Cryonics  

The Freeze Phil Campaign has been incubating for some time but was formally started, finally, in October 2012. The goal of this project is a legal, "Pre-Mortem Cryonic Suspension" for Philip Rhoades at an appropriate time and place for him and of his own choosing. The plan is to build a substantial campaign to force legislative change that will allow people more flexibility about their end of (current) life decisions ie in short, to allow people a legal "Pre-Mortem Cryonic Suspension."

My father died last year at age 89.  The last couple of decades of his life were worse than they should have been because of Alzheimer's Disease (AD).  Now, Dad's younger brother (my uncle) is in a similar state to Dad when he was the same age.  Clearly, most of the problem with AD is (epi)genetically-based.  I am fairly confident that if Homo sapiens can deal with our self-destructive tendencies and survive the Sixth Mass Extinction AND maintain current scientific and technological progress for another few decades - then there will almost certainly be early treatments to prevent the onset of AD - as well as treatments to reverse the symptoms of people already affected by AD. However, it will most likely be too late for me.

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There is not much doubt I am going down the same path as my father, uncle and other ancestors.  For two decades I have been active in Life Extension efforts including Cryonics and Neural Archives - but those last options for extending life (albeit involving a technological "resurrection" in the future) depends on the information in the brain being well enough preserved that there remains a "person" in the liquid nitrogen to reanimate.  In Australia, it is not a crime to kill yourself.

"I am looking for people who are interested in the project as I have outlined to help me develop some sort of Open Source project that will allow me to evolve Phi Rho from a simple (though amusing) chatbot to an entity that can increasingly act on my behalf."

 If, pre-mortem, you can be be cooled to -196C you are then legally "dead" (in Cryonics terms you are a "patient"). However there is great risk for anyone who helps you to get to that state.  I have been exploring options around that particular hurdle but the problem of continuing cognitive decline remains.  I do what I can to slow down the process.

There is, however, something else that I have been working on which I think will help me deal with my predicament.  A few years ago I bought a licence for the chatbot that won the 2012 Loebner Prize. Because of various health crises within the family I wasn't able to finish setting up a modified version of this chatbot for what I had intended at the time.  Now, I think I have a better use for it.  The homonid brain evolved, like other anatomical features, by duplication and divergent specialisation of various parts.  In a similar way, I think I can evolve my chatbot Avatar, Phi Rho, into something more.  I need to replace his current crude, quick-and-dirty memory of previous conversations with something more robust and scaleable and then I need to start adding AI and other modules as well as data dumps from the current wetware so Phi Rho becomes more and more like me.  If I can evolve Phi Rho into being what will eventually become a Distributed Autonomous Entity (DAE) with the evolutionary imperative of eventually scanning and decoding the information in the frozen brain of the original biological person (me) - then, over the next few years, there should be some protection from loss of information from dementia and freezing damage etc of the original biological brain.

Image Source - Jim Trifyllis/News Corp Australia

Since I retired last year, I don't have the resources that I used to have to pay developers etc to do the work that is too difficult or too slow for me do - so now I am looking for people who are interested in the project as I have outlined to help me develop some sort of Open Source project that will allow me to evolve Phi Rho from a simple (though amusing) chatbot to an entity that can increasingly act on my behalf - so that by the time my "Freeze By" date is up (scheduled for 2020 unless there are dramatic developments in the treatment and reversal of AD), there will be something of me that will be able to carry on in the world and which has an interest in the development of scanning technology that will, fundamentally, eventually, allow brain uploading and virtual people.

Links for further information:

http://freezephil.org
https://www.facebook.com/PhiRhoChat
http://philiprhoades.org

So if you are interested in this project and have some IT, AI etc ideas regarding a three-year development strategy for enhancing Phi Rho and are prepared to be involved (even if it is only to contribute constructive suggestions) then please feel free to contact me.  I can't promise any payment at the moment but the situation may change somewhat in the near future.  In the first place I am looking for Java people to upgrade Phi Rho's memory.

See you in the future.

By  Philip Rhoades	Embed
Philip Rhoades is an Executive Officer at the Cryonics Association of Australasia (http://cryonics.org.au), Executive Director, Neural Archives Foundation (http://neuralarchivesfoundation.org) as well as a member of the LifeBoat Foundation (http://lifeboat.com).

