Category Archives: Science Articles

What is the difference between dementia and Alzheimer’s disease?

This is probably the most common question I’m asked by my readers, so I decided to devote an entire article to clearing up the confusion. Doctors and scientists often throw around words like “dementia,” “Alzheimer’s,” and “mild cognitive impairment” without making it clear what the difference is between them. Understanding what each of these terms mean is important for being able to interpret articles and recognize how scientific findings may apply to you.

Let’s start with dementia. Dementia itself is actually not a disease, but a set of symptoms. The most well-known dementia symptom is memory loss, but it also includes other things such as difficulty communicating, impaired attention, poor judgement, and a decline in visual perception.

Dementia symptoms can be caused by many different diseases. The most common cause of dementia is Alzheimer’s disease, which makes up around 60% of all dementias. However, many other diseases can cause dementia, including Parkinson’s disease, vascular dementia, frontotemporal dementia, and Lewy body disease. Dementia is often referred to as an “umbrella term” for a range of symptoms than can be caused by multiple diseases.


Dementia is an “umbrella term” for a set of symptoms that can be caused by several different diseases. Image Source

I like to use an analogy to make this distinction a bit clearer. Think of Alzheimer’s disease like the flu. These are both diseases with a particular cause. Now think of some of the symptoms of having the flu: congestion, chills, nausea, and so on. There are many different diseases that can cause these symptoms, like a cold or sinus infection. In the same way, there are multiple diseases that can cause dementia symptoms.

To put it another way: everyone with Alzheimer’s disease has dementia, but not everyone with dementia has Alzheimer’s disease.

Now, there’s a third term you may have also heard thrown around: mild cognitive impairment, or MCI. It’s characterized by memory problems that are noticeable but not severe enough to interfere with daily life, such as forgetting appointments, losing your train of thought, and having trouble with planning or organization. Some people with MCI later progress to Alzheimer’s disease or other dementias, while others do not. Around 20% of adults over age 65 have MCI.


Mild cognitive impairment sometimes progresses to Alzheimer’s disease or other dementia-causing diseases. Image Source

So there you have it! To summarize:

  • Dementia is a set of symptoms that include memory loss, impaired attention, and and poor judgement.
  • Alzheimer’s is one of several diseases that can lead to dementia symptoms.
  • Mild cognitive impairment is a less serious memory problem than can, but does not always, progress to dementia.

Hopefully that helps to clear up some of the confusion surrounding these three terms! As always, feel free to comment or send me a message if there are any other topics you’d like me to explain.


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Vascular Damage May Affect Progression to Alzheimer’s Dementia


Guest author: Rachana Tank has a master’s degree in Neuropsychology from Maastricht University in the Netherlands. Her goal is to pursue a PhD in psychology exploring cognitive ageing, where her research interests lie.

As we grow older, we tend to become a little forgetful which is thought to be a normal part of ageing, but when does forgetfulness turn into abnormal ageing? Sometimes even slight but noticeable changes in thinking skills can be symptoms of an underlying issue. Alzheimer’s dementia is a continuous process, a progression taking place over many years, during which individuals experience considerable deficits before reaching clinical dementia. Stages leading up to Alzheimer’s dementia are referred to as predementia stages and are considered to be on the spectrum of Alzheimer’s dementia. In such stages, cognitive deficits are typically experienced as deterioration of memory, attention, and language skills.

Predementia stages can include individuals who self-report a decline in cognitive abilities (subjective cognitive impairments), or experience cognitive impairments that can be diagnosed by standardised testing (mild cognitive impairments). Both of these can, but not always, indicate an initial phase of neurodegeneration that may suggest they are in an early stage of Alzheimer’s dementia.


The difference between normal brain ageing (purple line) and stages of cognitive decline experienced as part of abnormal brain ageing in dementia. Image source

Individuals with subjective or mild cognitive impairments tend to have a higher incidence of future cognitive decline than the general population and more often show Alzheimer related pathology. However, it is still difficult to predict which individuals in these stages will progress to Alzheimer’s dementia.

