Source: Alzheimer’s health care update
Alzheimer’s death rate per state – 2015
Alzheimer’s death rate per state – 2015
Age-Adjusted* Alzheimer’s Disease Death Rates† Among Persons Aged ≥65 Years, by State§ — United States, 2015
New York is best place to age with South Carolina the highest in Alzheimer’s death rate.
https://www.cdc.gov/mmwr/volumes/66/wr/mm6627a6.htm?s_cid=mm6627a6_e
Alzheimer’s health care update
Drugs
- Pimavanserin for Agitation and Aggression in Alzheimer’s Disease (multiple sites)
- Crenezumab for Prodromal to Mild Alzheimer’s Disease (multiple sites)
Brain Imaging
- Alzheimer’s Disease Neuroimaging Initiative 3 (ADNI3) (multiple sites)
Caregiving
- Tele-Savvy Education Program for Dementia Caregivers (Atlanta, GA)
- Caring for the Caregiver Technology-Based Program (Miami, FL)
Exercise
- Exercise in Adults with Mild Memory Problems (EXERT) (multiple sites)
Other Dementias
- RVT-101 for Dementia with Lewy Bodies (HEADWAY-DLB) (multiple sites)
- Advancing Research and Treatment for Frontotemporal Lobar Degeneration (ARTFL) (multiple sites)
Registries
- Alzheimer’s Prevention Registry (nationwide)—get information and updates about participating in future Alzheimer’s prevention trials.
- GeneMatch (nationwide)—enroll to get matched to Alzheimer’s genetics studies.
- Brain Health Registry (nationwide)—sign up for an online study of brain health and learn about possible research-study opportunities.
Study of How We Look at Faces May Offer Insight Into Autism
How we look at other people’s faces is strongly influenced by our genes, scientists have found in new research that may be especially important for understanding autism because it suggests that people are born with neurological differences that affect how they develop socially.
The study, published on Wednesday in the journal Nature, adds new pieces to the nature-versus-nurture puzzle, suggesting that genetics underlie how children seek out formative social experiences like making eye contact or observing facial expressions. Experts said the study may also provide a road map for scientists searching for genes linked to autism.
“These are very convincing findings, novel findings,” said Charles A. Nelson III, a professor of pediatrics and neuroscience at Harvard Medical Schooland Boston Children’s Hospital, who was not involved in the research. “They seem to suggest that there’s a genetic underpinning that leads to different patterns of brain development, that leads some kids to develop autism.”
Dr. Nelson, an expert in child development and autism who was an independent reviewer of the study for Nature, said that while autism is known to have a genetic basis, how specific genes influence autism’s development remains undetermined.
The study provides detailed data on how children look at faces, including which features they focus on and when they move their eyes from one place to another. The information, Dr. Nelson said, could help scientists “work out the circuitry that controls these eye movements, and then we ought to be able to work out which genes are being expressed in that circuit.”
“That would be a big advance in autism,” he said.
In the study, scientists tracked the eye movements of 338 toddlers while they watched videos of motherly women as well as of children playing in a day care center. The toddlers, 18 months to 24 months old, included 250 children who were developing normally (41 pairs of identical twins, 42 pairs of nonidentical twins and 84 children unrelated to each other). There were also 88 children with autism.
Scientists study identical twins because 100 percent of their genes are the same, so if they share characteristics that are more individualized in other children, those traits are considered at least partly inherited. Nonidentical or fraternal twins share 50 percent of their DNA, so stark differences between identical and nonidentical twins suggest that those traits are strongly influenced by genes.
In the study, how much one identical twin looked at the eyes of people on screen matched the other identical twin 91 percent of the time. For fraternal twins, the match dropped to 35 percent. For unrelated children, when measured as pairs of the same age and sex, the match was 16 percent. And when the unrelated children were paired at random, their time spent looking at eyes did not match at all, said Warren Jones, the study’s senior author and an assistant professor of pediatrics at Emory University School of Medicine.
How much the children looked at mouths followed a similar pattern. And although each toddler watched the videos without other children present, identical twins often moved their eyes at nearly the same moment — as close as 16.7 milliseconds apart — and in the same direction.