Medical Technology  

Medical technology is constantly changing, and with it, we are introduced to more and more medical advancements each year. While great strides are being made in the world of medical robotics, there is also major advancement in the treatment and monitoring of cardiac disease, diabetes, and neurological conditions such as Alzheimer's disease that are becoming more commonplace in the population.

2017 has been no different in regard to medical advancements hitting the market. While some products are in the final stages of testing some of these devices are expected to hit the market in 2017 as soon as early spring. Listed below are five of the most amazing medical devices coming to the market this year.

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Thoratec's HeartMate

After St. Jude acquired Thoratec in 2015 it continued the production of the Thoratec's HeartMate. HeartMate is a left ventricular assist device. The assist device technology is used on cardiac patients in heart failure to help their heart continue to perform until they are able to receive a transplant. The device not only helps prolong the heart's function but helps keep the patient's body functioning well enough to be able to accept a transplant. The HeartMate is currently in the approval stage and since it is part way through the 12-month process, it is expected to be released by the end of 2017.

Medtronic's MinMed 670G System

Medtronic has come out with the MiniMed 670G as a closed loop system for personal insulin delivery. This system is the first hybrid closed loop and has been touted as the first artificial pancreas. The system helps to keep patient in their targeted glucose level for the longest amount of time throughout the day. The system received FDA approval in fall of 2016 and is expected to be manufactured and launched in spring of 2017.

Lotus Edge Transcatheter Aortic Valve

Created by Boston Scientific, the Lotus Edge Transcatheter Aortic Valve is the next generation of aortic valves. The Lotus Edge not only can be repositioned and retrieved once the patient has received the implant, but it provides for less chance of a chance of a pacemaker implant and paravalvular leak. The company is expected to go before the FDA for approval in May of this year and the manufacturers anticipate production in sizes including 21, 23, 25, and 27.

Johnson and Johnson OneTouch Via Insulin Delivery

Calibra Medical, a Johnson and Johnson Diabetes Care Company created the OneTouch Via On-Demand Delivery System to deliver insulin to the user easily and discreetly. It is worn on the abdomen and delivers a consistent quantity of insulin painlessly. The device is also discreetly wearable under the patient's clothing and has already been sent for FDA approval and it is expected to hit the market sometime this year.

Neuronex neuroAD Therapy System

Neuronex Medical has developed the neuroAD Therapy System for patients who suffer from Alzheimer's disease. The device utilizes cognitive therapy combined with focused transcranial magnetic stimulation, also referred to as TMS. The therapy produced by the device is created to help repair cognitive function in the brain. Neuronex neuroAD is still currently in the FDA testing phase, but the company is hoping to have the therapy approved by the end of the year.

Whether you are looking for advancements in the fields of neurology, cardiovascular health, or endocrinology, 2017 has advancements to help treat many of the conditions facing the population today. While the five devices listed above are some amazing medical advances hitting the market this year, there are much more in the early stages of testing that we will see emerge in the next few years. As medical technology continues to advance so will the ability to treat and fight disease. Whether it’s a medical document storage system like Integrity Support or a new kind of insulin pump, these are the technologies looking to change the way disease is fought.

By  Eileen O'Shanassy	Embed

Alzheimer's Disease  

A study has found concussions accelerate Alzheimer's disease-related brain atrophy and cognitive decline in people who are at genetic risk for the condition. The results demonstrate the importance of documenting head injuries even within the mild range as they may interact with genetic risk to produce negative long-term health consequences such as neurodegenerative disease.

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New research has found concussions accelerate Alzheimer’s disease-related brain atrophy and cognitive decline in people who are at genetic risk for the condition. The findings, which were published in the journal Brain, show promise for detecting the influence of concussion on neurodegeneration.

Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for developing neurodegenerative diseases such as late-onset Alzheimer’s disease, although it is unclear whether mild traumatic brain injury or concussion also increases this risk.

"Having a concussion was associated with lower cortical thickness in brain regions that are the first to be affected in Alzheimer’s disease."

Researchers from Boston University School of Medicine (BUSM) studied 160 Iraq and Afghanistan war veterans, some who had suffered one or more concussions and some who had never had a concussion. The researchers used MRI imaging, to determine the thickness of their cerebral cortex in seven regions that are the first to show atrophy in Alzheimer’s disease, as well as seven control regions.