Differentiating between those who will progress and who will not is a difficult task. However, biomarkers can be utilised to indicate the presence of Alzheimer’s pathology to detect and diagnose predementia stages. Namely, amyloid protein plaques and neurofibrillary tau tangles are the hallmarks of Alzheimer’s disease, with amyloid pathology being the earliest identifiable change in the brain. Although amyloid and tau have both been fundamental to understanding and estimating the pathological cascade, there is a lot of emerging evidence to suggest that it is not just tau and amyloid in isolation that contribute to progression of Alzheimer’s pathology and subsequent cognitive symptoms.

As evidence indicates there is more to consider than amyloid and tau, recent research, including my master’s research, investigates mixed Alzheimer’s pathology in early stages. Mixed pathology refers to hallmark Alzheimer pathology, such as amyloid and tau, that coexist with additional abnormalities such as vascular disease. Vascular disease is of particular interest in predementia stages as it is the most common disease to coexist with typical Alzheimer pathology early in the disease process.

Vascular disease can be defined as any condition that affects the arteries, veins, and capillaries responsible for carrying blood to and from the heart. Vascular damage can compromise brain health by reducing blood flow to vital areas, leading to loss of neurons. Such damage to the brain affects how well certain areas function, sometimes leading to decreased cognitive abilities such as language difficulties, attention problems or memory issues. There is evidence that vascular disease shortens time to progression when coexisting with traditional Alzheimer pathology. However, the mechanisms by which they may interact is not known.


Arterial plaques are one example of vascular disease. Image source

My research investigated mixed pathology in 269 memory clinic patients aged 39 or older with subjective or objective cognitive impairments. Levels of amyloid burden and vascular damage were recorded at baseline and at follow-up between 1 and 5 years later. Those who progressed to Alzheimer’s dementia were then compared to those who did not. Vascular damage was assessed using MRI scans, and level of amyloid pathology was determined via cerebrospinal fluid samples.

The results of my research found that Alzheimer’s disease patients with vascular damage had less amyloid in their brains than Alzheimer’s patients who did not have vascular damage. This suggests that vascular damage may worsen the effects of amyloid plaques on cognitive decline and Alzheimer’s. These findings are compatible with other studies that investigated vascular damage in relation to amyloid burden.

Different amounts of amyloid in patients did not show any direct relationship with vascular damage, suggesting that the presence or absence of vascular disease does not influence the presence of Abeta. However, both vascular damage and amyloid pathology increased the risk of progressing to Alzheimer’s dementia significantly, and 93% of individuals who progressed to Alzheimer’s dementia showed abnormal levels of both amyloid and vascular pathology, indicating that both contribute to the development of Alzheimer’s dementia. These research insights help us to better understand early stages and the influencing factors involved. This allows us to develop interventions, for example, promoting cardiovascular health in those at risk by encouraging memory clinic patients to participate in exercise programs.

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Macular Degeneration: Alzheimer’s Disease of the Eye?

Macular degeneration affects more than 10 million Americans, making it the leading cause of vision loss. It occurs when, for reasons that aren’t entirely understood, the central region of the retina (known as the “macula”) begins to deteriorate. The disease is considered incurable and usually occurs in people over the age of 55. Smokers and individuals of Caucasian decent are at an increased risk, as well as anyone with a family history of the disease.


This animation from the American Macular Degeneration Foundation shows the loss of central vision that occurs with this disease.

Surprisingly, there are many parallels between macular degeneration and Alzheimer’s disease. Though the two conditions may seem unrelated, both are believed to be caused by the buildup of a toxic protein called amyloid-beta. In Alzheimer’s disease, amyloid-beta plaques accumulate in the brain, while in macular degeneration, amyloid-beta forms fatty deposits behind the retina called “drusen.” Plaques and drusen appear to have similar composition of proteins and fats, and utilize the same mechanisms to damage surrounding tissue.


