Category Archives: Science Articles

Could We Ever Bring Back Alzheimer’s Patients’ Memories?

We spend our whole lives collecting memories. To many of us, these are far more precious than any of our material possessions. Perhaps this is why diseases like Alzheimer’s that rob us of our memories feel especially tragic and frightening.

There’s a lot of brilliant research being done on ways to prevent Alzheimer’s disease or to halt its progress, and each day the field is making great strides toward this goal. Yet many scientists are reluctant to address the elephant in the room: what about the memories that are already gone? Will we ever be able to bring back a lifetime of precious memories to a patient who’s forgotten them all? It’s a difficult question, one that no one can predict with absolute certainty, but here I’ll attempt to describe where our current research stands and the obstacles we must overcome if we’re ever to achieve this goal.

The Hunt for the Engram

Here’s a deceptively simple question for you: what is a memory? You might think you know the answer. Of course, memories are our way of looking pack on our past, the images you recall from your wedding day, the mouthwatering smell of your grandma’s brownies, the lyrics to your favorite song. But what are they really? Do memories exist in physical space, governed by simple chemical reactions like the rest of our bodies? Or are they more ethereal, an untouchable something that’s a part of us yet separate from our physical form? These questions have been a source of philosophical debate for centuries, going back to the time of Plato and Aristotle.

In the early 1900s, neuroscientist Richard Semon hypothesized that our brains undergo an enduring physical or chemical change whenever we form a new memory. He coined a new term, “engram,” to describe this physical manifestation of memory. The nature of the engram was a topic of considerable debate. Some, like William James, believed that each memory is stored within a single neuron. “Every brain-cell has its own individual consciousness, which no other cell knows anything about,” James famously wrote. According to this theory, there’s a cell for all your memories of your grandmother, a cell for memories of macaroni and cheese, a cell for memories of the color blue, and so on. Others took a more holistic approach to memory theory. They believed that memories were stored as a pattern of activity within a particular group of neurons, rather than in a single neuron.

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According to William James, everyone has a “grandmother cell” which contains all the memories you have of your grandmother. Image Source

For nearly a century, neuroscience lacked the proper tools to resolve this debate. Finally, in 2007, a revolutionary paper was published in the journal ScienceThe researchers in the study genetically engineered mice so that any neurons that became activated while learning a new behavior were permanently “tagged.” The researchers observed a particular group of neurons that were activated after learning the new behavior, but not in control mice that received no training. When the mice were exposed once again to the training, causing them to recall their previous memory, the same group of neurons became active. This was seen as the first proof that engrams existed within the brain and could be reactivated when recalling memories.

Subsequent research provided more concrete evidence that these neurons were indeed an engram. In one study, researchers placed rats in a cage where they received a foot shock. Normally, if the rats were placed in that cage again, they would remember the foot shock and display signs of fear such as “freezing.” However, when the researchers selectively destroyed the cells within that engram, the rats seemed to forget the memory and did not freeze when placed back in the cage.

The next breakthrough came in 2011 with the invention of optogenetics, which allows us manipulate the activity of individual neurons without destroying them. Using this technique, it was shown that activating the fear engram caused the rats to freeze, even if they weren’t in the cage where the shock happened. Conversely, inactivating the engram blocked the memory, so that the rats would not freeze when placed back in the cage where they had been shocked.

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Optogenetics allows researchers to directly manipulate neuronal activity using pulses of light. (Don’t worry, this is painless for the mouse!) Image Source

These studies show that engrams are probably formed by the activity of multiple neurons, casting doubt on James’s theory of one memory per cell. However, the mystery of the engram is not yet completely resolved. Today we are still trying to figure out what kinds of changes are occurring at the cellular and molecular level within these neurons when a memory is formed.

Alzheimer’s Disease: Memory Destroyer or Memory Blocker?