“We found that having a concussion was associated with lower cortical thickness in brain regions that are the first to be affected in Alzheimer’s disease,” explained corresponding author Jasmeet Hayes, PhD, assistant professor of psychiatry at BUSM and research psychologist at the National Center for PTSD, VA Boston Healthcare System. “Our results suggest that when combined with genetic factors, concussions may be associated with accelerated cortical thickness and memory decline in Alzheimer’s disease relevant areas.”

The researchers found that these brain abnormalities were found in a relatively young group, with the average age being 32 years old. “These findings show promise for detecting the influence of concussion on neurodegeneration early in one’s lifetime, thus it is important to document the occurrence and subsequent symptoms of a concussion, even if the person reports only having their “bell rung” and is able to shake it off fairly quickly, given that when combined with factors such as genetics, the concussion may produce negative long-term health consequences,” said Hayes.

The researchers hope that others can build upon these findings to find the precise concussion-related mechanisms that accelerate the onset of neurodegenerative diseases such as Alzheimer’s disease, chronic traumatic encephalopathy, Parkinson’s and others. “Treatments may then one day be developed to target those mechanisms and delay the onset of neurodegenerative pathology,” she added.

SOURCE  Science Daily

By  33rd Square

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Technology  

With Pokemon Go taking over nearly everyone's social feeds in the last week, 2016 will probably be looked back as a watershed moment for augmented reality technology. The year so far has also featured the rise of some other very important technology. Here are a few examples.

One thing that is certainly progressing at lightning fast speed is computer technology. New tech is constantly being released. As we saw with smartphones some years ago, new computer technology can fundamentally change the way people live. Below are some of the newest innovations in computer technology introduced in 2016 that are certain to make big waves soon.

A Digital Monitor of Alzheimer’s

As many people know, Alzheimer’s is a terrible disease that can cause elderly patients to lose their memory, personality and basic brain functions. However, thanks to a new application for computer tech, a cure may not be far off. This year, scientists have begun implementing artificial intelligence computer programs when analyzing MRI brain scans. The AI has the ability to detect which patients have early signs of Alzheimer’s with a remarkable degree of accuracy. This will allow doctors to begin treating those at risk for the disease much earlier than would have been the case without this technology.

Printed Circuit Boards

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Another piece of computer technology that has been garnering a lot of attention in 2016 is printed circuit boards, or PCBs. PCBs are created by adding copper tracks to glass fabricated plastic. The copper tracks act as a replacement for wiring from which components can be attached after holes are drilled into the board. PCBs are expected to be manufactured to be thinner and more compact with each passing year. With technology from companies like Streamline Circuits, printed circuit boards are making the inner workings of computers more versatile as time goes by.

Virtual Reality Could Solve Real Life Problems

Perhaps the technology making the biggest splash in 2016 is virtual reality. After years of VR only being the thing of science fiction, the tech is finally here. However, what you may not know is that VR may have some great applications for solving practical problems. Researchers at New York University in fact believe that the immersive simulations and collaborative learning that virtual reality can make possible could be applied towards tackling drug abuse and predicting climate change.

Wireless Charging

Most people today use computers in the form of smartphones and tablets. However, the days of traditional chargers for these devices may be soon over. New computer tech will soon be released that will allow these devices to be charged wirelessly. In fact, placing two smartphones using this new tech next to each other will allow them to share power and recharge each other.New technological developments are being introduced at a blinding pace. As new gadgets and computer tech make their way into our homes, they are certain to change our lives in unforeseen ways for the better.

By Dixie Somers

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Aging  

A vaccine to prevent and even reverse the early stages of Alzheimer's and dementia could be tested on humans within the next two to three years according to researchers in Australia. 

Researchers from South Australia's Flinders University have been working with US counterparts at the Institute of Molecular Medicine and University of California to develop the vaccine, which targets proteins in the brain that block neurons.

Flinders University medicine professor Nikolai Petrovsky said that over time, two proteins in the brain, amyloid-beta (a-beta) and tau, broke down and caused the condition. He told The Australian that the breakthrough was so significant, there was confidence it would eventually be used as a preventive vaccine, much like a flu shot, that could eradicate dementia.

The study has been published recently in the journal Nature Scientific Reports.

"Interestingly the second protein, which has been found more recently, which we are targeting … it turns out if you target tau with the vaccine you can actually reverse the disease even once it has developed"

"[The proteins are] a bit like the car in your driveway. You need to remove them from the brain otherwise if you left broken down cars in your driveway eventually you couldn't get out," he said. "Essentially that's what happens in people who get Alzheimer's or dementia is they have lots of these broken down proteins in the brain.

