "sleeps the mind momentarily to activate the senses (especially the olfactory).
One way to verify the effectiveness of the systems used is to take a look at what people consume. A majority of the country knows how harmful these food preferences are, yet many still choose to make decisions that affect their health and overall well being. The diets (if we can call it that way) that many have become comfortable with and are accustomed to are directly causing individuals to get sick quicker.
The following data refers to the components that are found in food served at most restaurants; Spanish omelet which contains 830 calories, 41 grams of fat, 280 grams of cholesterol, and 1560 milligrams of sodium. These nutrition facts are alarming for our well beings.
Restaurant chains are targeting our children, with intensive marketing campaigns about "junk food”. These companies spend about $2 Billion a year in marketing and advertising these products to hopefully induce children to go running to you begging for “candy, soda, etc”. That spending equates to approximately $5 million a day!!!
On a daily basis, our children watch approximately 10 advertisements related to food on television. Almost 98% of warnings about food, seen by our children, are related to products high in fat, sugar, or sodium. And close to 40% of our children’s diets consist of sugary products and unhealthy fats. Only 21% of children, between the ages of 6-19 years old, eat less than five servings a day of fruits and vegetables. One study found that when children are exposed to television with content related to food ad, they consume 45% more food than those who are not exposed to television.
In 2014 the food and beverage companies spent $60 billion lobbying Congress to prevent various regulations that could reduce the marketing of unhealthy foods as well as raising taxes on beverages. A study in 2010 found that more than half of the companies who advertised fruit in their products, did not actually contain any fruit ingredient. A second study found that 85% of products that claim to be healthy products, on the front labels, were not healthy at all.
If we continue down this gruesome path, it is anticipated that by 2050, one in every three adults in the United States will suffer from diabetes, and that medical costs attributed to poor diet will reach between $900 to $990 Billion dollars a year.
I think it is time that something should be done, to avoid chaos in our country's health industry, which seems imminent. It should be our due diligence to educate our children and tell them that the maximum consumption of sodium a day is 2,200 milligrams and not the average 3,200 mg that a child consumes on a daily basis. Avoid the temptation for those “fast” meals just because they are cheap and easy to obtain. Let’s educate our children about the detrimental effects of these foods and teach them about the number of benefits that come from healthy eating.
Remember the consumption of cigarettes in the 1990’s? We had to wait until the death poll reached millions in order to do take action and alleviate the problem. If our society continues to neglect the precautionary actions that are necessary to eradicate obesity, then we will essentially be faced with the same scenario as cigarette consumption, and I'm not exaggerating. Our children learn by imitating what we do, so let’s give them a good example by practicing the right actions and behavior. Make an effort and invite your children to help you while preparing meals to take advantage and explain to them the components that are necessary towards having a healthy diet. When taking trips to the supermarket, teach them how to read the nutritional facts found on the label, and teach them the pros and cons of consuming canned food vs. organic food. (It shouldn’t take too long)
That’s how we can educate our children, not only to be good citizens and respect the law, but also to eat healthier, practice more outdoor exercise, limit access to electronic games and television. Our country spends billions of dollars a year to reach other Planets and find extraterrestrial life... What for? To invite them for supper and share our, such called it, nutritional food preferences? It is certainly a shame that we say that we are an advanced civilization, in what way? We do not even know how to feed ourselves!!!
Of course, it is not our intention to insinuate you to develop a slender body type like Brad Pitt, Sylvester Stallone, Miss Universe Paulina Vega, or Jennifer Lopez, but to at least be healthy to avoid later problems in our lives, and the lives of our children.