Now that we have a better understanding of what exactly a memory is, I can return to my original question: can the memories lost by Alzheimer’s patients ever be rescued? The answer to this question depends on what is actually happening to the memories in this disease. If the engrams encoding these memories are destroyed, it seems unlikely that we could ever rebuild them. However, there is a more hopeful possibility. What if the memories are still present in the brain, but Alzheimer’s simply prevents us from accessing them?

This is essentially a question of what aspect of memory is lost in Alzheimer’s disease. Memory formation is divided into three stages:

  1. Encoding. Your brain translates the raw data obtained through your senses into a pattern of neuronal activity, which forms a short-term memory.
  2. Storage. If the memory is deemed by your brain to be important, it is transferred into long-term storage.
  3. Retrieval. Whenever you recall that memory, your brain accesses its stored engram and allows you to remember.

It is still not entirely clear which stage of memory is disrupted in Alzheimer’s disease. Are the patients simply unable to encode new memories? Can they form memories but not transfer them to long-term storage? Or maybe the memories are there but simply can’t be retrieved?

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A computer is a useful metaphor for understanding the stages of memory (even if it is a bit of an over-simplification). You encode information using the keyboard, which is stored on the hard drive or disk. When you want to retrieve that information, it is displayed on the monitor. Image Source

A study published last year in Nature took a step toward addressing this dilemma. Researchers used a mouse model of Alzheimer’s disease and selected mice that were 7 months old. This age group is a representation of early Alzheimer’s disease, when short-term memory is normal while long-term memory experiences deficits. Using the same foot-shock protocol I described before, they saw that the mice showed freezing behavior 1 hour after the training but had forgotten 24 hours later.

Next, the researchers used optogenetics to activate the engram associated with the fear memory 24 hours after the training period. This time, the mice showed freezing behavior, indicating that the memory had been recalled using the light stimulation. This result is encouraging because it suggests that, at least in the early stages of Alzheimer’s disease, memories can be consolidated into long-term storage, and the problem is simply an inability to retrieve them.

Will We Ever Rescue Lost Memories?

Our understanding of Alzheimer’s disease, and of the nature of memory itself, remain incomplete. The study I’ve just described does not address whether activating an engram can retrieve a memory formed months or even years ago. It also does not explore whether mice in later stages of the disease can have their memories revived in this way. Furthermore, at present we do not have a noninvasive method for activating particular engrams in humans.

However, it does provide at least of glimmer of hope. If it is the case that the memories of Alzheimer’s patients are still present in their brains, then the possibility of restoring the memories becomes much more feasible than if they were completely destroyed. It also suggests that emerging therapies like deep brain stimulation could one day be used to help restore memory.

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Deep brain stimulation uses an electrode to provide stimulation directly into the brain. These devices have had encouraging results for Parkinson’s disease and are now starting to be tested for Alzheimer’s. Image Source

Sometimes, people with Alzheimer’s disease will seem to momentarily remember something they had previously forgotten. They are plenty of videos of this online, such as this one, where a man suffers from severe dementia and yet can inexplicably recall the lyrics to his favorite songs; or this one, where a woman with Alzheimer’s recognizes her daughter after having forgotten her. Perhaps those other memories are not gone but just inaccessible. Perhaps the memories are still buried deep inside their brains, just waiting for the right stimulus to bring them back to the surface.

 

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How Sleep “Cleans” Your Brain and Fends Off Alzheimer’s Disease

Sleep: we spend nearly a third of our lives doing it, yet only recently have we begun to understand its true purpose. You’ve probably read countless articles about how getting enough sleep is important for preventing a variety of diseases, including diabetes, depression, and even Alzheimer’s. However, while strong correlations have existed for decades, until recently there was still little evidence to show why we sleep or how it fends off disease.

As some of you may know, I’m currently living in Switzerland, where I’m conducting research at EPFL over the summer. My research is on the connection between sleep deprivation and Alzheimer’s disease, so for me it’s especially important to help others understand why sleep is so important for your brain’s overall health. A few recent breakthroughs in sleep science research have revolutionized the field and brought about an exciting new era of neuroscience, particularly for Alzheimer’s disease research.

