The Myopia Pandemic

August 28, 2015 by

Aug. 28, 2015

By Medical Discovery News

The Myopia Pandemic

You’ve probably heard of pandemics – the plague, influenza, HIV – but you might not have seen coverage of the growing myopia pandemic. Before you consider bathing in sanitizer, you should know that myopia isn’t contagious. Another word for it is nearsightedness.

Myopia is a condition in which close objects are seen clearly but distant objects are blurred due to the elongation of the eye or too much curvature of the cornea. This causes light entering the eye focusing in front of the retina rather than on it. Myopia is different than hyperopia, which is the kind of nearsightedness that comes from growing older. In fact, the myopia pandemic is primarily affecting young people.

It currently affects 90 percent of the young adults in China, although 60 years ago it was 10-20 percent. In the United States and Europe it affects about half of all young adults, double what it was 50 years ago. Seoul has the highest incidence: 96.5 percent of young people in South Korea’s capital have myopia. An estimated 2.5 billion people will experience myopia by 2020.

Vision issues can be corrected with glasses, contact lenses, or surgery, but none of those fix the underlying defect. Eye elongation can stretch and thin parts of the inner eye, which can increase the risk of retinal detachment, glaucoma, cataracts, and even blindness.

Genetic causes have been discounted, so this rapid change has to come from something in the environment. More than 400 years ago, Johannes Kepler, an astronomer and expert in optics, wrote that his intense studying led to nearsightedness. Today, students are not only studying a great deal but are also spending much of their time with cell phones, tablets, computers, and video games, primarily indoors.

Intense periods of reading and studying were disproved as a cause of myopia during a study in 2000. Seven years later, scientists from Ohio State University followed more than 500 eight- and nine-year-olds with healthy vision and tracked the time they spent outdoors. After five years, 20 percent had developed myopia, which correlated to the time they spent indoors. This was confirmed one year later, when scientists in Australia studied 4,000 students and also reported that the amount of time spent indoors was the important factor.

It’s probably because the retina of the eye produces and releases more dopamine, a neurotransmitter, during the day to signal the eye to switch from night to daytime vision. Indoor light disrupts this cycle, affecting eye development. Only 30 percent of Australian children who spent three or more hours outside each day had myopia. A systematic review paper aggregated previous studies and concluded that each hour of each week spent outside reduces a child’s chance of developing myopia by 2 percent.

Researchers are examining possible ways to control the development of myopia, such as altering the way contact lenses focus light, producing eye drops that block neurotransmitter release, and using artificial lights like those used to treat seasonal affective disorder, also known as winter depression. Of course, having children play or simply be outside seems the best option, and it has other health benefits too.

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Obesity and Diabetes – Is Your Gut in Control?

August 28, 2015 by

Aug. 21, 2015

By Medical Discovery News

Your body is like a forest, providing a home to microscopic flora and fauna. In fact, your body is home to up to 100 times more microbes than your own cells, which make up your microbiome. While we provide them residence, these microbes help us out by providing a first line of defense against disease trying to invade our bodies, even breaking down food during digestion and producing vitamins. Now, the microbes that live in the digestive tract are helping us understand diabetes better.

According to the Human Microbiome Project sponsored by the National Institutes of Health, the microbiome plays a huge role in human health. When the microbiome is altered or imbalanced, it can cause conditions like obesity, irritable bowel syndrome, skin disease, urogenital infection, allergy, and can even affect emotion and behavior.

Recently, scientists from Israel discovered another surprising effect of the microbiome while investigating the use of artificial sweeteners in relation to glucose intolerance and diabetes. Artificial sweeteners such as saccharin, sucralose, and aspartame are commonly used in weight loss strategies because they do not add calories while still satisfying sweet cravings. However, artificial sweeteners are not always effective in managing weight and glucose, and scientists at the Weizmann Institute of Science may have figured out why.

Through experimentation they observed that adding artificial sweeteners to the diets of mice caused significant metabolic changes, including increasing blood sugar levels more than mice fed regular sugar. It didn’t matter whether the mouse was obese or at a normal weight, they all reacted the same. Dietary changes can alter the populations of bacteria in our guts, so the study addressed whether those changes affected blood glucose levels as well. After being treated with saccharin for nine days, the populations of gut bacteria in the mice shifted dramatically and corresponded with an increase in their glycemic index. Specifically, the bacterial group Bacteroidetes increased while the group Clostridiales decreased. These changes in bacterial populations is associated with obesity in mice and people.