“It’s a really remarkable set of findings in that it really shows that genetic factors are driving differences in the way that toddlers are looking at faces,” said Brad Duchaine, a professor of psychological and brain sciences at Dartmouth, who was not involved in the study. “This suggests that genetic differences drive this important aspect of the way that we interact with others.”
Dr. Jones, whose co-authors include Dr. John Constantino, director of child and adolescent psychiatry at Washington University School of Medicine in St. Louis, and Ami Klin, director of the Marcus Autism Center at Children’s Healthcare of Atlanta, said: “When we started to get the results back, I thought that I had the wrong data because the match between identical twins was so strong. I thought I might have mistakenly matched data from the same twin.”
With the children with autism, the researchers found that, compared with typically developing toddlers, they spent significantly less time looking at faces and more time looking at objects. That difference was especially pronounced with the day care videos, scenes presenting many more things to look at than the close-up videos of women talking to the camera, Dr. Jones said. When watching the day care videos, toddlers with autism looked at faces half as often as typical children did, and at objects almost twice as much.
The difference was so consistent that researchers could identify most children with autism just by looking at the eye-tracking results, Dr. Jones said. That result reinforced previous research in which Dr. Jones, Dr. Klin and colleagues showed that babies from 2 months to 6 months old who looked less at people’s eyes in videos were more likely to be given an autisim diagnosis at age 3 and that eye-tracking could provide an early behavioral indicator of autism.
Experts said that because the study shows that a social behavior that is significantly different in children with autism is strongly influenced by genetics, it might help scientists home in on specific genes to better understand autism or at least a key autism characteristic.
Even when identical twins watched completely different videos, their results matched. “How much Twin 1 looked at the eyes in a video that Twin 2 didn’t get to see predicted how much Twin 2 would look at the eyes in a different video,” Dr. Jones said.
That suggests, he said, that the genetically driven behavior involves “seeking out” social information found in the eyes rather than “merely responding to” facial features, a finding that could help pinpoint “what is disrupted in children with autism as they develop and learn about the world.”
Dr. Nelson said one question for further research was “how specific are these phenomena to autism, or might you see them in other neurological disorders?”
Another question is “how does this actually affect longer-term development of the brain,” said Matthew Peterson, a postdoctoral researcher at the Massachusetts Institute of Technology, whose studies have found that “everybody has a preferred location or position on the face where they will always look when they identify someone” — higher or lower on the face; toward the eyes, nose or mouth.
In the new study, researchers also tested the typically developing children again at age 3 and found that identical twins still strongly matched in how much they looked at eyes and mouths. That suggests that compared with genes, “that experience they’re having in that year — that’s not having much of an influence,” said Dr. Duchaine, whose work has found genetic roots to face recognition.
Still, Dr. Nelson cautioned against overemphasizing the direct role of genes. “Twins have identical DNA, but they don’t have identical experiences and they don’t have the same brains,” he said.
Most likely, through evolution, we came to have “genes that regulate the formation of the neural circuits that underpin how we visually inspect the social world,” he said.
“That,” he said, “helps ensure that we are social beings.”
Health in France
Source: Health in France
Health in France
Average life expectancy in France at birth is 81 years.[1][2]
Contents
[hide]
Healthcare issues in France
Obesity in France
Even though French are among the thinner Europeans (see chart below), obesity in France has been increasingly cited as a major health issue in recent years. It is now considered a political issue whereas just a few years prior it would only have been an issue reported on television talk shows or in women’s magazines.[3] There is a myth about French people not getting overweight or obese[4] however France is only ranked as the 128th fattest country in the World,[5] one of the lowest rank among developed countries and French food has long been studied for its healthy diet.