Diagram of a normal eye and an eye with macular degeneration. Image Source

The similarities between these two diseases don’t end there. Older people with macular degeneration are three times as likely to have cognitive impairment, suggesting that the same processes leading to amyloid-beta accumulation in the retina could also be occurring in the brain. This makes sense, since the retina and the brain are both part of the central nervous system. Additionally, several mouse models of Alzheimer’s disease exhibit amyloid-beta buildup in both the brain and the retina, further cementing the link between the two conditions.

The emerging connection between Alzheimer’s and macular degeneration has several important consequences. If amyloid-beta buildup in the retina could be a sign of a similar process happening in the brain, it raises the possibility that eye exams could serve as a non-invasive method to screen people for Alzheimer’s disease. Clinical trials for this idea are still ongoing, but the early results seem encouraging. These eye exams could potentially allow for earlier Alzheimer’s diagnosis or a lower risk of misdiagnosis.

This relationship also suggests that people with Alzheimer’s disease could be at a greater risk of macular degeneration, or vice versa. If you or a loved one is experiencing dementia, it’s recommended to minimize the risk of macular degeneration by receiving regular eye exams, protecting the eyes from sunlight, and maintaining a healthy diet.


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What Naked Mole Rats Can Teach Us About Alzheimer’s Disease

Yes, you read that title correctly. I’m talking about naked mole rats, the burrowing hairless rodents with a face only a mother could love. You might just know them for their strange appearance, but naked mole rats have fascinated scientists for decades due to their extreme longevity. They are by far the longest-lived rodent species, with a maximum lifespan of more than 30 years, compared to only 2 years for your typical mouse. They also are practically immune to cancer, for reasons we don’t entirely understand.

So what does this have to do with Alzheimer’s? Well, another one of the naked mole rat’s strange quirks is that is possesses extremely high levels of amyloid-beta, the toxic protein that is believed to cause Alzheimer’s disease. In humans, amyloid-beta aggregates into sticky plaques in the brain, which can cause a whole host of problems. Amazingly, naked mole rats have even higher amyloid-beta levels than 3xTg-AD mice, which are an Alzheimer’s mouse model genetically engineered to over-produce amyloid-beta. However, the amyloid-beta found in naked mole rats is less sticky and does not tend to form plaques, despite being just as toxic to neurons. Additionally, while amyloid-beta in humans increases as we age, its levels remain constant in naked mole rats. This suggests that amyloid-beta could be harmless (or possibly even beneficial) when it’s present in its non-sticky form. A 2015 report also found that the brains of old naked mole rats look more like what you’d expect to see in a baby animal’s brain, with high numbers of new neurons constantly being formed.

The fact that naked mole rats possess exceedingly high levels of amyloid-beta throughout their lifespan, yet do not develop Alzheimer’s disease, makes them an extremely useful research subject. If scientists can unravel what makes these rodents so resistant to amyloid-beta, we might be able to apply this finding to humans in the form of a treatment for Alzheimer’s disease. So even though they may not be the cutest creatures, you might someday have the naked mole rat to thank for keeping your brain healthy!

Here are some more fun facts about naked mole rats! They have no sense of pain and are nearly blind. They are almost entirely cold-blooded, relying on their environment to regulate body temperature. In order to live underground, naked mole rats have evolved very low rates of breathing and metabolism, and can survive for up to 5 hours in low-oxygen conditions. They live in eusocial colonies similar to ants or bees, with a single queen that produces all the colony’s offspring.


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Alzheimer’s and Coconut Oil: What Does the Science Say?

Coconut oil has certainly been a health craze over the past few years, with people claiming it can do everything from whiten your teeth to promote weight loss. Recently I’ve had several readers ask me to look into claims that coconut oil could treat or cure Alzheimer’s disease. So let’s dive into the details and figure out whether coconut oil could really be healthy for your brain.