When they administered antibiotics to reverse this and return the bacterial populations to a healthy state, it also countered the effects of saccharin, returning glucose levels to normal. To take it a step further, researchers took feces from saccharin-consuming mice showing glucose intolerance and transplanted them into other mice that had never consumed saccharin. Remarkably, those mice started showing signs of glucose intolerance.

In a study of 400 people, those who consumed artificial sweeteners had a gut microbiome that was vastly different from those who did not. They had a group of people consume high levels of artificial sweeteners for seven days, and like the rats their glucose levels increased and their microbiomes changed.

Overall, these studies show that artificial sweeteners may induce glucose intolerance instead of preventing it due to the intimate connection between the bacteria that live in our digestive systems and our metabolic state. In the future, expect to see diagnostic and therapeutic procedures that utilize our microbial friends.

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A Cause of Sporadic ALS

August 28, 2015 by

Aug. 14, 2015

By Medical Discovery News

A Cause of Sporadic ALS

When the groundbreaking theoretical physicist Stephen Hawking was diagnosed with amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s disease at 21, he was given two years to live. Now he is 73 years old. How has he managed to survive this invariably fatal disease for so long? We may not have all the answers when it comes to ALS, but one study has brought us closer to understanding its cause.

ALS is a devastating, progressive neurodegenerative disorder characterized by gradual degeneration and death of motor neurons responsible for controlling voluntary muscles, resulting in the loss of all voluntary movement including the face, arms, and legs. The disease becomes life-threatening when the muscles in the diaphragm and the chest wall fail and the patient requires a ventilator to breathe. Most people with ALS die from respiratory failure three to five years after the onset of symptoms. Only 10 percent survive 10 years or longer.

One tragic aspect of ALS is patients usually retain their awareness, intelligence, taste, sense of smell, hearing, and touch recognition, making them acutely aware of their deteriorating condition. ALS is one of the most common neuromuscular diseases, afflicting 12,000 people in the United States. Some 90-95 percent of all ALS cases are sporadic, so they have no family history. The remaining cases, called familial ALS, have a genetic component.

While its cause has long been sought after, recently scientists conducted the largest genetic sequencing study of ALS patients thus far. The genetic information of nearly 3,000 ALS patients and over 6,400 control subjects were sequenced, leading to the identification of a new gene associated with ALS. It took a study of this size to detect such a rare gene variant, as it is only mutated in about 2 percent of sporadic ALS cases.

The gene, TANK-Binding Kinase 1 (TBK1), is involved in a cell system that degrades and recycles waste. Scientists are trying to link mutations in the gene with the accumulation of protein aggregates that are killing motor neurons. TBK1 is also important to the immune response. Scientists have long thought inflammation in the brain plays a role in ALS. Since TBK1 tamps down inflammation, a mutation in the gene could interfere with that function.

Researchers are also studying a gene, OPTN, that interacts with TBK1. Together they regulate cell waste disposal and inflammation. Scientists are experimenting on mice engineered with mutations in both genes to determine how they contribute to ALS. These models will also be used to develop future therapies. However, genetic profiling of ALS patients will be necessary to determine which therapy is appropriate depending on the gene that is mutated.

Since ALS can be caused by dozens of gene mutations, the more we can identify, the better scientists can understand their influence on the pathways that lead to this disease.

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The Plague: It was the Gerbils

August 28, 2015 by

Aug. 7, 2015

By Medical Discovery News

In the past 800 years, many things have been blamed for the plague that swept through Europe in the Middle Ages: the alignment of the planets, bad air, lack of proper hygiene, black rats, and their fleas. Now scientists have data that suggests the climate in Central Asia at that time influenced the size of the great gerbil population, which triggered cycles of plague in Europe. These furry little rodents carried the plague bacterium, as did the fleas that fed on them. When the gerbil population shrank, the fleas found alternate hosts like horses, humans, and eventually rats, which then made their way to Europe and triggered the plague pandemics.