| Country | Average weight | BMI[6] | Daily Calorie Intake | Source |
|---|---|---|---|---|
| United Kingdom | 80 kg | 29 | 2,200 | [7] |
| Italy | 74 kg | 26 | 2,100 | |
| Germany | 73.5 kg | 26 | 2,400 | |
| France | 68 kg | 24 | 2,200 |
Public health
France, as all EU countries, is under an EU directive to reduce sewage discharge to sensitive areas. In 2006, France was only 40% in compliance, one of the lowest achieving countries in the EU with regard to this waste-water treatment standard[8]
Statistics
| Total population (2015) | 64,395,000 |
|---|---|
| Gross national income per capita (PPP international $, 2013) | 37 |
| Life expectancy at birth m/f (years, 2015) | 79/85 |
| Probability of dying under five (per 1 000 live births, 0) | not available |
| Probability of dying between 15 and 60 years m/f (per 1 000 population, 2015) | 104/51 |
| Total expenditure on health per capita (Intl $, 2014) | 4,508 |
| Total expenditure on health as % of GDP (2014) | 11.5 |
Missing Link Discovered Between Immune Cells and Alzheimer’s Disease
Source: Cornell University
By studying the effects of immune cells that surround blood vessels in the brain, Weill Cornell Medicine researchers have discovered a new pathway involving these cells that may contribute to the cause of Alzheimer’s disease.
One of the hallmarks of Alzheimer’s disease is the accumulation of plaque deposits, or abnormal protein fragments, from a peptide called amyloid-beta. Amyloid-beta destroys neurons and damages brain blood vessels with the help of highly reactive molecules, called free radicals, which are derived from oxygen. For their study, published May 17 in Circulation Research, the researchers sought to determine which cells in the brain were responsible for producing the free radicals, also known as reactive oxygen species (ROS).
“These free radicals are nasty molecules that paralyze the vessels so that they can’t function normally. As a result, brain cells are deprived of the blood supply of oxygen and glucose they need to function properly,” said senior study author Dr. Costantino Iadecola, director of the Feil Family Brain and Mind Research Institute and the Anne Parrish Titzell Professor of Neurology at Weill Cornell Medicine.
In their study, the investigators examined cells in the brain called perivascular macrophages (PVM), which surround blood vessels and pick up and remove damaging metabolic byproducts floating around the brain. The team focused on these cells because amyloid-beta tends to accumulate in the vascular space where PVM are located.
“We saw that when cells are exposed to amyloid beta, these PVM start producing free radicals like crazy,” Iadecola said.
To determine whether the PVM were involved in the ROS production, the researchers removed PVM by injecting into the brains of mice spherical lipid droplets called liposomes that contained the drug clodronate.
“The liposomes acted as a kind of Trojan horse,” said Laibaik Park, assistant professor of research in neuroscience in the Feil Family Brain and Mind Research Institute, and first author of the study. “The PVM digest the lipids and sets the drug loose into the cell, forcing them to die.”
Park and Iadecola administered the liposomes in mice with Alzheimer’s disease; ROS paralyzed the blood vessels in the rodents. Remarkably, the team found that the blood vessels in these mice appeared to work normally once rid of PVM, despite the presence of amyloid-beta. “This showed that without the PVM, amyloid-beta was unable to exert its damaging effects on brain blood vessels,” Park said.
The researchers then sought to learn what caused the PVM to produce ROS. Previous studies showed that macrophages have innate immune receptors on their surface called CD36 that help them bind and interact with other immune cells and proteins. The next step was to determine what happens when CD36 was not present, Iadecola said.
To remove the CD36 receptors from PVM, the researchers first used radiation to destroy the PVM. Then, old PVM were replaced through a bone marrow transplant with new PVM that did not have the receptor.
“When we did that, it was as good as getting rid of the whole macrophage, proving that the presence of CD36 on PVM was necessary for the ROS production and vascular damage to occur,” Iadecola said.
The researchers ultimately discovered that when amyloid beta binds to the CD36 receptor of PVM, a signaling pathway is triggered, which causes an enzyme called NADPH oxidase to produce free radicals.
“It was previously thought that amyloid-beta was going to work its way from the brain into the wall of blood vessels, reaching endothelial cells, which would be the source of the radicals,” Iadecola said. “But in reality, amyloid-beta globs onto the macrophages to activate them. This makes perfect sense because endothelial cells are inside the vessels away from brain amyloid-beta, while PVM are outside the vessel continuously bathed by amyloid-beta coming from the brain.”
