Category: alzheimer’s disease

Potential Vaccine and Oral Medication for Alzheimer’s Disease in Human Trials

Focusing on Prevention

Researchers from the University of Southern California (USC) Keck School of Medicine are tackling Alzheimer’s disease (AD) proactively by focusing on prevention. AD, the sixth-leading cause of death in the US which affects 47 million people worldwide, is the subject of a new study and series of clinical trials testing both a vaccine and oral medication. Both interventions aim to prevent or delay AD in older at risk adults.

This focus on prevention is a new approach to fighting AD. “One of the challenges in developing new medications for Alzheimer’s is that researchers tend to test medications on people with more advanced Alzheimer’s, and the medications are simply not proving to be effective,” Lon Schneider, Keck School professor of psychiatry and study lead investigator, told Neuroscience News. “By intervening 10 to 12 years before Alzheimer’s manifests, we may be able to stop it before it begins or delay the symptoms.”

The APOE4 Gene

According to Schneider, approximately half of all AD patients carry the apolipoprotein e4 (APOE4) gene, which can be inherited from either parent. Around one-quarter of the population carries one APOE4 gene, while two to three percent of the population carry two copies, one from each parent. Participants must have two copies of the gene to qualify for the study; interested adults ages 60 to 75 with normal cognition must undergo genetic testing for the APOE4 gene. If the vaccine, the oral medication, or both prove effective in treating people with two copies of the APOE4 gene, it is highly likely to be effective for other at-risk people.

 

Image Credit: Boku wa Kage/Wiki Commons
Amyloid beta fibrils. Image Credit: Boku wa Kage/Wiki Commons

Participants are randomly assigned a vaccine, an oral medication, a placebo vaccine, or a placebo oral medication which they will take for five to eight years. Both the vaccine and the oral medication target amyloid beta, the primary component of amyloid plaques in the brain and a major cause of AD, but in two different ways. The vaccine assists in the development of amyloid beta antibodies, while the oral medication blocks an enzyme that makes amyloid beta.

“If we are able to show that the vaccine or oral medication is effective at delaying Alzheimer’s among people at higher risk, then this would strongly imply that we are on the right track for developing treatments,” Schneider said to Neuroscience News. “If we can delay the onset of Alzheimer’s by five years, for example, the incidence of the illness would drop by half. It would also give individuals five more years without symptoms of the illness.”

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New Research Suggests Memory Loss in Alzheimer’s Patients May be Reversible

A Targeted Approach

New research from a team at MIT indicates symptoms of Alzheimer’s disease (AD) affecting patient’s memories may be reversible. AD causes memory loss by setting up genetic “blockades” formed when the enzyme HCAC2 condenses the genes of the brain responsible for memory. Eventually, those genes become useless; unexpressed, the genes are unable to cause the formation of new memories or retrieval of existing ones.

Clearly, blocking HCAC2 in the brain is an obvious fix; however, it has to date been impossible, in that all prior attempts have negatively affected the internal organs which require other enzymes in the histone deacetylase (HDAC) family for normal function. Researchers at MIT have now found something they hope might be the answer: LED lights which they use to prevent HCAC2 alone from binding with Sp3, its genetic blockade formation partner in crime (and Alzheimer’s).

Image Credit: jarmoluk/Pixabay
This research was spurred by the 2007 discovery that blocking HDAC activity in mice reversed memory loss. Human cells contain around one dozen forms of HDAC, and the team found later that it is HDAC2 that causes the memory-linked gene blockade, and that HDAC2 levels are elevated in Alzheimer’s patients.

Finding The Right Match

The trick was determining a way to target HDAC2 specifically without affecting HDAC1 levels and hurting white blood cell production as a result. To do this, the team analyzed postmortem brain samples of both healthy people and those with Alzheimer’s disease, assessing gene expression data. They found that there were more than 2,000 genes at levels that nearly matched HDAC2 levels. They then needed to test the best candidates; doing this allowed them to isolate the Sp3 gene.

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“This is exciting because for the first time we have found a specific mechanism by which HDAC2 regulates synaptic gene expression,” Director of MIT’s Picower Institute for Learning and study lead author Li-Huei Tsai explained to MIT News. “If we can remove the blockade by inhibiting HDAC2 activity or reducing HDAC2 levels, then we can restore expression of all these genes necessary for learning and memory.”