The plague was caused by the bacterium Yersinia pestis. It is transmitted to humans through the bite of a flea that has fed on an infected rodent. Plague outbreaks have afflicted humans for thousands of years and changed the course of history. The first recorded plague pandemic began in 541 and was named the Justinian Plague after the 6th century Byzantine emperor. Frequent outbreaks for the next 200 years are likely to have killed over 25 million people. The second pandemic, called the Great Plague or the Black Death, began in China and spread westward along trade routes to Constantinople and into Europe. About 60 percent of Europeans died, eliminating entire towns.

The third pandemic, or Modern Plague, also began in China and spread to Hong Kong by 1894. Rats hitching rides on steamships spread the plague to port cities around the world for the next 20 years, killing about 10 million people. By then scientists were able to identify the bacterium responsible and how it spread. Efforts to control the rat population eventually ended the pandemic. It continued to infect people (although in much smaller numbers than before) during the 20th century, such as in Vietnam during the war. The bacterium is still in the reservoir of wild rodents, and today most cases of plague are in sub-Saharan Africa and Madagascar. The plague can be effectively treated with common antibiotics, but if left untreated it has a high mortality rate.

Since there are still lots of rats in Europe, some wonder, why is there no plague? Researchers proposed that each time, the plague actually started in Asia. To test their theory, they examined climate records using the rings of trees. The incidence of plague did not correlate with climate changes in Europe, but it did with changes in Asia. It was already known that the Asian great gerbil carries Yersinia pestis, and when the weather in Asia was good, gerbils thrived, but when it turned bad, their population would crash. Then their fleas would seek another host such as human traders and their pack animals, who spread the plague to other parts of the world. They found no evidence that rodents in Europe carried Yersinia pestis, so that would explain why cases of the plague disappeared between pandemics.

So don’t worry about the little gerbils in the pet store – they are not carrying the plague.

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A Way Our of Our Antibiotic Crisis

August 28, 2015 by

July 24, 2015

By Medical Discovery News

A petri dish

Antibiotic resistance occurs when strains of bacteria that infect people – such as staph, tuberculosis, and gonorrhea – do not respond to antibiotic treatments. In America, 2 million people become infected with resistant bacteria every year and at least 23,000 die each year because of those infections. If nothing is done to stop or slow the resistance of bacteria to antibiotics, the World Health Organization (WHO) warns that we will find ourselves in a post-antibiotic world, in which minor injuries and common infections will be life-threatening once again.

The crisis arose primarily from three conditions. First, when people are given a weeks’ worth of antibiotics and stop taking them as soon as symptoms improve, they often expose the bacteria causing their infection to the medicine without killing it. This allows the bacteria to quickly mutate to further avoid the effects of the antibiotic. Second, antibiotics are over-prescribed. Most common illnesses like the cold, flu, sore throat, bronchitis, and ear infection are caused by viruses, not bacteria, so antibiotics are essentially useless against them. Yet they are prescribed 60-70 percent of the time for these infections. This once again provides bacteria in the body unnecessary contact with antibiotics. Third, tons of antibiotics are used every year in the agriculture industry. They are fed to livestock on a regular basis with feed to promote growth and theoretically for good health. But animals are also prone to bacterial infections, and now, to antibiotic-resistant bacteria, which spreads to humans who eat their meat or who eat crops that have been fertilized by the livestock. The good news is that the Food and Drug Administration (FDA) is working to focus antibiotic use on bacterial infections and regulate its use in livestock.

An easy solution to this problem might be to create new antibiotics, but it’s not that simple. It takes an average of 12 years and millions of dollars to research new antibiotics and make them available on the market, which is a huge investment considering they are normally only taken for up to 10 days. But there’s an even bigger challenge: microbiologists can only cultivate about 1 percent of all bacteria in the lab, including specimens that live in and on the human body. The ability to grow diverse bacteria is important because most antibiotics actually come from bacteria, produced as a defense against other microbes.

Slava Epstein, a professor of microbial ecology at Northeastern University, came up with an ingenious approach to solving this problem. He speculated that we are unable to grow these bacteria in the lab because we were not providing the essential nutrients they needed to grow. Working with soil bacteria, which are a huge source for developing antibiotics, he created the iChip. The iChip allows bacteria to grow directly in soil, which is their natural environment, while being monitored.

