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MCI and Anosognosia: She Didn’t Know She Couldn’t Walk

My mother’s first fall, at age ninety-two, seemed like an accident. Her rubber-soled sandals caught on the carpet in the activities room of her senior apartment complex and she plunged forward catching her arm on the piano bench. After minor surgery to repair the wound, and a short hospital stay, she began a course of physician therapy; but the falls continued. Injuries were rare and minor. Still the increasing frequency was distressing.

When I suggested a walker, Mom told me, “I don’t need one. I can walk perfectly well. I just lose my balance sometimes.” I puzzled over that response for days. Was it possible she didn’t remember all the falls? Did she really think she could walk safely without assistance?

It was not until after she died that I came upon the concept of anosognosia, from the Greek a-without, nosos-disease, gnosis-knowledge: without (lack of) knowledge of disease. People with anosognosia are unaware of their illness or deficits. It is most often associated with mental illness and is the primary reason for medication non-compliance in psychiatric patients.

It also affects seniors with age-related brain changes, including mild cognitive impairment. Unaware of her weakness and impaired balance, my mother had not understood that she couldn’t walk without falling. And because she did not believe she was impaired, she could not imagine why she should use a walker.

Anosognosia is often assessed with the Clinical Insight Rating (CIR) scale that identifies lack of knowledge/insight in four domains: understanding the reason for the visit (to the physician); awareness of cognitive deficit; awareness of functional deficit; and/or perception of disease progression. Mom’s lack of insight pertained to her functional deficit. Although her anosognosia resulted from an aging brain and associated (and increasing) cognitive impairment, she was sadly aware of her memory problems and disordered thoughts. People with more severe forms of dementia (including Alzheimer’s disease) are more likely to exhibit anosognosia of cognitive deficit, while those with mental illness, brain tumors, or stroke, often exhibit lack of awareness in multiple domains.

At the time, I thought my mother’s refusal to accept help stemmed from her fierce independence. I knew she had trouble thinking clearly, but I still tried to reason with her, hoping that in time she would acknowledge her functional decline and her need for assistance. But neuropsychological testing shows that patients with anosognosia score lower on composite indices of both memory and executive function. Facts and evidence are not persuasive to anyone with a pathological lack of insight.

Looking back, I now understand that Mom’s falls probably signaled her progression to “mild cognitive impairment” or MCI. The Mayo Clinic defines MCI as an intermediate stage between the expected cognitive decline of normal aging and the more-serious decline of dementia; it is often assessed using the Mini Mental Status Exam (MMSE). Studies have shown that the rate of falls increases with each unit decrease in the MMSE, and that insight can be equally impaired in persons with MCI or more advanced dementia.

I wish my mother had received a diagnosis of MCI, but it is not surprising that she didn’t. Most people with MCI can and do live independently, as my mother did, and are able to fulfill basic social roles. They are typically capable of most activities of daily living, although on close observation they take more time to complete them than unimpaired individuals. My mother’s mental decline was almost imperceptible at first, and as it progressed, I did not know enough to ask whether her symptoms were evidence of a specific diagnosis.

Knowing she had MCI would not have helped my mother, but it would have helped me. I would have done my research and uncovered her anosognosia. I would have realized that her reluctance to use a walker was grounded in her understanding of her abilities, wrong as that understanding was. I would have felt more comfortable taking over some of her decision-making.

Eventually, a physical therapist convinced my mother to use the walker for one week, promising that she could stop if she didn’t like it. Within two days, she began referring to it as her Cadillac. After that, her rate of falling decreased substantially.

References

De Carolis A, Corigliano V, Comparelli A, Sepe-Monti M, Cipollini V, Orzi F, Ferracuti S, Giubilei F: Neuropsychological patterns underlying anosognosia in people with cognitive impairment. Dement Geriatr Cogn Disord. 2012;34:216–223. doi:10.1159/000343488

De Carolis A, Cipollini V, Corigliano V, Comparelli A, Sepe-Monti M, Orzi F, Ferracuti S, Giubilei F: Anosognosia in people with cognitive impairment: Association with cognitive deficits and behavioral disturbances. Dement Geriatr Cogn Disord; 2015;5:42-50. doi:10.1159/000367987

Vogel A, Hasselbalch SG, Gade A, Ziebell M, Waldemar G: Cognitive and functional neuroimaging correlate for anosognosia in mild cognitive impairment and Alzheimer’s disease. Int J Geriatr Psychiatry 2005;20:238–246. doi:10.1002/gps.1272