This AD research is in the early stages yet, having only been conducted with mice. No usable remedy for humans will be forthcoming for some time, but even so, this is one of the most promising semblances of a cure for Alzheimer’s to date, with the potential to help more than 5.5 million Americans and almost 44 million worldwide.

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New Test Allows For Easier and Earlier Detection of Alzheimer’s

Early Detection

A new blood test has been found to be able to detect buildups of beta-amyloid in the brain, the cause of the plaques that characterize the development of Alzheimer’s disease. Although the role that these clumps of beta-amyloid play in the brains of Alzheimer’s patients is unknown, monitoring their presence has been a reliable way to watch for the disease. Unfortunately, watching for the build-up of these plaques in the brain has only been possible through PET-scans, which are expensive and not widely available, or with spinal tap procedures, which are invasive and can only be administered by a, relatively, select few practitioners.

In this new study, researchers have developed a simple blood test to screen for Alzheimer’s risk that anyone from general practitioners to nurses in clinics could use. This simple to administer screening would be able to identify thousands of at-risk patients, allowing them to start treatment before brain damage and irreversible memory loss occurs. In fact, with this kind of basic screening tool, monitoring for Alzheimer’s disease could be as widespread and quick as checking your cholesterol and blood sugar.

Image Credit: PublicDomainPictures/Pixabay
Image Credit: PublicDomainPictures/Pixabay
This test was developed to measure relative amounts of different types of beta-amyloids, since the researchers were able to determine, using PET scans, that ratios of beta-amyloid varieties in the blood correspond with how much beta-amyloid has aggregated in the brain. This development is critically important, since the number of Americans with Alzheimer’s disease could rise from 5 to 16 million by 2050.

Preventing Alzheimer’s Disease

Although there is not yet any silver bullet treatment for Alzheimer’s disease, there are promising treatments on the horizon — some that reverse symptoms, and others that slow the progression of the disease. However, the most important way to fight Alzheimer’s right now is through prevention. As scientists study why some brains resist the disease more than others and how we might prevent the disease entirely, evidence shows that lifestyle interventions including healthy diet and exercise can reduce the risk of Alzheimer’s disease by as much as 30 percent. Earlier detection with a blood test would make lifestyle interventions more effective.

Beta-amyloid plaques begin to accumulate 15 to 20 years before a person exhibits the symptoms of Alzheimer’s disease. Positive test results wouldn’t guarantee that a patient would develop the disease, but they would signal possible risk while suggesting a need for lifestyle changes.

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A New Drug Can Fix Abnormal Brain Activity in Alzheimer’s Disease

Alzheimer’s Breakthrough

For the first time, researchers have shown that a common epilepsy drug can normalise disrupted brain activity in patients with Alzheimer’s disease.

A New Drug Can Fix Abnormal Brain Activity in Alzheimer’s Disease
Image Source: NIA-NIH

The incurable condition already affects one in ten people over the age of 65, so in the widespread scientific search for new therapies this research result is a highly promising development.

Alzheimer’s patients are known to be at an increased risk of developing epilepsy, but the vast majority don’t experience any seizures with noticeable symptoms.

But research has suggested that, in many such patients, seizure-like brain activity is still going on undetected, possibly even leading to some of the cognitive symptoms that patients experience.

That’s why a team from Beth Israel Deaconess Medical Center (BIDMC) at Harvard Medical School turned to an anti-seizure medication to see whether it might have any effect on the brain activity of patients with mild Alzheimer’s disease.

LEV

The drug in question was levetiracetam (LEV for short), commonly used for treating seizures in epilepsy patients. It’s been tested before in mouse models of Alzheimer’s disease, showing benefits for normalising brain activity and even reversing some cognitive deficits.

Previous studies have also shown that low doses of LEV can improve memory in people with ‘amnestic mild cognitive impairment’, a memory deficit that’s known to be a risk factor for Alzheimer’s.

Now researchers have finally tested the drug in actual Alzheimer’s disease patients, and even though this was just a small feasibility study, the results look promising indeed.

The team, led by neurologist Daniel Z. Press from BIDMC, measured the effects of a single dose of LEV in seven patients with diagnosed mild Alzheimer’s disease.