To date, about 24 potential antimicrobials have been identified from 50,000 bacteria that remain unable to grow in the lab. With possibly billions of bacteria left to grow and examine, the number of new drugs awaiting discovery is seemingly endless.

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The Genetic of Autism

August 28, 2015 by

July 17, 2015

By Medical Discovery News

The Genetics of Autism

In the past decade, autism has garnered a lot of media attention. Lately much of the focus has been on finding the cause. Much is still a mystery, despite confirming that vaccines and parenting are not responsible. Now a new study of twins has given us another clue, revealing that the influence of genetics on the development of autism may be between 56 and 95 percent.

According to the Centers for Disease Control, one in 68 children have autism, a neurodegenerative disorder that exists on a spectrum, meaning its symptoms and their severity varies tremendously. A hallmark feature of autism is impaired social interaction, noticeable even in babies. Those with autism find it difficult to interpret what others are thinking or feeling because they miss the social clues most take for granted. Other symptoms can include repetitive movements such as spinning or rocking, speech delays, and self-destructive behaviors. Children with autism can also have a variety of other conditions including epilepsy, Tourette’s syndrome, learning disabilities, and attention deficit disorder (ADD).

The cause of autism is probably rooted in genetics and environment. Comparing sets of twins is a well-established way of clarifying the extent of both these influences. Scientists in London studied over 6,400 pairs of twins in England and Wales between 1994 and 1996, all raised by their parents in the same environments. The data they collected revealed that the chance of identical twins having autism was 77-99 percent, whereas the chance of non-identical twins having autism was 22-65 percent. This suggests that additive genetic factors contribute to 56-95 percent of autism cases. This is far higher than previous estimates, which assumed environmental influences were more of a factor.

While no one gene has been attributed to autism, the majority of the genes that are associated seem to be linked to one specific symptom. For example, the gene EN2 is often studied for its role in autism because it is critical to midbrain and cerebellum development. Reelin, a protein found mainly in the brain, also plays an important role in autism development. In adults, reelin is important to learning and memory and is critical to inducing and maintaining long-term neuronal connections. Autistic individuals consistently show elevated levels of serotonin, otherwise known as the feel-good hormone. This has led researchers to examine the role of genes involved in serotonin regulation as potential causes of autism. Another hormone system called arginine-vasopressin affects social behavior, so one of the genes that regulates it is a candidate for autism as well. These are just a few of the many genes being studied.

As more people become aware of autism and more children are diagnosed, the pressure is building to further understand this disorder. Discovering the causes might translate to better diagnostics and treatment for autism.

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How a Heart Fails

July 12, 2015 by

July 10, 2015

By Medical Discovery News

A heart

What exactly causes a heart to fail? It may come down to a simple protein, which scientists recently identified as having an important role in how a heart goes from weakening to failing.

Your heart is a strong, muscular pump slightly larger than your fist that pushes blood through your body. Blood delivers the necessary oxygen and nutrients to all cells in all the organs. Every minute, your heart pumps five quarts of blood. Human hearts have four chambers: two atria on top and two ventricles on bottom. Oxygenated blood leaves the lungs, enters the left atrium, moves to the left ventricle, and is then pumped out of the heart to the rest of the body. After it circulates, blood returns to the heart, enters the right atrium, moves to the right ventricle, and is then sent back to the lungs for a fresh dose of oxygen. Although your heart beats 100,000 times each day, the four chambers must go through a series of highly organized contractions to accomplish this.

Any disruption of this process can have serious consequences such as heart failure, which is clinically defined as a chronic, progressive weakening of the heart’s ability to circulate enough blood to meet the body’s demands. To compensate, the heart enlarges, which increases contractions and the volume of blood pumped. Blood vessels elsewhere in the body narrow to keep blood pressure normal. Blood can even be diverted from less important organs, ensuring more vital organs like the brain and heart are satisfied. However, such responses mask the underlying problem: the weakening heart, which continues to worsen. Ultimately, the body can no longer compensate for the heart, which is when it will start to fail.

Scientists at the University of California, San Diego School of Medicine studied the cellular changes in weakened hearts to better understand the transition from the compensatory stage, when it works harder to pump blood, to the decompensation, when it fails to pump blood sufficiently. They were especially interested in a RNA-processing protein called RBFox2 because it is involved in the heart’s early development and its continuing functions. When genes are expressed, DNA is transcribed into RNA, which is then processed and eventually used to make proteins such as RBFox2.