"Essentially what we have designed is a vaccine that makes the immune system produce antibodies and those antibodies act like tow trucks so they come to your driveway, they latch on to the breakdown protein or car and they pull it out of the driveway."

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"So by developing a vaccine against a-beta it seems to work in the animals best if you give it before they get Alzheimer's or dementia and it doesn't work so well once they have developed the disease," he said.

"Interestingly the second protein, which has been found more recently, which we are targeting … it turns out if you target tau with the vaccine you can actually reverse the disease even once it has developed."

Professor Petrovsky said having a vaccine targeting both proteins was a key feature.

"Given the demand for a vaccine, if we show it is successful in the early stages we expect this will be pulled through and turned into product very, very quickly."

"It could be used both to give people at a particular age, say 50 years of age when they are perfectly fine, to stop them developing dementia, but potentially also could be given to people at least in the early stages of dementia to actually try and reverse the process," he said.

He said the vaccine was being "bankrolled by the world's biggest government" and unless researchers hit a roadblock it would be tested on humans within the next two to three years.

"Certainty the US Government is very committed to this program; this year they have allocated $1 billion for research into treatments of Alzheimer's including our vaccine," he said.

SOURCE  ABC Online

By 33rd Square

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Alzheimer's Disease  

Being a caregiver for an individual with Alzheimer’s is a loving, selfless act, but it comes with its share of stress and challenges. However, there are many ways to make the experience feel less overwhelming. Here are a few tips caregivers can try to make the journey a little easier.

Someone in the United States develops Alzheimer’s every 67 seconds. As the disease progresses, it becomes increasingly difficult for sufferers to care for themselves, and oftentimes a loved one steps in to help with day-to-day life.

Being a caregiver for an individual with Alzheimer’s is a loving, selfless act, but it comes with its share of stress and challenges. However, there are many ways to make the experience feel less overwhelming. Here are a few tips caregivers can try to make the journey a little easier:

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Know the early indicators

Absentmindedness is not the same as clinically-diagnosed Alzheimer’s disease or dementia. Knowing the difference between normal forgetfulness (like not recalling the name of a new acquaintance or a recently-visited restaurant) and a regular pattern of inability to retain information that impacts daily life (such as a medication schedule or even personal hygiene habits) can help caregivers identify when to seek additional medical treatment. This list helps distinguish between harmless “senior moments” that come with aging and red flags that Alzheimer’s may be progressing.

Plan some activities

"No matter what, caring for those who can no longer care for themselves is a tremendously compassionate act, and you have already made their lives better simply by bearing that responsibility."

An Alzheimer’s diagnosis shouldn’t feel like a jail sentence for caregivers or their ailing loved one. Planning some fun things to do inside and outside the home can break up the humdrum of trying to get through the day. Going outside by visiting the park, stopping by a local museum, or making a trek to a place that holds fond memories may provide both of you a break from the monotony that this disease sometimes imposes upon people.

Adjust your approach to communication

Severe memory impairment and mood swings are characteristics of the illness that can put a wrench in communication skills. Trying to remain patient is the first step in learning how to cope with these changes. This article from the National Institute on Aging offers other helpful advice for making the transition as smooth as possible, such as maintaining eye contact, being aware of body language, and encouraging a mutual conversation as often as possible.

Consider a four-legged friend

This guide demonstrates how special service dogs may help treat Alzheimer’s symptoms, and provide assistance to caregivers who are juggling other responsibilities such as careers and raising a family. Having a dog, even one who hasn’t received the rigorous training required to be classified as a service or therapy dog, may still provide emotional benefits to caregivers and their loved ones.

An Alzheimer’s diagnosis can feel like a devastating blow to sufferers and their loved ones. However, there are many things you can do as a caregiver to help make daily life a little less stressful for both of you. It’s also important to remember that no matter what, caring for those who can no longer care for themselves is a tremendously compassionate act, and you have already made their lives better simply by bearing that responsibility.


Top Image via Pixabay

By Vee Cecil

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Author Bio - Vee Cecil is a wellness coach, personal trainer, and bootcamp instructor. Vee is passionate about studying and sharing her findings in wellness through her recently-launched blog.

 Aging  

A study tying the aging process to the deterioration of tightly packaged bundles of cellular DNA could lead to methods of preventing and treating age-related diseases such as cancer, diabetes and Alzheimer's disease.