The study was double-blinded, and all patients received a total of three injections – either a low dose of LEV, a higher dose, or a placebo.

Before and after each injection, the patients were given an electroencephalogram (EEG) which can detect disrupted electrical activity in the brain even when there are no obvious symptoms of a seizure.

The patients also took standardised cognitive tests to measure the various abilities affected by Alzheimer’s, such as memory, language abilities and executive function.

The results showed that when patients received the higher dose of LEV, it appeared to reduce abnormalities of brain activity patterns which are typical in Alzheimer’s patients and which the researchers detected before administration of the drug. But there was no improvement in cognitive test scores.

It’s important to note that the team didn’t have a control group without Alzheimer’s, and they say in the study that this “prevents us from determining whether the effects would also be seen in healthy ageing.”

But there is some previous research to indicate that LEV doesn’t change EEG patterns in healthy volunteers. The dosage of the drug will also have to be investigated more thoroughly, to see how patients would fare with smaller doses over longer periods of time.

“Chronic administration would be required to better delineate any potential long-term benefits of the drug,” the team writes in the paper.

But even with the small sample size and other limitations, the effects of the medication look so promising the researchers are now calling for a larger study to further investigate the potential of LEV as an Alzheimer’s treatment.

“It’s worth noting, we did not demonstrate any improvement in cognitive function after a single dose of medication in this study,” says Press.

“It’s too early to use the drug widely, but we’re preparing for a larger, longer study.”

Whether an epilepsy drug could indeed become a treatment option for managing Alzheimer’s symptoms remains to be seen, but over decades of hard work scientists have certainly been making progress in tackling this disease.

Last year another team reported highly promising results in a preliminary trial for a drug that can clear the toxic protein build-up in the brain. This treatment is now being investigated in a large-scale study with results expected in 2020.

And just last week we finally had a close-up look at one of the key proteins involved in Alzheimer’s. Mapping the tau protein’s molecular structure is a significant step towards devising new drugs that can target it.

The study was published in the Journal of Alzheimer’s Disease.

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A New Technique Transforms Human Skin Into Brain Cells

From Skin to Brain

The brain is one of the most vital organs in the human body, so damage to the brain from injury or aging can have major impacts on people’s quality of life. Neurological disorders represent some of today’s most devastating medical conditions that are also difficult to treat. Among these is Alzheimer’s disease.

Usually, research involving Alzheimer’s rely on brain cells from mice. Now, neurobiologists from the University of California, Irvine (UCI) have developed a method that could allow the use of human cells instead of animal ones to help understand neurological diseases better.

In their study, which was published in the journal Neuron, the researchers found a way to transform human skin cells into stem cells and program them into microglial cells. The latter make up about 10 to 15 percent of the brain and are involved in the removing dead cells and debris, as well as managing inflammation. Micgrolia are instramental in neural network development and maintenance, explained researcher Mathew Blurton Jones, from UCI’s Department of Neurobiology & Behavior.

“Microglia play an important role in Alzheimer’s and other diseases of the central nervous system. Recent research has revealed that newly discovered Alzheimer’s-risk genes influence microglia behavior,” Jones said in an interview for a UCI press release. “Using these cells, we can understand the biology of these genes and test potential new therapies.”

A Renewable Method

The skin cells had been donated by patients from UCI’s Alzheimer’s Disease Research Center. These were first subjected to a genetic process to convert them into induced pluripotent stem (iPS) cells — adult cells modified to behave as an embryonic stem cell, allowing them to become other kinds of cells. These iPS cells were then exposed to differentiation factors designed to imitate the environment of developing microglia, which transformed them into the brain cells.

“This discovery provides a powerful new approach to better model human disease and develop new therapies,” said UCI MIND associate researcher Wayne Poon in the press release. The researchers, in effect, have developed “a renewable and high-throughput method for understanding the role of inflammation in Alzheimer’s disease using human cells,” according to researcher Edsel Abud in the same source.

In other words, by using human microglia instead of those from mice, the researchers have developed a more accurate tool to study neurological diseases and to develop more targeted treatment approaches. In the case of Alzheimer’s, they studied the genetic and physical interactions between the disease’s pathology and the induced microglia cells. “These translational studies will better inform disease-modulating therapeutic strategies,” Abud added in the press release.