Ketones and Where to Find Them

Most explanations for coconut oil’s supposed miraculous properties focus on its high ketone content. The “ketogenic diet,” sometimes shortened to the “keto diet,” has recently seen a surge in popularity. The idea behind the keto diet is to shift your body’s primary energy source from carbohydrates to ketones. Normally, the carbs in the food you eat are converted into glucose (aka sugar), which your body then uses for energy. However, when your carb intake is very low, a backup mechanisms called ketogenesis kicks in. Your liver starts breaking down fat into ketones, another type of energy-storing molecule similar to glucose but with a different chemical structure.

To induce ketosis, people cut back on their intake of carbs to less than 20 grams per day (equivalent to half a cup of pasta or one slice of bread), compared to the 225 to 335 grams that most people consume daily. To compensate for the reduced calories, they also increase their consumption of fats. Coconut oil is especially popular in keto diets because it is rich in medium-chain triglycerides, a type of fat that your body can easily convert into ketones. By maintaining a low-carb diet for an extended period of time, your body shifts toward utilizing fat as its primary energy source. As a result, your pancreas starts producing lower levels of insulin, the hormone that tells your body to store glucose as fat. The idea then is that less of what you eat gets stored as body fat and more gets burned for energy, and so you lose weight.

An overview of the ketogenic diet. Image Source

How Ketones Affect the Brain

In general, most studies have suggested that the keto diet could be an effective weight loss tool, though research on its longer-term effects remains limited. But what effect does it have on the brain? The idea that coconut oil and other ketogenic foods could help with Alzheimer’s disease comes from studies showing that Alzheimer’s patients have lower glucose metabolism in their brains. This means that their brains have trouble utilizing glucose for energy, which could result in cognitive impairment. This tends to be worse in people with diabetes, perhaps one of the reasons why diabetics are at an increased risk of Alzheimer’s. (See Alzheimer’s Disease: Diabetes of the Brain?)

That’s where coconut oil might come in. Since their brains have trouble metabolizing glucose, perhaps Alzheimer’s patients could substitute ketones as an alternative source of energy. Research shows that ketone metabolism in normal in Alzheimer’s brains, providing hope that this could be a possibility. A recent study also showed that neurons incubated with coconut oil and then exposed to amyloid-beta (a toxic protein associated with Alzheimer’s disease) had increased survival compared to neurons not treated with coconut oil.

Unfortunately, clinical trials in humans are lacking. I was only able to find one small study from Spain, in which 22 Alzheimer’s patients were given 40 mL of coconut oil daily for three weeks. They found that these patients scored better on a memory test than others who did not receive coconut oil. However, the sample size was very small and they also did not include a placebo in the control group, so it’s difficult to say how meaningful these results really are. Other clinical trials studying different types of ketogenic compounds to treat Alzheimer’s disease have seen only limited success in a small subset of participants.

What’s the Verdict?

While it’s possible that it could help you lose weight or provide other health benefits, there’s just not enough evidence to say whether or not coconut oil and other ketogenic foods could reduce the risk of Alzheimer’s disease. On the other hand, there are some possible risks associated with it. Consumption of coconut oil in large quantities can lead to gastrointestinal problems, and its high saturated fat content also makes it a risk factor for heart disease or obesity. However, incorporating a small amount of coconut oil into your diet could be beneficial if you offset those calories with reduced carb intake. That being said, it’s unlikely that coconut oil or any ketogenic diet alone will be enough to dramatically alter your risk of Alzheimer’s disease. (To learn about real ways you can reduce your risk, see How to Reduce your Dementia Risk in 2017)


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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.


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.


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?


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.


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.

I’m currently writing this article from Switzerland, where I’m conducting research at the EPFL Brain Mind Institute 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.


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.


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.


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.

Screenshot 2017-06-11 at 3.02.17 PM

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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