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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Alzheimer’s Patients May Experience “Silent Seizures”

If you’ve read our recent article on sleep science, you know that neurons release amyloid-beta (a toxic protein implicated in Alzheimer’s disease) during periods of activity. The protein is excreted as a waste product whenever neurons fire an electrical signal. This is probably why patients with epilepsy often have large amyloid-beta plaques in their brains, as the fast pulses of activity created by seizures cause neurons to excrete large amounts of the protein. Based on this observation, some have theorized that the buildup of amyloid-beta in Alzheimer’s disease could be caused by hyperactive neurons.

In a paper published recently in Nature Medicine, researchers used electrodes to monitor neuronal activity in the medial temporal lobe (MTL) of two patients with early Alzheimer’s disease. The MTL is highly vulnerable to amyloid plaque buildup in Alzheimer’s disease and contains structures important for memory, including the hippocampus and entorhinal cortex. Typically a scalp EEG is used for measuring seizure activity, but because the MTL is buried deep within the brain, it’s difficult to observe in this way. The researchers got around this problem by inserting electrodes directly into the patients’ MTL.

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This figure shows the placement of the electrodes in one of the patients.

Patient 1 showed high neuronal activity in the MTL, ranging from 400 spikes per hour when awake to 850 spikes per hour during sleep. The electrodes recorded three small seizures during the 12-hour monitoring period, all of which occurred during sleep. One caused the patient to awaken, while the others had no noticeable effect. When the patient was treated with levetiracetam, an antiepileptic drug, the spiking activity in the MTL was reduced by 65% and she experienced no further seizures for the next 48 hours before the electrodes were removed.

The second patient had comparatively lower neuronal activity: about 16 spikes per hour when awake and 190 spikes per hour during sleep. Mood disturbances prevented her from being administered the levetiracetam.

In both patients, 95% of the spikes and all of the seizures in their MTL were not detectable by EEG, which was recording at the same time as the electrodes. Thus these clinically silent seizures have remained unknown until now, invisible to both patients and doctors. This new electrode recording method shows that patients in the early stages of Alzheimer’s disease may have hyperactive neurons in the MTL, a possible explanation for why this region is often affected by high amyloid-beta levels. If this is the case, some patients may benefit from antiepileptic drugs to prevent Alzheimer’s disease from progressing further.

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While EEG (pictured here) is an easy and noninvasive method of measuring neuronal activity, this study showed that is cannot reliably detect seizures in subcortical structures like the hippocampus.

With only two patients, it’s hard to say whether this study generalizes to the rest of the population. These patients could be exceptions to the rule and display unusually high MTL activity. However, the study is certainly intriguing and merits further investigation with a larger number of test subjects.

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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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Sleep Apnea May Contribute to Alzheimer’s Disease

*Thank you all for your patience during my one-month hiatus. To read about my adventures backpacking across Europe or my current internship researching Alzheimer’s disease in Switzerland, check out my travel blog, Brains and Backpacks.*

 

Around 3-7% of adults suffer from obstructive sleep apnea, a condition in which the upper airway tract periodically collapses during sleep. This can lead to loud snoring and poor sleep quality. If left untreated, it can contribute to a multitude of health conditions and decreased overall quality of life. Among these possible complications is Alzheimer’s disease. People with Alzheimer’s are five times more likely to have obstructive sleep apnea than the general population.

Recent evidence has provided more direct proof for the link between sleep apnea and Alzheimer’s. In an editorial published in the journal Oncotarget, researchers from Tokyo’s National Institute of Neuroscience described their recent work investigating a new mouse model of Alzheimer’s disease. To do so, they subjected the mice to intermittent hypoxia by decreasing oxygen levels in their cages for one minute, followed by two minutes of normal oxygen levels. This cycle repeated for eight hours per day while the mice slept for periods ranging from 5 to 28 days. This type of model has been used before to simulate the effects of sleep apnea.