Sure enough, levels of RBFox2 were dramatically reduced in the hearts of mice with a condition similar to heart failure. Then they genetically engineered mice without RBFox2, which developed symptoms of heart failure. Not only are low levels of this protein connected to weakened heart muscle, without enough of it, the body cannot compensate and the heart declines more quickly. However, we still don’t know why levels of RBFox2 decline during the transition to the decompensatory phase of heart failure.

In the future, this research might be used to develop treatments that reverse the decline of RBFox2 and effectively slow or prevent heart failure.

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An Unwelcome Gift from Gorillas

July 2, 2015 by

July 3, 2015

By Medical Discovery News

Gorilla

You probably know that Acquired Immunodeficiency Syndrome (AIDS), which has affected 79 million people and killed 39 million since 1981, is the result of Human Immunodeficiency Virus (HIV). What you may not know is that there are several different types of this virus and they did not all come from the same source, making the search for HIV’s origins lengthy and complicated.

There are four groups of HIV-1: M, N, O, and P. Each of them was transmitted between African primates as simian immunodeficiency viruses (SIVs) before infecting humans, and each crossed species to humans independently. More than 40 African primates carry SIVs, which emerged up to 6 million years ago. It is likely that transmission to humans has occurred many times when hunters where exposed to the blood and tissues of infected animals. However the isolation of humans in Africa limited the spread of SIVs that crossed into humans until the last century.

It was not until modern travel allowed infected humans to move from the bush to cities and from there to other cities and countries that an HIV strain such as M took hold among humans, leading to a global pandemic. Group M causes more than 90 percent of AIDS cases and currently affects 40 million people worldwide. We already know that it came from chimpanzees in southern Cameroon. Group N also came from chimpanzees, but has infected less than 20 people.

Group O has infected about 100,000 people in Cameroon, Chad, Gabon, Niger, Nigeria, Senegal, and Togo. Although anti-retroviral drug combinations have made HIV infections survivable, many in Africa and the developing world do not have access to these treatments. Group P has only been isolated from two people. The origins of groups O and P were previously unknown, but now their source has been definitely confirmed: gorillas.

Scientists gathered fecal samples from western lowland, eastern lowland, and mountain gorillas, screening them for SIV antibodies and genetic information. Despite testing many wild troops of gorillas throughout Cameroon, Gabon, the Democratic Republic of Congo, and Uganda, the virus was identified at only four sites. Two strains of SIVs from southwestern Cameroon resembled HIV Group P and one from central Cameroon resembled Group O.

Not only does this data prove that gorillas were the immediate source of groups O and P, but the genetic information revealed that the viruses originated through a cross-species transmission from chimpanzees to gorillas. These are the same chimpanzees that infected humans, leading to groups M and N. Chimpanzees and gorillas share the same habitat, so the virus could have infected a gorilla if it bit a chimpanzee with SIV or was exposed to its blood or tissues.

Understanding the origins of HIV in humans is crucial if we want to prepare for additional viruses, especially SIV variants, entering the human population in the future, which will remain a risk as long as humans continue to hunt and eat primates.

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Microlesions in Epilepsy

June 26, 2015 by

June 26, 2015

By Medical Discovery News

Humans have been recording and diagnosing epilepsy for at least 4,000 years, but it only began to be understood a few hundred years ago. While doctors noticed some epileptic patients had brain lesions, others did not have any that were visible – until now. Using a combination of gene expression analysis, mathematical modeling, and microscopy, scientists have found microlesions in the brains of epilepsy patients, which may explain the cause of seizures in some people.

Epilepsy is characterized by unpredictable seizures that result from groups of neurons firing abnormally. Some people experience symptoms prior to a seizure that allows them to prepare. In some cases, seizures can include jerking, uncontrolled movements, and loss of consciousness. In others, the seizure may only cause confusion, muscle spasms, or a staring spell. Epilepsy patients experience repeated seizure episodes.