Astudy tying the aging process to the deterioration of tightly packaged bundles of cellular DNA could lead to methods of preventing and treating age-related diseases such as cancer, diabetes and Alzheimer’s disease, as detailed in Science.

In the study, scientists at the Salk Institute and the Chinese Academy of Science found that the genetic mutations underlying Werner syndrome, a disorder that leads to premature aging and death like progeria, resulted in the deterioration of bundles of DNA known as heterochromatin.

The discovery, made possible through a combination of cutting-edge stem cell and gene-editing technologies, could lead to ways of countering age-related physiological declines by preventing or reversing damage to heterochromatin.

The top image shows normal human cells (left) and genetically modified cells developed by the Salk scientists to model Werner syndrome (right), which showed signs of aging, including their large size.

“Our findings show that the gene mutation that causes Werner syndrome results in the disorganization of heterochromatin, and that this disruption of normal DNA packaging is a key driver of aging,” says Juan Carlos Izpisua Belmonte, a senior author on the paper. “This has implications beyond Werner syndrome, as it identifies a central mechanism of aging–heterochromatin disorganization–which has been shown to be reversible.”

Werner syndrome is a genetic disorder that causes people to age more rapidly than normal. It affects around one in every 200,000 people in the United States. People with the disorder suffer age-related diseases early in life, including cataracts, type 2 diabetes, hardening of the arteries, osteoporosis and cancer, and most die in their late 40s or early 50s.

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The disease is caused by a mutation to the Werner syndrome RecQ helicase-like gene, known as the WRN gene for short, which generates the WRN protein. Previous studies showed that the normal form of the protein is an enzyme that maintains the structure and integrity of a person’s DNA. When the protein is mutated in Werner syndrome it disrupts the replication and repair of DNA and the expression of genes, which was thought to cause premature aging. However, it was unclear exactly how the mutated WRN protein disrupted these critical cellular processes.

"Accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging. This begs the question of whether we can reverse these alterations–like remodeling an old house or car–to prevent, or even reverse, age-related declines and diseases."

In their study, the Salk scientists sought to determine precisely how the mutated WRN protein causes so much cellular mayhem. To do this, they created a cellular model of Werner syndrome by using a cutting-edge gene-editing technology to delete WRN gene in human stem cells. This stem cell model of the disease gave the scientists the unprecedented ability to study rapidly aging cells in the laboratory. The resulting cells mimicked the genetic mutation seen in actual Werner syndrome patients, so the cells began to age more rapidly than normal. On closer examination, the scientists found that the deletion of the WRN gene also led to disruptions to the structure of heterochromatin, the tightly packed DNA found in a cell’s nucleus.

This bundling of DNA acts as a switchboard for controlling genes’ activity and directs a cell’s complex molecular machinery. On the outside of the heterochromatin bundles are chemical markers, known as epigenetic tags, which control the structure of the heterochromatin. For instance, alterations to these chemical switches can change the architecture of the heterochromatin, causing genes to be expressed or silenced.

The Salk researchers discovered that deletion of the WRN gene leads to heterochromatin disorganization, pointing to an important role for the WRN protein in maintaining heterochromatin. And, indeed, in further experiments, they showed that the protein interacts directly with molecular structures known to stabilize heterochromatin–revealing a kind of smoking gun that, for the first time, directly links mutated WRN protein to heterochromatin destabilization.

“Our study connects the dots between Werner syndrome and heterochromatin disorganization, outlining a molecular mechanism by which a genetic mutation leads to a general disruption of cellular processes by disrupting epigenetic regulation,” says Izpisua Belmonte. “More broadly, it suggests that accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging. This begs the question of whether we can reverse these alterations–like remodeling an old house or car–to prevent, or even reverse, age-related declines and diseases.”

Izpisua Belmonte added that more extensive studies will be needed to fully understand the role of heterochromatin disorganization in aging, including how it interacts with other cellular processes implicated in aging, such as shortening of the end of chromosomes, known as telomeres. In addition, the Izpisua Belmonte team is developing epigenetic editing technologies to reverse epigenetic alterations with a role in human aging and disease.

SOURCE  Salk Institute for Biological Studies

By 33rd Square

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 Alzheimer's Disease  

Researchers discovered an innovative drug-free approach breaks apart the neurotoxic amyloid plaques associated with Alzheimer's. Human clinical trials, are at least two years away.