When the researcher’s examined the mice’s hippocampi, the part of the brain responsible for long-term memory formation, they observed that many of the processes associated with aging were also triggered by the intermittent hypoxia. This suggests that sleep apnea could lead to an increased rate of aging in the brain. The mice also had high levels of hyperphosphorylated tau, a toxic protein that forms tangles in the brains of Alzheimer’s patients. These results are in line with other recent studies, which have shown that intermittent hypoxia causes neurons to become hyperexcited and produce greater amounts of amyloid-beta, another protein involved in Alzheimer’s disease.

The authors suggested that this protocol could be useful in developing new animal models of Alzheimer’s disease, since it triggers many of the disease’s pathological signatures using only an environmental stimulus. The models could be applied for studying how aging and sleep disruptions contribute to development of Alzheimer’s over time.

At present, there is not yet enough concrete evidence to conclude a direct link between sleep apnea and Alzheimer’s disease. However, if you or a loved one experiences sleep apnea or other sleep disorders, there would certainly be no harm in seeking medical help. Correcting sleep problems can lead to greater quality of life and reduced risk of many medical conditions. Perhaps Alzheimer’s is among them.

One-Month Hiatus from AlzScience

Hi everyone! Thanks for your amazing support for AlzScience thus far. I wanted to let my subscribers know that I will be taking a brief hiatus from AlzScience during the month of May. I’m taking a backpacking trip across Europe and won’t have the time or the internet access to post articles regularly. (To follow me on my journey, check out my travel blog, Brains and Backpacks.) At the end of May I’ll begin a summer internship in Switzerland, where I’ll be able to resume writing articles. Until then, stay curious!

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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Probiotics May Improve Cognitive Function in Alzheimer’s Disease

The gut microbiome has recently become the focus of a lot of biomedical research, as we begin to understand how important the microbes living in our gastrointestinal tracts are for our overall health. While it’s still unclear what exactly makes your gut microbes healthy or unhealthy, previous research has shown that probiotics shift the balance in the right direction. Probiotics are live bacterial or yeast cultures often found in fermented foods like yogurt, sauerkraut, and pickles. These cultures seem to increase the proportion of “good” microbes in your gut. While the gut microbiome is clearly important for gastrointestinal health, recent studies suggest that it can also influence the brain. Scientists have coined the term “microbe-gut-brain axis” to describe this close relationship.

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The brain and the gut microbiome are closely related and can influence each other’s function. Image Source

In a study published in Frontiers in Aging Neuroscience, researchers from Iran attempted to determine whether probiotics could be beneficial for dementia patients. They randomly divided sixty patients diagnosed with Alzheimer’s disease into two groups. One group received milk containing a mixture of probiotics, while the other group received regular milk as a control. The study had a double-blind design, meaning neither the researchers or the subjects knew who received each type of milk until after the data analysis was completed. This design helps to ensure that unconscious biases do not influence the results. Additionally, none of the subjects were allowed to consume probiotic-rich foods like yogurt during the study, ensuring that any gut microbiome differences would be due to the experiment and not any dietary interference.

After twelve weeks consuming the milk on a daily basis, the subjects took a mini-mental state exam, which is used to assess memory and cognition. The probiotic group scored an average of 28% better on the exam compared to their score before starting the treatment. In contrast, the control group’s score decreased by an average of 5%. This difference was statistically significant, indicating that the probiotics substantially improved memory in these subjects.

The researchers also tested the subjects’ blood for many different biochemicals. The probiotic group had improved markers of insulin metabolism, suggesting that the treatment might be helpful in reducing the risk of insulin resistance, a condition associated with type 2 diabetes. They also had lower levels of triglycerides, a type of body fat.

Despite the sample size of this study being fairly small, the dramatic improvement in cognitive status after only three months of probiotic treatment suggests that the gut microbiome could be intimately involved in dementia. Probiotics have no known health detriments, and are proven to assist in gastrointestinal health. While we wait for larger studies to provide a conclusive answer on probiotics’ utility in Alzheimer’s disease, it can’t hurt to try increasing them in our diets, or in the diet of a loved one with dementia.

 

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