Genetic studies have long suggested that the brain’s innate immune cells, like microglia and macrophages, contribute to Alzheimer’s disease, but how these cells damaged the brain was not known. “Our study identifies a novel way in which immune cells could contribute to Alzheimer’s disease, and provide a new therapeutic approach to suppress their damaging effects,” Iadecola said.
Researchers will now seek to develop methods that block CD36 or NADPH oxidase in the cells, which may reduce the amount of amyloid-beta in the brain and potentially slow the progression of Alzheimer’s disease. “Delaying the process may give you more years with a healthy mind,” Iadecola said.
He also added that the maintenance of blood vessel health is crucial for a wide variety of brain diseases. “Our research shows that even in a disease that doesn’t start with a blood vessel, by making the vessels work better, there may be a beneficial effect,” Iadecola said. “Beside Alzheimer’s disease, our study provides us with a new way to look at vascular risk factors that cause stroke and dementia, like hypertension and diabetes, because in these conditions these PVM cells were not previously considered as major players.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Molly Schulson – Cornell University
Image Source: NeuroscienceNews.com image is credited to the researchers.
Original Reserch: Abstract for “Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides” by Laibaik Park, Ken Uekawa, Lidia Garcia-Bonilla, Kenzo Koizumi, Michelle Murphy, Rose Pitstick, Linda H Younkin, Steven G Younkin, Ping Zhou, Geroge A Carlson, Josef Anrather, and Costantino Iadecola in Circulation Research. Published online May 17 doi:10.1161/CIRCRESAHA.117.311054
CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Cornell University “Purpose in Life by Day Linked to Better Sleep at Night.” NeuroscienceNews. NeuroscienceNews, 12 July 2017.
<http://neurosciencenews.com/alzheimers-immune-cells-7069/>.
<http://neurosciencenews.com/alzheimers-immune-cells-7069/>.
Abstract
Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides
Rationale: Increasing evidence indicates that alterations of the cerebral microcirculation may play a role in Alzheimer’s disease (AD), the leading cause of late-life dementia. The amyloid-β peptide (Aβ), a key pathogenic factor in AD, induces profound alterations in neurovascular regulation through the innate immunity receptor CD36, which, in turn, activates a Nox2-containing NADPH oxidase leading to cerebrovascular oxidative stress. Brain perivascular macrophages (PVM) located in the perivascular space, a major site of brain Aβ collection and clearance, are juxtaposed to the wall of intracerebral resistance vessels and are a powerful source of reactive oxygen species (ROS).
Objective: We tested the hypothesis that PVM are the main source of ROS responsible for the cerebrovascular actions of Aβ, and that CD36 and Nox2 in PVM are the molecular substrates of the effect.
Methods and Results: Selective depletion of PVM using intracerebroventricular injection of clodronate abrogates the ROS production and cerebrovascular dysfunction induced by Aβ applied directly to the cerebral cortex, administered intravascularly or overproduced in the brain of transgenic mice expressing mutated forms of the amyloid precursor protein (Tg2576 mice). In addition, using bone marrow chimeras we demonstrate that PVM are the cells expressing CD36 and Nox2 responsible for the dysfunction. Thus, deletion of CD36 or Nox2 from PVM abrogates the deleterious vascular effects of Aβ, whereas wild-type PVM reconstitute the vascular dysfunction in CD36-null mice.
Conclusions: The data identify PVM as a previously unrecognized effector of the damaging neurovascular actions of Aβ and unveil a new mechanism by which brain-resident innate immune cells and their receptors may contribute to the pathobiology of AD.
“Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides” by Laibaik Park, Ken Uekawa, Lidia Garcia-Bonilla, Kenzo Koizumi, Michelle Murphy, Rose Pitstick, Linda H Younkin, Steven G Younkin, Ping Zhou, Geroge A Carlson, Josef Anrather, and Costantino Iadecola in Circulation Research. Published online May 17 doi:10.1161/CIRCRESAHA.117.311054
Lawsuit says California healthcare system discriminates
Lawsuit says California healthcare system discriminatesA lawsuit filed Wednesday alleges that the state’s healthcare system is discriminatory because it provides unequal care to the 13.5 million people who are enrolled in Medi-Cal, the health insurance program for low-income Californians. The suit alleges that Medi-Cal patients face big obstacles in getting timely access to care because the state pays providers so little for their services that many doctors decline to accept Medi-Cal patients. |
Creative Minds: Reprogramming the Brain
Creative Minds: Reprogramming the Brain
by
Caption: Neuronal circuits in the mouse retina. Cone photoreceptors (red) enable color vision; bipolar neurons (magenta) relay information further along the circuit; and a subtype of bipolar neuron (green) helps process signals sensed by other photoreceptors in dim light.
Credit: Brian Liu and Melanie Samuel, Baylor College of Medicine, Houston.
When most people think of reprogramming something, they probably think of writing code for a computer or typing commands into their smartphone. Melanie Samuel thinks of brain circuits, the networks of interconnected neurons that allow different parts of the brain to work together in processing information.
Samuel, a researcher at Baylor College of Medicine, Houston, wants to learn to reprogram the connections, or synapses, of brain circuits that function less well in aging and disease and limit our memory and ability to learn. She has received a 2016 NIH Director’s New Innovator Award to decipher the molecular cues that encourage the repair of damaged synapses or enable neurons to form new connections with other neurons. Because extensive synapse loss is central to most degenerative brain diseases, Samuel’s reprogramming efforts could help point the way to preventing or correcting wiring defects before they advance to serious and potentially irreversible cognitive problems.
When most people think of reprogramming something, they probably think of writing code for a computer or typing commands into their smartphone.
The human brain is wired with a vast number of circuits. They travel winding, contorted paths through the densely packed neurons in the human brain, making them extremely difficult to study. Samuel will start in less expansive and daunting neural terrain.
She has chosen to focus first on synapses in the mouse retina, the complex neural tissue that lines the back of the eye. The retina is also a good place to start because some of its circuits can restructure to help keep them in working order.
As a postdoctoral student, Samuel discovered that two specific proteins are needed to maintain healthy synapses in the retinas of older mice. This suggested it might be possible to target particular molecules and pathways to keep neural cells of the retina connected and doing their job [1]. Because previous studies have shown parallels between pathways in the retina and brain, Samuel began thinking that similar molecules and pathways might exist in the brain.
Melanie Samuel thinks of brain circuits, the networks of interconnected neurons that allow different parts of the brain to work together in processing information.Samuel, a researcher at Baylor College of Medicine, Houston, wants to learn to reprogram the connections, or synapses, of brain circuits that function less well in aging and disease and limit our memory and ability to learn.
She has received a 2016 NIH Director’s New Innovator Award to decipher the molecular cues that encourage the repair of damaged synapses or enable neurons to form new connections with other neurons.
Because extensive synapse loss is central to most degenerative brain diseases, Samuel’s reprogramming efforts could help point the way to preventing or correcting wiring defects before they advance to serious and potentially irreversible cognitive problems.Photo portrait of a smiling young woman ” data-medium-
Now, Samuel will use the New Innovator Award to look for more of these essential proteins in the mouse retina to provide leads for future studies in humans. As part of the effort, Samuel and her colleagues will develop a range of specialized technologies to manipulate and visualize individual synapses in the retina. Among them are state-of-the-art 3D imaging tools that will allow them to map the locations of individual molecules inside a synapse.
In another project, Samuel’s team will systematically examine mice in which genes have been knocked out, or inactivated, one by one in search of those that are involved in wiring the retina. The project is well underway, and they now have a list of several candidate genes for further testing.
Samuel will take her leads in the retina and soon study them within the more complex wiring of the mouse brain. If all goes well, she can begin to test which pathways are responsible for wiring the nervous system and repairing or remodeling synapses. The answers may be complex: her team’s preliminary data suggest that different synapses use distinct molecular codes to regulate the remodeling process. The group has also found that certain parts of a circuit are more flexible structurally, suggesting they might be more amenable to reprogramming.