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cientists have found that non-invasive ultrasound technology can be used to treat Alzheimer’s disease and restore memory. University of Queensland researchers discovered that the innovative drug-free approach breaks apart the neurotoxic amyloid plaques that result in memory loss and cognitive decline.

The findings were published in the journal Science Translational Medicine.

Queensland Brain Institute Founding Director Professor Perry Bartlett said the discovery – a result of ‘game-changing’ work performed at the institute's Clem Jones Centre for Ageing Dementia Research – was made possible through the support of the State and Federal Governments and philanthropic support led by the Clem Jones Foundation.

“I believe the work opens up an entirely novel avenue for future therapeutic treatment.”

"The word ‘breakthrough’ is often mis-used, but in this case I think this really does fundamentally change our understanding of how to treat this disease, and I foresee a great future for this approach."

Clem Jones Centre for Ageing Dementia Research director Professor Jürgen Götz said the new treatment method could revolutionize Alzheimer’s treatment by restoring memory.

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“We’re extremely excited by this innovation of treating Alzheimer’s without using drug therapeutics,” Professor Götz said.

“The ultrasound waves oscillate tremendously quickly, activating microglial cells that digest and remove the amyloid plaques that destroy brain synapses. The word ‘breakthrough’ is often mis-used, but in this case I think this really does fundamentally change our understanding of how to treat this disease, and I foresee a great future for this approach.”

“With an ageing population placing an increasing burden on the health system, an important factor is cost, and other potential drug treatments using antibodies will be expensive,” Professor Götz said.

“In contrast, this method uses relatively inexpensive ultrasound and microbubble technology which is non-invasive and appears highly effective.

The approach is able to temporarily open the blood-brain barrier, activating mechanisms that clear toxic protein clumps and restoring memory functions.

“With our approach the blood-brain barrier’s opening is only temporary for a few hours, so it quickly restores its protective role,” Professor Götz said.

Research has been conducted using mice with an Alzheimer’s model, with the next step being to scale the research in higher animal models ahead of human clinical trials, which are at least two years away.

“This treatment restored memory function to the same level of normal healthy mice,” Professor Götz said.

“We’re also working on seeing whether this method clears toxic protein aggregates in neurodegenerative diseases other than Alzheimer’s and whether this also restores executive functions, including decision-making and motor control.”


SOURCE  University of Queensland

By 33rd Square

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 Medicine  

In the developed world it is often easy to take medical care for granted.  Here are a few of the ways doctors are changing the world by preventing diseases and helping injured patients.

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oday, people have forgotten that there was a time before there were physicians available to treat illnesses and injuries. While everyone may see shows on television depicting physicians working in hospitals and private practices, they forget that doctors are changing the world in numerous ways to prevent diseases and assist injured patients. The world of medicine has changed since the time of bloodletting to get rid of an illness or operating on patients without anesthesia.

Offering Charitable Medical Care

In many parts of the world there is no access to medical care, leading to the public having simple problems that are easily fixed but are untreated. While in the United States a child with a cleft palate or lip is operated on quickly, in third world countries, there is no access to surgeons to correct this common congenital defect. Nonprofit health care and medical organizations provide surgical procedures to repair congenital defects with volunteer physicians worldwide.

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Getting Involved in Politics

Physicians are getting involved in politics to make changes in how the government views health care for the public. In the United States, physicians have always had a presence in the government with approximately 20 currently serving as members of the United States Congress. They are often instrumental in helping other politicians understand the high cost of health care and how it is inaccessible to many citizens. The physicians serving in political roles are trained in a wide assortment of specialties, leading to providing vital information to the public.

More Physician Owned Hospitals

With many physicians frustrated with the bureaucracy involved in medical care in the United States, many are grouping together to control their own medical facilities. These physicians want to advocate for better medical care for patients rather than constantly worrying about the cost of treatments and insurance. Patients give physician owned medical facilities, like Nueterra, high scores for personalized treatment that indicates the hospital really cares about patients.

Promoting New Medical Treatments

Physicians work directly with patients and medical conditions, making them the best professionals to think of new medical treatments. Instead of new surgical techniques and treatments being inventing by researchers in a laboratory, physicians are taking the lead by devising unique solutions for devastating diseases such as cancer, acquired immune deficiency disorder and Alzheimer’s disease. Finding a cure for medical conditions is what many physicians did long ago before bureaucrats changed the system.