Furthermore, they are now using these induced microglia cells in three-dimensional brain models. The goal is to understand the interaction between microglia and other brain cells, and how these influence the development of Alzheimer’s and other neurological diseases.

This is all made possible by reprogrammable stem cells. Indeed, this study is one more example of how stem cells are changing medicine.

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A New Genetic Test Predicts If and When You’ll Develop Alzheimer’s

In the US, there are 5.5 million Americans with Alzheimer’s — a disease defined by the progressive deterioration of brain function, most often affecting thinking and memory, that typically begins during middle or old age. Among the 5.5 million patients, the vast majority are at least 65 years old, while an estimated 200,000 suffer from what’s known as early-onset Alzheimer’s.

Assessing someone’s lifetime risk of contracting the disease is of concern not just to patients and families, but also healthcare providers. Alzheimer’s risk factors are notoriously hard to identify, but getting that information as early as possible can help prepare patients and families to manage the disease, and in many cases support preventative efforts.

Gaining more insight into a patient’s risk may soon become remarkably easier: researchers from the University of California San Diego (UCSD) School of Medicine and University of California San Francisco (UCSF) have created a genetic test that can calculate a patient’s age-specific risk of Alzheimer’s.

The method looks for 31 genetic markers, gathered from over 70,000 individuals, including patients suffering from Alzheimer’s as well as healthy elderly patients. Scientists based the test on background genetic variations which, individually, have a tiny influence on Alzheimer’s — but collectively, their effect is substantial enough that they can accurately predict an individual’s risk of developing the disease.

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Breakthrough

“Preventing the development of dementia symptoms is the holy grail of Alzheimer’s research but to succeed we first need accurate methods to predict who is most likely to develop the condition. This study’s approach was fairly successful at predicting the likelihood of someone developing dementia over the coming year, but needs to be tested further in mixed, non-US populations,” said James Pickett, head of research at Alzheimer’s Society in a report published by The Guardian.

It should be noted that scoring high on this genetic test doesn’t automatically mean someone will develop Alzheimer’s. Nor does it imply that scoring low means someone would be considered immune to the disease. Genetics is one of several factors that determines a person’s risk for developing any disease, including Alzheimer’s.

“From a clinical perspective, the [test] provides a novel way not just to assess an individual’s lifetime risk of developing Alzheimer’s disease, but also to predict the age of disease onset,” said senior author Dr Anders Dale, of the University of California San Diego School of Medicine.

While we have yet to find a viable treatment for the disease, experts believe that we are getting close. To that end, they assert that once a cure is found, it would still need to be administered as early as possible in the course of the disease, to ensure that damage done to the brain is at a minimum.

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A Drug That Could Slow Parkinson’s and Alzheimer’s Is Heading to Major Testing

On to the Next Level

A drug that has already been approved to treat leukemia is now closer to being approved for use against the debilitating brain diseases, parkinson’s and alzheimer’s. There are more than 5 million people currently living with Alzheimer’s disease in the US and another million living with parkinson’s. This drug has the potential to change the lives of not just these millions of sufferers, but also their countless friends and family who suffer along with them.

Currently, there are no approved drugs to slow or halt the progression of the diseases. These patients typically take medications and treatments to address the specific symptoms of their disease, which have their own deleterious side-effects. However, in a previous study, the drug known as nilotinib, “significantly increased brain dopamine (the chemical lost as a result of neuronal destruction) and reduced toxic proteins linked to disease progression.”

“It was such a small trial, there was no placebo control and it really wasn’t designed to assess efficacy,” says J. Paul Taylor, chair of the cell and molecular biology department at St. Jude Children’s Research Hospital. But, researchers are remaining prudent.  To further test and prove the efficacy of this drug, twin trials will be conducted at Georgetown.

“This is going to help us identify what might have been a placebo effect and what is truly the effect of the medication,” says Fernando Pagan, medical director of the translational neurotherapeutics program at Georgetown.

*4* Drug to Treat Parkinson’s and Alzheimer’s Have Moved to a New Phase Toward Approval

Fueling Optimism

Years of research studying these neurodegenerative diseases has allowed for new treatments like this to be developed. A better understanding of how these diseases work and how they impact the brains of sufferers is leading to better potential treatments.