The Brain: A Dumping Ground for Neuronal Waste

While you’re awake, the 100 billion neurons in your brain are hard at work. Through an incredibly complex network of connections and signals, your neurons keep your heart pumping, your muscles moving, and your attention focused on the task at hand. Every time a neuron fires a signal, it undergoes a series of chemical reactions to produce neurotransmitters, which it uses to communicate with other cells. These reactions also produce waste byproducts that need to be disposed of. The neuron packages the waste into vesicles and excretes them into the fluid that surrounds cells in the brain. How these waste products were cleared from the fluid remained a mystery for a long time. More on that in a bit.

These waste products used to not be seen as particularly important to study. But in 2005, a group of scientists came up with a crazy idea that would end up shaking the foundations of Alzheimer’s research: what if amyloid-beta is one of these byproducts of neuronal activity? As a bit of background, amyloid-beta is a protein that forms sticky plaques in the brains of people with Alzheimer’s disease. At large enough sizes, these plaques become toxic to neurons, resulting in neurodegeneration. This is believed to be one of the main driving forces behind the development of Alzheimer’s disease. At the time, we  knew that amyloid-beta came from neurons, but were unsure what caused the neurons to produce it or how to stop them.

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This is what an amyloid-beta plaque looks like inside a real brain. Image Source

The researchers tested their hypothesis using mice genetically engineered to produce human amyloid-beta. They surgically implanted an electrode in the mice’s brains, which was used to measure the neurons’ activity levels. They also implanted a microdialysis probe, which sampled the mice’s brain fluid periodically to monitor levels of amyloid-beta. When the researchers electrically stimulated the mice’s brains, causing neurons to become highly active, they saw an abrupt increase in amyloid-beta levels in the area of stimulation. Conversely, when they used drugs to decrease neuronal activity, amyloid-beta levels dropped.

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This is one of the figures from that study. Panel A shoes the mice’s EEG activity (a measure of neuronal firing) before and after the electrical stimulation. Panel B shoes the immediate increase in amyloid-beta levels after stimulation, while Panel C shoes the decrease after drug treatment to reduce neuronal activity.

The results of this landmark study were published in the journal Neuron and have since been cited hundreds of times by other papers. Many other studies have confirmed the initial results and expanded into other model organisms. The revelation that amyloid-beta is excreted during neuronal activity was huge, because until then we’d assumed that only “diseased” neurons were releasing the toxic protein. This new research showed that not only were healthy neurons releasing amyloid-beta, but they did so every time they were activated.

Sleep: The Good Kind of “Brainwashing”

This brings us back to the question I brought up earlier: how does the brain get rid of all these waste products? If amyloid-beta and other toxic byproducts of neuronal activity were allowed to accumulate unchecked, we’d probably all develop Alzheimer’s disease in infancy. The brain must have some way of cleaning itself. We knew that the waste products eventually ended up being flushed into the cerebrospinal fluid, but no one was sure how exactly it got there from within the brain.

The answer finally came in 2012 with the discovery of the glymphatic system. Researchers found that cerebrospinal fluid was able to enter the brain through a cavity called the subarachnoid space, and flush out toxins via drainage vessels running parallel to the veins. They demonstrated that this pathway was capable of clearing away amyloid-beta from the brain in mice.

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The recently-discovered glymphatic system pumps cerebrospinal fluid through the subarachnoid space into the brain, where it flushes out toxins (including amyloid-beta) through vessels surrounding the veins. Image Source

Only a year later, another breakthrough came. A paper published in Science revealed that the glymphatic system was intricately linked with sleep. During sleep, the channels that carry fluid through your brain expand by 60%, resulting in enhanced glymphatic drainage. The researchers showed that in sleeping mice, the expanded glymphatic vessels cleared away amyloid-beta from the brain twice as quickly as they did when the mice were awake. This paper received a lot of attention because it shed light on a likely function of sleep: to allow the brain to clean itself. New studies quickly came forward with additional evidence, showing that amyloid-beta levels in your brain increase throughout the day and then decrease again when you sleep.