The Public Wants Physician Owned Hospital Medical Care

Many physicians are fighting for their rights to operate hospitals despite the government’s plans to make it more difficult. With the government taking control of more health care insurance plans, there are new regulations in place to make it harder for physician owned hospitals to receive reimbursements. The general public is voicing their opinions concerning these regulations because they want a higher level of medical care.

By Meghan Belnap

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 Aging  

People aged 80 and above, but with memories that are as sharp as those of healthy persons decades younger—SuperAgers—have distinctly different brains than those of normal people, according to new imaging and analysis.

SuperAgers, aged 80 and above, have distinctly different looking brains than those of normal older people, according to new research. The work is the initial stages of revealing why the memories of these cognitively older individuals don’t seem to suffer the usual effects of aging.

SuperAgers have memories that are as sharp as those of healthy persons decades younger.

Understanding their unique “brain signature” will enable scientists to decipher the genetic or molecular source and may foster the development of strategies to protect the memories of normal aging persons as well as treat dementia.

Published 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 University’s Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University Feinberg School of Medicine.

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Their typical brain signature has three common components when compared with normal persons of similar ages: a thicker region of the cortex; significantly fewer tangles (a primary marker of Alzheimer’s disease) and a whopping supply of spindle neurons, also called, von Economo neurons (VENs), which have been linked to higher social intelligence.

VEN cells are also present in such species as whales, elephants, dolphins and higher apes.

“The brains of the SuperAgers are either wired differently or have structural differences when compared to normal individuals of the same age,” said Changiz Geula, study senior author and a research professor at the Cognitive Neurology and Alzheimer’s Disease Center. “It may be one factor, such as expression of a specific gene, or a combination of factors that offers protection.”

“Identifying the factors that contribute to the SuperAgers’ unusual memory capacity may allow us to offer strategies to help the growing population of ‘normal’ elderly maintain their cognitive function and guide future therapies to treat certain dementias,” said Tamar Gefen, the first study author and a clinical neuropsychology doctoral candidate at Feinberg.

"Identifying the factors that contribute to the SuperAgers’ unusual memory capacity may allow us to offer strategies to help the growing population of ‘normal’ elderly maintain their cognitive function and guide future therapies to treat certain dementias."

MRI imaging and an analysis of the SuperAger brains after death show the following brain signature:

MRI imaging showed the anterior cingulate cortex of SuperAgers (31 subjects) was not only significantly thicker than the same area in aged individuals with normal cognitive performance (21 subjects), but also larger than the same area in a group of much younger, middle-aged individuals (ages 50 to 60, 18 subjects). This region is indirectly related to memory through its influence on related functions such as cognitive control, executive function, conflict resolution, motivation and perseverance. 

Analysis of the brains of five SuperAgers showed the anterior cingulate cortex had approximately 87 percent less tangles than age-matched controls and 92 percent less tangles than individuals with mild cognitive impairment. The neurofibrillary brain tangles, twisted fibers consisting of the protein tau, strangle and eventually kill neurons. 

The number of von Economo neurons was approximately three to five times higher in the anterior cingulate of SuperAgers compared with age-matched controls and individuals with mild cognitive impairment.

 “It’s thought that these von Economo neurons play a critical role in the rapid transmission of behaviorally relevant information related to social interactions,” Geula said, “which is how they may relate to better memory capacity.”

Studies like this, will probably have you ask what it takes to be among the SuperAgers. Unfortunately, there aren't yet any clear answers, Emily Rogalski, an assistant research professor at Northwestern has said.

"Genetics are likely to play a role. And, in general, a healthy lifestyle is supportive of good memory. But in our experience, some of our SuperAgers have been smoking a pack of cigarettes for the last 20 years. Others have never touched them. Some go to the gym three to five days a week. Others don't exercise. Some are still working and others have never worked. It seems there might be more than one route to being a SuperAger."


SOURCE  Northwestern University

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 Neuroscience  

Researchers  have uncovered a new memory regulator in the brain involving adenosine receptors, which may offer a potential treatment to improve memory in Alzheimer’s disease.

S
cientists from the Gladstone Institutes have shown that decreasing the number of A2A adenosine receptors in a particular type of brain cells called astrocytes improved memory in healthy mice. What’s more, reducing receptor levels also prevented memory impairments in a mouse model of Alzheimer’s disease.