Epilepsy is a relatively common brain disorder affecting about 1 percent of people – 65 million worldwide, 3 million in the United States. Some causes of epilepsy are strokes, brain tumors or infections, traumatic brain injuries, lack of oxygen to the brain, genetic disorders such as Down syndrome, and neurological diseases such as Alzheimer’s. However, for two-thirds of people with epilepsy, there is no known cause. Not all seizures are related to epilepsy, as they can also be caused by low blood sugar, high fever, and withdrawal from drugs and alcohol.

Epilepsy can be treated using anti-seizure medications that control the spread of seizure in the brain, but about one-third of epileptic patients don’t respond to current medications. Some cases are treated by surgically removing or killing cells in the region of the brain that are responsible for the aberrant electrical signaling. If neither of those are options, a device can be implanted that stimulates the vagus nerve, which is part the autonomic nervous system that controls involuntary bodily functions such as heart rate and digestion.

In some people with epilepsy, the cause was traced to a visible abnormality in the brain. Now, scientists have identified millimeter-sized microlesions that could explain why a seemingly normal brain suffers seizures. Scientists compared the genes expressed in the microlesions of 15 people with epilepsy. Using mathematical modeling called cluster analysis, they discovered 11 groups of genes that were either expressed too much or too little in brain tissues experiencing the high electrical activity that causes seizures.

Based upon what these genes encoded, they predicted certain brain cells would be reduced and immune response or inflammation would increase in the microlesions. That’s exactly what they found when they stained those sections of the brain and examined them under a microscope. Brain cells lost communication with each other, limiting the brain’s communication network. This probably leads to the abnormal electrical signals that trigger seizures.

This conclusion still needs to be confirmed, but in the future it may guide the development of new treatments for epilepsy.

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The Dollars and Sense of Alzheimer’s

June 19, 2015 by

June 19, 2015

By Medical Discovery News

As people age, they begin to worry about developing dementia and its most common cause, Alzheimer’s. Alzheimer’s is a neurodegenerative disease that can affect your cognitive abilities, the ability to function in daily life, and orientation. If that’s not devastating enough, those with Alzheimer’s only live four to eight years on average after diagnosis.

In America, Alzheimer’s is the 6th leading cause of death. Today 5.1 million of those 65 or older are living with this disease, a number that is only expected to grow as the population ages – by 2050 it is projected to affect 13.5 million of those 65 or older. The few drugs readily available only moderate the symptoms, as there is no way to cure, slow, or prevent Alzheimer’s.

Recently, the Alzheimer’s Association published a report called “Changing the Trajectory of Alzheimer’s Disease: How a Treatment by 2025 Saves Lives and Dollars.” It focuses on the costs associated with a theoretical treatment that could delay the onset of Alzheimer’s for five years. If such a thing were discovered, it could have a huge impact on people’s lives and their financial.

Since Alzheimer’s is a disease of older Americans, treatments for it are mostly funded by Medicaid and Medicare. Currently, Medicare covers 80 percent of the total costs of Alzheimer’s care in America, which equates to $153 billion. By 2050, the total costs of caring for those with Alzheimer’s is expected to rise to $1.1 trillion, with Medicare allocating one-third of all its expenses to treating it.

Within the Alzheimer’s population, a higher proportion will be in severe stages of the disease by 2050, as opposed to early or moderate stages. In the early stage of the disease, people can continue everyday functions and may appear symptom-free. They do have deficits in their abilities to think and learn, but the financial impact and burden on family members are low. In the moderate stage, memory lapses, inability to express thoughts, and confusion become apparent. Finally, in the severe stage, people have trouble taking care of themselves and require extensive daily care. In 2050, almost half of those affected will be in the severe stage.

The Alzheimer’s Assocation presents a case for funding biomedical research now, before the human and economic costs can be realized. For the sake of argument, they describe a hypothetical new treatment that would delay the onset of Alzheimer’s symptoms by five years. If such a thing were available by 2025, it would save $220 billion in its first five years. By 2050, 6 million fewer people would be affected by Alzheimer’s, saving families $90 billion in healthcare costs and the federal government $367 billion. Even if such research costs $2 billion a year starting today, a way to delay Alzheimer’s by just five years would pay for itself within three years.

Research from very basic studies on the brain to translational research leading to new therapeutics and early diagnostics are desperately needed. There are many promising studies that suggest a delay in the progression or even cure for Alzheimer’s are possible.

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