How Sleep Deprivation Can Poison Your Brain

In less than 10 years, our understanding of sleep and Alzheimer’s disease has been turned upside down. We now know that during the day, when neurons are highly active, they release amyloid-beta into the brain fluid. Then when you sleep, your brain’s glymphatic vessels expand and flush away the amyloid-beta and other waste products before they can accumulate to toxic levels. This newly-discovered relationship brings up an ominous possibility: could sleep deprivation reduce amyloid-beta clearance and thus lead to Alzheimer’s disease?

Correlational studies suggest the answer may be yes. Elderly people with insomnia and other sleep disorders are at an increased risk of dementia and have higher levels of amyloid-beta in their brains. A recent study suggested an even more troubling possibility. The paper showed that chronic sleep deprivation may cause neurons to become hyperactive, so that they excrete greater amounts of amyloid-beta into the brain. In turn, this amyloid-beta can interact with other neurons to make it harder to sleep, creating a vicious cycle that could spiral out of control and perhaps lead to Alzheimer’s disease.

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The authors suggested that sleep deprivation could start a vicious cycle, with amyloid-beta deposition increasing exponentially.

The possibility that sleep deprivation could contribute to Alzheimer’s disease is deeply concerning. The CDC reports that 1 in 3 adults routinely do not get at least 7 hours of sleep per night. The problem may be even more severe for elderly people, of whom nearly half report sleep disturbances. By not getting enough sleep, we could be accumulating toxic levels of amyloid-beta in our brains and setting ourselves up for Alzheimer’s disease as we age.

Despite being rather frightening, these recent findings also come with an aspect of hope. While seemingly a major risk factor for Alzheimer’s disease, sleep deprivation is also preventable. By prioritizing sleep as a vital facet of overall health, as well as seeking medical assistance for sleep disorders like insomnia and sleep apnea, we may all be able to reduce our risk for Alzheimer’s and perhaps even other brain diseases. So put down that phone, turn off the lights and head to bed at a reasonable hour tonight. You’ll wake up with a squeaky clean brain in the morning!

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Homocysteine and Dementia: Impact of Nutrition on Neurodegeneration

This week’s article is a guest post by Dr. Nafisa Jadavji, a research associate and lecturer at Carleton University and the University of Ottawa. To submit your own guest post to AlzScience, please contact us.

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High levels of homocysteine have been implicated in neurodegenerative diseases, such as dementia, mild cognitive impairment, and Alzheimer’s disease. Homocysteine can be measured in blood easily, which has led to several studies in humans reporting that elevated levels of homocysteine lead to increased risk of developing neurodegenerative diseases or affect progression. Interestingly, homocysteine levels in our bodies increase as we age.

Vascular cognitive impairment (VCI) is the second leading cause of dementia after Alzheimer’s disease.  VCI is the result of reduced blood flow to the brain, however, the pathology is not well understood. Reduced blood flow ben be a result of age and health (e.g. high cholesterol). The clinical presentation of VCI varies, most the patients have some degree of cognitive decline. There are currently no treatments for VCI since the actual pathology remains unknown.

Nutrition is a risk factor for VCI, specifically high levels of homocysteine. High levels of homocysteine can be reduced by B-vitamins, like folates or folic acid. Folates are the natural occurring form of the vitamin, these are often found in food such as green leafy vegetables or liver. Whereas folic acid is the chemically synthesized form that is often taken in supplemental form.

My research program focuses on how nutrition affects the brain, specifically how folates affect neurodegeneration.

Using a mouse model of VCI we have reported that deficiencies in folates, either dietary or genetic, affect the onset and progression of VCI. Using the Morris water maze task, we report that mice with VCI and folate deficiency performed significantly worse compared to controls. We assessed changes in the brain using MRI and interestingly found that folate deficiency changed the vasculature in the brain of mice with VCI. Because of either a genetic or dietary folate deficiency, all the mice had increased levels of homocysteine. However, we did not observe any significant association between elevated levels of homocysteine and behavioral impairment or changes in the brain tissue of VCI affected mice.