Trials will be conducted for a year. According to the press release, “The clinical trial is a phase II, randomized, double-blind, placebo-controlled study designed to evaluate the safety and tolerability of low doses of nilotinib, the efficacy on disease biomarkers, and clinical outcomes in people with mid-stage Parkinson’s disease.” The other trial will evaluate the same for alzheimer’s.

NPR spoke with Jonathan Lessin, a retired anesthesiologist who is living with parkinson’s. He expressed great excitement for the potential of this drug. “I’m very optimistic,” he says. “I’ve seen it cure Parkinson’s in mice. I’ve seen people who can talk again, walk again, which is very encouraging.”

Taylor says, “If the results of this trial don’t turn out to be as exciting as the very tiny trial suggested, I would not get too pessimistic because there are other developments that are in the wings.”

It would be fantastic if these trials prove the efficacy and safety of this treatment. However, even if this drug turns out to be a dud, there is still plenty to hope for and work towards.

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You Can Rewire Your Brain to Have a Super Memory

Mnemonic Jocks

We know the brains of “memory athletes” are different—but it’s not because they started out that way. The tasks that elite mnemonic athletes undertake in competitions may seem impossible to most of us, no matter how intelligent we are. Memorizing 500 digits in five minutes, for example, or thousands of random words in sequence. Yet new research shows that most people can successfully master and apply the memorization techniques that memory athletes use. Even more fascinating, research indicates that as we apply these techniques, we literally rewire our brains on a large scale.

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The Radboud University research team, led by Martin Dresler, compared the minds of memory champions to those of people in the general population using brain scans and behavioral tests. These comparisons revealed a different pattern of brain connectivity in the brains of top memory athletes versus the controls. The team also found that the changes to brain connection patterns caused by learning a common memorization technique began to appear after a period of weeks. Not surprisingly, these subjects were able to significantly improve their memory skills and exhibit behaviors similar to those of memory athletes.

It makes sense that learning new skills throughout our lives could be healthy for our brains, but there isn’t complete scientific evidence for its efficacy. However, some research links specific changes in the brain to certain skills. For example, one study showed that taxi drivers in London developed more gray matter in their hippocampi as they learned to navigate the streets of the city, and therefore had larger-than-average memory centers. The scientists were able to definitively say that not only did the drivers have larger memory centers built up by their time on the roads, but that the development of this form of memory might inhibit development in other areas.

Hit The (Brain) Gym

“I think the interesting part is that not only can you boost memory in a similar way behaviorally in normal subjects compared to memory athletes,” Dresler says, “but on the brain level you see a reflection of that behavioral increase, and you drive the brains of naive subjects into the patterns of the best memorizers in the world.”

The results of this study concur with recent findings that some Alzheimer’s patients appear to be resistant to memory loss. The idea that the typical plaques associated with Alzheimer’s may be present in a brain that continues to function normally suggests there may be protective factors involved, or practices we can adopt to maintain healthier minds as we age. The results of this super memorizer study certainly imply that rewiring the brain is within reach for most of us.

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Noted Scientists Who Passed Away in 2016

Noted_Scientists_Who_Passed_Away_in_2016_Rev4

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New Evidence Shows That Air Pollution Causes Alzheimer’s and Dementia

Neurodegeneration

Smog and soot is doing a lot more than just obscuring city skylines—according to several studies, air pollution has become so severe that it might increase a person’s risk of Alzheimer’s disease and other types of dementia.

The dangers that inhaling pollution impose on our respiratory system are well documented. Asthma, lung cancer, and even heart disease have been proven to be linked to this exposure. Now, there’s mounting evidence that what lurks in our air could also harm the brain, speeding up cognitive aging that can lead to more serious, debilitating neurological diseases.

Current research is focused on the effects that ultrafine pollutant particles in the air, referred to as PM2.5, have. The smaller these particles are, the more damage they could cause within DNA and other cellular structures.

 

Image Credit: C. Bickel / Science

According to one 11-year epidemiological study conducted by University of Southern California (USC) researchers,  exposure to above-normal levels of polluted air may double the risk of dementia. The study focused on older women who lived in places where air pollutants exceeded the Environmental Protection Agency’s (EPA) standard of safety (12 µg/m3). If these results could be shown in a larger group, they could be linked to around 21 percent of dementia cases worldwide.

Supporting USC’s findings, researchers from the University of Toronto have also reported that residents who live within 50 meters of a major thoroughfare were 12 percent more likely to develop dementia due to higher exposure to fine pollutants.