Samuel and her team have a long way to go. But the details that they discover in the months and years ahead will help to provide a basic understanding of how failing brain circuits might be patched up or reprogrammed. It will exciting to see what they find.
U.S. Says Taxpayers Lost $1.3 Billion in Health-Care Fraud Cases
U.S. Says Taxpayers Lost $1.3 Billion in Health-Care Fraud Cases
ByJuly 13, 2017, 7:22 AM PDT
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Attorney General Jeff Sessions announces nationwide sweep
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Hundreds charged in illegal drug and treatment billing schemes
More than four hundred people were charged in a sweeping crackdown on health-care fraud that cost taxpayers $1.3 billion, in part through bogus treatment programs that contributed to the country’s opioid epidemic, Attorney General Jeff Sessions said on Thursday.
Sessions called the nationwide takedown the largest in U.S. history, with doctors and other individuals charged for improperly prescribing and distributing opioids and other narcotics and billing Medicaid and Medicare. Of the 412 people charged, 56 were doctors and 120 cases were related to opioids, Sessions said. Arrests were made in cities including Chicago, Detroit, Los Angeles and Miami, as well as in southern Florida, which is home to hundreds of residential drug addiction treatment centers.
“Too many trusted medical professionals like doctors and nurses and pharmacists have chosen to violate their oaths and put greed ahead of their patients,” said Sessions, speaking at a press conference at the Justice Department in Washington. “Amazingly, some have made the practices into multimillion dollar criminal enterprises. They seem oblivious to the disastrous consequences of their greed.”
Federal prosecutors, some of whom have been working on cases for a year or more, were directed to accelerate their efforts in time for Thursday’s announcement, a person familiar with the matter said. The Government Accountability Office did an investigation and found last year that the sign-up process for the Affordable Care Act exchanges was “vulnerable to fraud.”
Obamacare Fight
The health-care fraud takedown comes as a fight brews in Congress over how much money to allot for opioid treatment and as Republicans spar over how to repeal or replace the ACA. Some Republicans want more funding to help states combat the opioid addiction epidemic, which is estimated to have killed 33,000 Americans last year. Changes to a Senate bill expected to be released later Thursday may include more money, but it’s unclear if it will secure the 50 votes needed to pass.
More than 500,000 people received high amounts of opioid painkillers out of the 43.6 million who were signed up for Medicare’s optional prescription drug benefit last year, according to a report on opioid use released Thursday by the Office of Inspector General for the Department of Health and Human Services, which investigates waste, fraud and abuse in government health programs, including Medicare and Medicaid. A high amount is considered equivalent to 12 Vicodin 10 milligram tablets or 16 Percocet 5 milligram pills a day for at least three months.
The report also identified 401 doctors who had questionable prescribing practices and were either giving opioids to patients who already received a high number or those who appeared to be doctor shopping. Those doctors wrote a total of 256,260 opioid prescriptions at risk of abusing the painkillers, costing Medicare $66.5 million. Oxycodone was the most commonly prescribed opioid.
Opioid Epidemic
More than 33,000 Americans died from opioid overdoses in 2015, according to the National Institute on Drug Abuse. About 19,000 of those deaths are linked to heroin and synthetic opioids such as fentanyl. The overdose numbers are typically updated at the end of the year.
Southern Florida has the biggest concentration of residential treatment centers in the country — hundreds are based mainly in single-family homes in and around Delray Beach, a small town in Palm Beach County, north of Miami. A December 2016 grand jury report commissioned by the State Attorney for Palm Beach County found addiction treatment centers to be rife with operators who use deceptive marketing, illegal patient brokering and fraudulent insurance claims to profit from addicts.
Fraudulent claims became so rampant that Cigna Corp., the fourth-biggest U.S. health insurer, quit Florida’s Obamacare market in the fall of 2015, ahead of the sign-up period for 2016 plans. At the time, the company blamed fraudulent and abusive practices by drug-treatment centers for driving up its costs.
‘Category 5 hurricane’: White House under siege by Trump Jr.’s Russia revelations
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GOP Makes Horrifying Announcement About Trump’s Wall
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