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In the Morris water maze, a mouse is placed in a pool and must swim to find a hidden platform. The mouse’s memory is measured based on how long it takes to find the platform after it’s placed in the pool a second time. Image source

Our results suggest that it is not elevated levels of homocysteine making the brain more vulnerable to damage, but the deficiency in folates, either dietary or genetic that changes the brain. In the cell, folates are involved in DNA synthesis and repair as well as methylation. These are vital functions for normal cell function. Therefore, reduced levels of folate may be changing the cells in the brain and making them more vulnerable to any types of damage. I would like to suggest that high levels of homocysteine may just be out put measurement of some sort of deficiency (e.g. reduced dietary intake of folates). Several studies using brain cells that are grown in petri dishes have reported that extremely high levels of homocysteine need to be added to cells to cause damage. These levels are usually not observed in humans.

In terms of future directions, more research is required to understand how deficiencies in folates, homocysteine and other nutrients that reduce levels of homocysteine like choline change cells in the brain throughout life and how these changes are related to neurodegeneration.

For more information about my research please visit my personal website.

 

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How Alzheimer’s and Depression are Linked to Hearing Loss (Reblog)

Our article this week is a reblog from the New Generation Hearing Blog. It’s a fairly short article, but I like that sheds light on the little-known connection between brain health and hearing loss. Click the link below to give it a read!

 

There are at least 38 million people who suffer from hearing loss throughout America. Many senior citizens expect to lose their hearing over time but few know that it could increase the chances for depression and even increase the risk of Alzheimer’s disease. In fact, hearing loss can influence every aspect of an individual’s life […]

via How Alzheimer’s and Depression are Linked to Hearing Loss — New Generation Hearing Blog

 

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Marijuana and Alzheimer’s: What Does the Science Say?

The legalization of marijuana, whether for medical or recreational use, has been the subject of a lot of recent debate. In states where it is legal, many doctors prescribe cannabis to treat a variety of ailments including multiple sclerosis, chronic pain, and severe nausea from chemotherapy. Additionally, several studies (such as this one) have suggested that the drug’s primary active ingredient, THC, may also be useful in treating the harmful inflammation associated with Alzheimer’s disease.

The Endocannabinoid System

The reason that marijuana and other cannabinoids can get you high is because of their chemical similarity to a family of molecules produced in our own bodies called endocannabinoids. Endocannabinoids are a vital part of the brain’s signaling network and help to modulate multiple sensations including mood, pain, and hunger. THC is chemically similar to our endocannabinoids and can bind to their receptors, resulting in overactivation of the endocannabinoid system. This leads to a variety of effects including reduced focus, poor coordination, and a pleasant “high.”

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Endocannabinoids and natural or synthetic cannabinoids all activate the same receptors in the brain. Image Source

Interestingly, the endocannabinoid system seems to become less active during aging. Aged rats have fewer endocannabinoid receptors present on their neurons in multiple brain regions including the hippocampus, which is considered the brain’s memory center. Unfortunately there has been little research on whether the endocannabinoid system is further disrupted by Alzheimer’s disease. The few studies that have been attempted on this topic have yielded conflicting results, and more research is needed to tease out the answer. One intriguing hint comes from a study that used a drug to increase endocannabinoid levels in the brains of Alzheimer’s mice. These mice had reduced cellular damage and memory impairment, suggesting that kickstarting the endocannabinoid system could be beneficial for neurodegeneration.

THC as an Alzheimer’s Treatment

Though our understanding of the endocannabinoid system remains poor, multiple studies have suggested that cannabinoid drugs could be a feasible treatment for Alzheimer’s disease. In one study, a group of mice with a mutation simulating Alzheimer’s disease were treated with several types of synthetic cannabinoids. This resulted in reduced inflammation and improved cognitive function. Other studies have utilized cannabidiol, a component of marijuana that does not produce any psychoactive effects, with similarly encouraging results.