The study has been published in Nature Neuroscience, the findings suggest that astrocytes—star-shaped cells that are abundant in the brain and support neuronal function—are important regulators of information storage, and their dysfunction might lead to memory decline in disease.

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“Our findings have provided us not only with a new perspective on the role of astrocytes in cognition, but also with an exciting drug target to enhance memory and maybe even stave off memory decline in Alzheimer’s disease,” says senior author Lennart Mucke, MD, director of the Gladstone Institute of Neurological Disease and professor of neurology and neuroscience at the University of California, San Francisco. “Next, we will explore the therapeutic implications of our discovery by repurposing available drugs that block these adenosine receptors and are well tolerated in humans.”

"Our findings have provided us not only with a new perspective on the role of astrocytes in cognition, but also with an exciting drug target to enhance memory and maybe even stave off memory decline in Alzheimer’s disease."

The researchers focused on astrocytes after their initial finding that patients with Alzheimer’s disease have unusually high numbers of adenosine receptors in these cells. However, whether this increase was linked to cognitive ability was unknown. solve this mystery, the scientists generated mice with normal or reduced levels of A2A receptors in astrocytes and compared them on tests of learning and memory.

While the mice showed no differences in learning, those that had fewer adenosine receptors performed better on tests of long-term memory. Moreover, reducing the number of receptors improved memory in older mice that often have memory deficits.

Taking this one step further, the researchers performed the same experiments in a mouse model of Alzheimer’s disease to see if these astrocytic adenosine receptors were also involved in memory loss associated with the disease. Once again, decreasing the number of receptors improved memory, even in the presence of amyloid plaques characteristic of Alzheimer’s.

The scientists say that they were surprised the effect of manipulating astrocytes was restricted to long-term memory with no changes occurring in learning or general behaviors. “Given the many roles of astrocytes in the brain, one might expect a global disruption of brain function,” says lead author Anna Orr, PhD, a staff scientist at Gladstone. “Instead, we see a very specific effect on memory retention.”

SOURCE  Gladstone Institutes

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 Alzheimer's Disease  

Microglia cells in the brain chew up toxic substances and cell debris, calm inflammation and make nerve-cell-nurturing substances. New research shows that keeping them on the job may prevent neurodegeneration and Alzheimer's disease.

Alzheimer's could be prevented and even cured by boosting the brain's own immune response, scientists at Stanford University believe.

Researchers discovered that nerve cells die because cells which are supposed to clear the brain of bacteria, viruses and dangerous deposits, stop working.

These specialized nerve cells, called microglia make up about 10-15 percent of all the cells in the brain, actually resemble immune cells considerably more than they do nerve cells. Microglia function properly when people are young, but when they age, a single protein called EP2 stops them operating efficiently.

"Microglia are the brain’s beat cops. Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology."

Now scientists have shown that blocking EP2 allows the microglia to function normally again so they can deal with amyloid-beta plaques which damage nerve cells in Alzheimer's disease.
The researchers found that, in mice, blocking EP2 with a drug reversed memory loss and myriad other Alzheimer’s-like features in the animal models.

“Microglia are the brain’s beat cops,” said Dr Katrin Andreasson, Professor of neurology and neurological sciences at Stanford University School of Medicine.

“Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology.”

The study has been published in the Journal of Clinical Investigation.

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Microglial cells are the front-line soldiers of the brain, monitoring their surroundings for suspicious activities and materials by probing its local environment. If they spot trouble, microglia release substances that recruit other microglia to the scene, said Andreasson.

Microglia protect the brain against invading bacteria and viruses by gobbling them up also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells including clusters of amyloid-beta which aggregate as gummy deposits and break the connections between neurons, causing loss of memory and spatial awareness. These clusters are believed to play a substantial role in causing Alzheimer’s.

“The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation,” added Dr Andreasson. “If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation.”

The scientists discovered that in young mice, the microglia kept the sticky plaques under control. But when experiments were done on older mice, the protein EP2 swung into action and stopped the microglia producing enzymes which digested the plaques.

Similarly mice which were genetically engineered not to have EP2 did not develop Alzheimer's disease, even when injected with a solution of amyloid-beta, suggesting that their cells were getting rid of the protein naturally.

In the mice who developed Alzheimer's-like disease, blocking EP2 reversed memory decline.
Now Stanford is hoping to produce a compound which only blocks EP2 to prevent unnecessary side effects.


SOURCE  Stanford University Top Image Hagop Kaneboughazian

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