One of the earliest observations of how air pollution affects the brain was based on a study that looked at its effects in aging dogs in Mexico City. According to Neuroscientist Lilian Calderon-Garciduenas, dogs who lived in polluted areas of the city displayed disorientation and couldn’t recognize owners. When the dogs died, they found that these dogs had elevated plaque levels, similar to what is associated with Alzheimer’s disease.

In a separate study where scientists exposed mice to aerosolized pollutants, it was found that mice exposed to pollution showed signs of Alzheimer’s disease and memory loss, as well as other signs of brain damage.

The Air We Breathe

Despite the severity of these claims, experts are quick to point out that the research is still young, and the correlation between pollution and neurodegeneration has to be studied further.

Until this correlation can be supported further, it might be helpful to study the ramifications of the Anthropocene—an era marked by climate change, air pollution, population growth, and significant rainforest loss—and what we can do about our environment.

In 2013, China was forced to shut down the city of Harbin, a major city in the world’s biggest industrial nation with over 11 million residents, due to smog. Last year, NASA and the California Institute of Technology illustrated the severity of pollution originating from Asia and how it affects cloud development in regions as far as North America, strengthening tropical cyclones. And this year, Beijing and Tianjin, major urban centers in China, issued red alerts due to heavy, toxic smog that enveloped the cities.

Because of our dependence on fossil fuels, considered to be the biggest pollutant to date, it’s hard to completely eliminate air pollution. But while we are unable to control the air itself, we do have the ability to control what goes in it, and at the end of the day, we can continue working to protect ourselves. So, as research continues and the case against pollution grows, we can try to think of ways to limit our own impacts on the environment.

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The 2017 Breakthrough Prizes

Breakthrough_PrizeV5

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Humanity May Have Reached its Maximum Lifespan

A Halt to Progress?

It’s no secret that lifespans have been getting longer—whether in the U.S. or in other developed countries. Whereas at the beginning of the 20th Century global life expectancy rarely exceeded 50 years, it has now reached an average that’s regularly in the 80s in Japan and Canada —and in the United States it’s reached a high of 78 years.

The reasons for this dramatic increase are numerous, and largely have to do with the extraordinary evolution in medical technology, healthcare, and general standards of living that occurred during the 20th Century and continue in the opening decades of the 21st. Vaccination programs have defeated smallpox, polio, measles and other diseases that formerly carried off thousands. Meanwhile, the decline in smoking and the creation of new drugs to ameliorate blood pressure and cholesterol have warded off the ubiquitous specter of heart disease.

The projected percentage change in the world's population by age, 2010-2050. Credit: United Nations, World Population Prospects: The 2010 Revision.
The projected percentage change in the world’s population by age, 2010-2050. Credit: United Nations, World Population Prospects: The 2010 Revision.

So why does life expectancy seem to be leveling off? What’s undoing—or at least matching, move-for-move—the recent remarkable gains in lifespans? Incredibly, the culprit this time isn’t some virulent pathogen, some unexpected new cancer or disease epidemic; nothing so terrifying as that at all. It’s obesity—a “lifestyle disease” brought on by our unhealthy dietary habits.

And this one’s a great deal tougher to defeat than those earlier epidemics. You can’t vaccinate it away; you can’t inoculate a person against further occurrences. Obesity undoes virtually every gain made in the fight against heart disease and stroke—it raises blood pressure, cholesterol, and heightens the risk for diabetes.

This all brings up some disturbing questions: have we reached the end of the line when it comes to living longer and healthier lives? Is there a point at which diminishing returns just mean any gains in lifespan are bound to be insignificant and temporary?

The Future of Longevity

The answer, fortunately, is probably not. Geriatric medicine has come a long way, and promising headway is being made in research into geroprotective drugs and compounds such as carnosine, the diabetes drug metformin, and the fungal compound rapamycin—an immunosuppressive which seems to induce cells to husband resources, thereby stretching cellular lifespans and by extension the health and life expectancy of the entire organism.

Meanwhile, there are great strides to be made in combating Alzheimer’s, the neurodegenerative disorder that is the great scourge of the elderly. Even if obesity hadn’t arrived to level off the gains made against cardiovascular disease, there’s still that fearful wall to healthy aging erected by dementia. But research into tau proteins and amyloid beta proteins, and drugs like verubecestat and the anti-inflammatory NTRX-07, have shown great promise.