Apart from the tentative successes of synthetic cannabinoids, THC has also shown some potential as an Alzheimer’s treatment. Acetylcholinesterase inhibitors, the only class of Alzheimer’s drugs currently available, were shown to be less effective than THC at preventing toxic plaque buildup in the brain. Another study found that a mixture of THC and cannabidiol was successful at improving Alzheimer’s disease in rats.

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Acetylcholinesterase breaks down acetylcholine in the brain. Alzheimer’s drugs inhibit this process to improve memory. However, THC may be even more effective than our current drugs. Image Source

Safety and Efficacy in Humans

Even fewer studies have examined the effects of cannabinoids in humans. The best we have to go on so far is a few small clinical trials comprising 60 subjects in total. A synthetic version of THC called dronabinol was shown to significantly improve behavioral symptoms for many of the Alzheimer’s patients. Some side effects were reported (including tiredness and delirium) but none were severe enough to cause patients to withdraw from the trials.

Despite these encouraging results, a review paper on this topic pointed out several problems with these clinical trials. In addition to the very small sample size, many of the trials were not randomized and included only a short treatment period of between two and seven weeks. These complications make it difficult to draw conclusions from these results.

What’s the Verdict?

Unfortunately, there is simply not enough data yet to determine the safety and effectiveness of marijuana or other cannabinoids to treat Alzheimer’s disease. Based on the promising results that I described above, the topic certainly warrants further study. We can only hope that policy-makers will see past their fear of illicit drugs to provide funding for research into cannabinoids’ effects on the brain.

Further reading: Cannabinoids in late-onset Alzheimer’s disease

 

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How to Reduce Your Dementia Risk in 2017

2017 is almost upon us, and that means it’s time for New Year’s resolutions. Many of us resolve to lose weight, quit smoking, or spend less money. However, I’d like to suggest a new resolution for you to try out this year: improving the health of your brain. Though Alzheimer’s disease and other dementias are not completely preventable, there are a variety of steps you can take to substantially reduce your risk. The younger an age you start implementing these simple lifestyle changes, the more benefits you will reap, but it’s never too late to start protecting your brain.

Tip #1: Improve Your Oral Hygiene

Nearly half of all adults in America have periodontitis, a severe form of gum disease that gradually destroys the bone sockets holding your teeth in place, resulting in tooth loss. Recent evidence suggests that the bacteria  that cause periodontitis may be able to enter the brain, and their presence has been correlated with reduced cognitive function. Protect your mouth and your brain by brushing twice per day, flossing once per day, and visiting the dentist twice per year. To read more see How Oral Hygiene Protects Your Brain From Dementia

Tip #2: Get Your Daily Dose of Vitamin D

A recent meta-analysis concluded that vitamin D deficiency is a strong risk factor for dementia. Vitamin D is not easily obtained through food, but our bodies can synthesize it when our bare skin (without sunscreen) is exposed to sunlight. The time required to meet your daily dose of vitamin D depends on your skin tone, the amount of sunlight available, and how much skin you have exposed. On a sunny summer day, 10-15 minutes is often enough. You may want to consider taking vitamin D supplements during the winter, if you live in an often-cloudy area, or if you do not go outside every day.

Tip #3: Reduce Your Risk of Diabetes

Nearly 30 million Americans (around 10% of the total population) have diabetes, and another 86 million are prediabetic. People with diabetes have an approximately 54% higher risk of Alzheimer’s disease. According to the NIH’s Diabetes Prevention Program, even people at high risk of diabetes can prevent the disease through a combination of weight loss (5-7% of your total body weight), a healthy diet, and regular exercise. The National Diabetes Education Program offers lots of great tips for transitioning to a healthier lifestyle. To read more see Alzheimer’s Disease: Diabetes of the Brain?

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The impact of dietary choices on the risk of type 2 diabetes. Source

Tip #4: Get Your Brain Health Checkup

Healthy Brains is a website created by the Cleveland Clinic Lou Ruvo Center for Brain Health. The website is centered around the six pillars of brain health: physical exercise, food/nutrition, medical health, sleep/relaxation, mental fitness, and social interaction. One of my favorite parts about the site is the Brain Health Checkup, a free quiz that takes around 20 minutes to complete. After taking the quiz, you can read personalized tips on how to improve your brain health. Click here to check it out.

 Tip #5: Get Enough Sleep

You’ve probably heard a million times about the health consequences of sleep deprivation, but did you know that it may also increase the risk of Alzheimer’s? The Baltimore Longitudinal Study on Aging found that people over the age of 70 who report little sleep or low-quality sleep have higher levels of amyloid beta (a toxic protein linked to Alzheimer’s disease) in their brains. Additionally, a 2013 study found that amyloid beta and other toxic substances can actually be flushed out of the brain during sleep.

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Age-based recommendations from the National Sleep Foundation. Source

Tip #6: Adopt the Mediterranean Diet

The Mediterranean diet is often praised for its cardiovascular benefits, but recent studies show that it’s also great for your brain. This diet, commonly consumed in places like Italy and Greece, has been linked to a reduced risk of Alzheimer’s and improved cognitive function in older adults, as well as a longer average lifespan. The Mediterranean diet is characterized by high consumption of plant-based foods including fruits, vegetables (especially leafy greens), whole grains, legumes, and nuts. Red meat and dairy are consumed no more than a few times per month, replaced instead by poultry or fish.

Tip #7: Be Socially Active

Engaging in social interactions is a great way to stimulate your brain, and having a large social network is correlated with a reduced risk of dementia. While a causal relationship is difficult to determine, social engagement has also been shown to improve overall quality of life, especially for older adults. For introverts, there are many ways to be socially active besides going out with friends. These could include adopting a pet, conversing on social media websites, volunteering, or joining a community group.

Tip #8: Get More Exercise

This one might already on your list of resolutions, but here’s one more reason to get off the couch. Studies have consistently shown that people who get regular physical exercise have a substantially lower risk of Alzheimer’s disease and other dementias. Aerobic exercise, such as walking, jogging, biking, or dancing, seem to have the biggest protective effect on brain health. The CDC recommends that adults get 2.5 hours of moderate aerobic activity or 1.25 hours of vigorous aerobic activity each week, plus at least two sessions of muscle strength training.

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The many benefits of exercise for your brain. Source

Tip #9: Protect Your Brain From Injuries

Traumatic brain injuries (TBI’s), which may be the result of contact sports, falls, or car accidents, affect nearly 1.7 million Americans each year. TBI’s, including mild injuries that do not necessarily cause a concussion, have been repeatedly linked to an increased risk of Alzheimer’s disease. TBI’s are especially damaging in children, whose brains are still in the process of developing. Minimize your risk of a TBI by wearing a helmet when playing contact sports, installing house fixtures to protect from falls, and always wearing a seatbelt while driving.

Tip #10: Never Stop Learning

Lifelong education, whether formal or informal, is vital for keeping your brain active and maintaining proper cognitive function. Formal education could include taking classes at a nearby community college or online, teaching yourself a new language, or learning to play an instrument. More informal types of mental stimulation could include reading, doing crossword puzzles, social interaction, or attending musical or theatrical performances.

 

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Sniffing Out Dementia: What Your Nose Can Tell You About Your Brain

Detecting Alzheimer’s disease can be tricky, especially in its earliest stages.  Alzheimer’s is frequently misdiagnosed, due in part to the expensiveness and complexity of the current diagnostic tools. According to a 2012 examination of the National Institute on Aging’s Alzheimer’s Disease Centers, physicians may fail to detect more than 1 in 10 Alzheimer’s cases.

Alarmingly, some centers also had a false positive rate of more than 50%, meaning that half of the patients who were diagnosed with Alzheimer’s actually did not have the disease. The symptoms of these individuals may have been due to other conditions such as vascular dementia or thyroid dysfunction. An incorrect diagnosis could have resulted in the true cause of these patients’ memory loss going untreated (see Is It Really Alzheimer’s? 10 common misdiagnoses you should know about).