Even if none of these treatments represent the hoped-for panacea for aging, they seem to be pointing in the right direction. Some combination of them, or of future incarnations developed from research into their effects, is likely to greatly extend human lifespans in the future, and—more importantly—allow those greater lifespans to be healthy and productive.

However, the way in which we choose to live those longer lives is another matter altogether. Unhealthy choices will come back to haunt us later in life, and the diseases of obesity and poor diet can still undo all the miraculous and marvelous technology we devise to stave off the inevitable.

Unfortunately, no cures for a self-destructive mentality are anywhere on the horizon.

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Breakthrough Treatment Proven to Prolong Life

New Advance

An international team of researchers has developed and tested a drug on mice to treat Alzheimer’s disease. The results of the testing is very promising, suggesting that not only does the drug mitigate symptoms, but also increases life-span in patients with the debilitating disease. The team’s findings have been published in the Journal of Clinical Investigation.

According to author Professor Andrew Tobin, the drug targets a particular protein (M1 muscarinic receptor) that is associated with the disease and activates it, having a positive effect on cognition. Different drugs were previously tested on this protein but had too many adverse side-effects to make them practical as effective treatments. The class of drug used in these trials, however, did not manifest any of these adverse side-effects in the subject mice. Professor Tobin explained that the team, including Dr. Sophie Bradley, “found that these drugs can not only improve symptoms of brain degeneration, such as cognitive decline, but can also extend the life-span of these terminally-sick mice,” when administered daily.

Image credit: Thomas Deerinck/NCMIR/Science Source
Image credit: Thomas Deerinck/NCMIR/Science Source

Long Road

Since the trials are still at the animal testing phase, there is no guarantee that these drugs will have the same impact on humans. Even if this particular treatment does not live up to its early promise, it’s providing important discoveries about the disease itself that could play a vital role in the research ahead.

Current treatments simply serve to mask or relieve patient symptoms. There is no cure for the disease, but with each new research project undertaken, there is hope for healing.

The goal of Alzhiemer’s treatments seems to be shifting toward not only improving symptoms of the disease, but also to slow down the deleterious disease progression, thus extending life-span. It will take a lot of time and an ever-accumulating pool of professional knowledge, but with results as promising as these, there is always hope.

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We May Be Able to Treat Alzheimer’s With Light

Hope in Light

In the United States alone, well over five million people are currently living with Alzheimer’s disease. The disease is debilitating for its sufferers and not much easier on their friends and family, who sit by practically helpless as the disease robs their loved one of their mind and body. Now, one company is investigating a promising new approach to help these patients and their families.

Cognito Theraputics is looking into using light to help fight the disease as noninvasively as possible. The therapy they are developing uses light flickering at a specific frequency (40 Hz) to induce brainwaves known as gamma oscillations. As Li-Huei Tsai, one of the study’s senior authors, told the Los Angeles Times, “We just directly recruit other neurons and other cell types in the brain to sort of enable the brain’s inner ability to repair itself.”

In the experiment, mice were exposed to a strip of LEDs flickering at 40 Hz for different durations. After exposure for a single hour, production of beta amyloids, a type of protein associated with Alzheimer’s, was reduced by half in the subjects’ visual cortex, although the levels returned to where they started an hour after treatment. When the mice were exposed to the therapy for an hour a day for seven days, they showed a significant reduction in both beta amyloid plaques and free-floating amyloids.

The researchers are still testing to see how long the levels remain reduced, but their current research has been published in the journal Nature.

The Road Ahead

Of course, with any trial done on mice, there is a big chance that the results will not be replicated in humans, so researchers are urging caution. “It’s a big ‘if,’ because so many things have been shown to work in mice, only to fail in humans,” says Tsai. “But if humans behave similarly to mice in response to this treatment, I would say the potential is just enormous, because it’s so noninvasive, and it’s so accessible.”

The company is still far from the human trial stage and even further from FDA approval. Nevertheless, their research gives hope for those countless millions directly or indirectly impacted by Alzheimer’s. At the very least, the research could provide new insight into how the immune system may be equipped to battle the disease without the need for invasive treatments.

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