However, there might be a simpler and more cost-effective way to help diagnose Alzheimer’s disease: your sense of smell. As strange as it sounds, your nose can provide some key insight into the health of your brain.

Sniffing Out Dementia

Just like vision and hearing, our sense of smell tends to gradually deteriorate as we get older. Anosmia, the complete inability to smell, affects more than 50% of people over the age of 65 and 75% of people over 80. This likely contributes to the loss of appetite that many elderly people experience, as our sense of smell is closely tied to our ability to taste and enjoy food. Changes in the nose’s smell receptors and in the parts of the brain responsible for olfactory processing are likely to blame for age-related anosmia.

While anosmia is common among all elderly individuals, it seems to be especially prevalent in certain neurological conditions, including dementia. The frequency of anosmia among dementia patients has been known since the 1970s, but only recently has this observation begun to attract the attention of researchers.

The ability to identify different odors is frequently impaired in early-stage Alzheimer’s patients, with complete anosmia appearing in the later stages of the disease. A small study involving 90 patients with mild cognitive impairment found that individuals with greater olfactory impairment were more likely to progress to Alzheimer’s disease during the two-year study period. Many of these patients were unaware of their own inability to smell.

#AlzFact: Peanut butter might help identify early-stage Alzheimer’s. A small study from the University of Floria found that Alzheimer’s patients have difficulty smelling peanut butter, especially with the left nostril.

An olfactory assessment called the Pocket Smell Test has shown promise as a diagnostic tool for Alzheimer’s disease. In a small 60-patient study, this simple three-item test was able to distinguish Alzheimer’s from vascular dementia and major depressive disorder with 95% accuracy, a dramatic improvement from the 50% false-positive rate by NIA physicians that I described earlier. All of the Alzheimer’s patients in the study had two or three incorrect responses to the smell test, while nearly all of the vascular dementia and depression patients had zero or one incorrect response.

Another small study suggested that smell tests could also be used to distinguish Alzheimer’s from semantic dementia, frontotemporal dementia, and corticobasal dementia. Notably, smell tests would probably be less useful for distinguishing Alzheimer’s from Parkinson’s disease, since anosmia seems to be equally common in these two conditions. However, simple smell-detection tests could serve as an inexpensive method to improve the accuracy of Alzheimer’s diagnoses when combined with more traditional diagnostic tools.

Could Infections Be To Blame?

The reasons for the prevalence of anosmia in patients with Alzheimer’s or other dementias remain poorly understood. One interesting hypothesis, first proposed back in 1986, posits that the olfactory nerve (which transmits smell information from the nose to the brain) could serve as a potential entry point for environmental toxins or microbial agents to reach the brain. This has since been dubbed the olfactory vector hypothesis.

The brain is protected from external agents by the blood-brain barrier, which prevents most microbes and chemical substances from crossing between the nervous system and the blood. Olfactory neurons are unusual in that they are directly exposed to the external environment, making them vulnerable to infiltration. Unlike any other sensory cells, olfactory neurons connect directly to the brain without any intermediate synapses. Microbes can taken advantage of this direct connection as an ideal route to bypass the blood-brain barrier.

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Olfactory neurons (shown in yellow) serve as a direct connection between the nasal cavity and the brain. Image source

Animal studies show that the viruses that cause polio, influenza, rabies, hepatitis, and herpes are all capable of infecting the brain via the olfactory nerve. In addition, many environmental toxins including metals, chemicals, and nanoparticles can be taken up by olfactory neurons and transported to the brain. This may help explain why prolonged exposure to air pollution or certain industrial chemicals can greatly increase the risk of Alzheimer’s (see Air Pollution, Aluminum, and Vitamin D Deficiency Linked to Dementia Risk).

The olfactory vector hypothesis remains a speculative model, and more evidence is needed to prove whether infiltration of the brain by external agents via the olfactory nerve can lead to Alzheimer’s. It is an intriguing idea that certainly warrants further study.

 

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