Lin F, Vance DE, Gleason CE, Heidrich, SM: Taking care of older adults with mild cognitive impairment: An update for nurses. J Gerontol Nurs. 2012 December; 38(12): 22–37. doi:10.3928/00989134-20121106-02

Gleason CE, Gangnon RE, Fischer BL, Mahoney JE: Increased risk for falling associated with subtle cognitive impairment: Secondary analysis of a randomized clinical trial. Dement Geriatr Cogn Disord 2009;27:557–563. doi:10.1159/000228257

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David And Goliath: The Art of Turning All Weaknesses Into Strengths

Hello, everyone! I’m Arda Cigin, founder of Stoic-Leaders.com and in this article, I’m about to change your whole mindset towards all “disadvantages” and “less than stellar situations”.

How?

I’ll be telling you about the battle between David and Goliath as an instructive case study to understand how advantages can actually be the source of our greatest weakness, and vice versa.

And then, I’ll give you many practical solutions and mindset shifts that you can apply to your life today to turn disadvantages circumstances into your greatest strengths.

But before we get into the insights, for those who may not know, let’s analyze David and Goliath’s timeless story.

– Why even tell a story?

I want to tell a story because the human brain relates through stories, not facts and theories. If you truly want to take away an action plan at the end of this article, pay attention to this timeless story.

 

The Instructive Story of David and Goliath

Goliath is this giant who is six-foot nine, wearing a bronze helmet and full body armor. He is carrying a javelin, a spear, and a sword.

Why? Because he is about to go into a fierce battle.

The giant, Goliath was about to fight with a fledgling shepherd boy named, David.

David, as a fragile young man, inherently knew he was incomparably weak to his opponent, yet he wanted to take the stand and confront the wrath of Goliath nonetheless.

Is David’s confidence misplaced? Maybe there is more to David than meets the eye…

Only time will tell.

Naturally, everyone judged David to have no chance against Goliath. Most people who looked at this combat duo would bet their money on Goliath.

And trust me. You would too.

If we were to observe Goliath, he was prepared for close combat since he was wearing heavy armor and was armed with various spears and swords.

What many didn’t know was that the great and almighty Goliath, who was regarded as the supreme winner of this fight, had one fatal, characteristic flaw:

He had awful eye-sight.

That being said, the fight started.

At the beginning of the battle, Goliath shouted the words “Come to me!”.

Yet do not mistake this as an arrogant battle cry. Goliath needed David to be in arm’s-length so that he could see David and defeat him. It was more of a desperate cry than anything else, a definite side effect of his weak eyesight.

If you think about it, Goliath didn’t excel in close combat just because he chose to do so. He had no other option but to excel in close combat.

Remember his awful eye-sight? If he were to be a strong warrior, he can not be a long-ranged one like an archer. Combined with his bulky physical nature, a simple fault in eye-sight turned Goliath into a wrathful close-ranged warrior with almost-blind eyes.

Goliath was on, what Robert Greene calls, the “death ground”.

He was trapped and had no other option. Either he was going to master close combat or he’d lead his life as a blind giant. With the help of outside pressures and internal obstacles, he became the best in his niche—ruthless close combat.

David, the fragile young man, may be a shepherd but he was a smart boy. He was not going to fight with Goliath in close combat. That would be foolish.

Therefore, he’d prepared himself for a long-ranged combat—a kind of fight Goliath was not prepared for.

As Goliath started to get agitated, David took out his trusty slingshot, swiftly positioned a rock, pulled the end of the sling and shot right at the forehead of the giant.

Goliath couldn’t even see the rock because of his faulty eyesight.

The speed at which the rock traveled was more than enough to put Goliath into a deep slumber he’d never wake up from.

And so the shepherd boy won the fight he was predestined to lose. All the cards were stacked against him, or so it appeared.

A supremely disadvantageous fragile man came to be victorious against a supremely advantageous killing machine.

Naturally, everyone was shocked. They told themselves how lucky David was.

But this has nothing to do with luck.

All the spectators were wrong. There was one thing David was far superior to Goliath in.

It was neither his size nor his strength, but his ability to think strategically.

And this exact strategy that David had used to kill Goliath will be the topic of our discussion today.

______

Most often in life, strategic thinking is the secret ingredient to turning unfavorable situations into favorable ones

Understand: Strategic minds will always rise victorious—whatever the circumstance, whoever the enemy.

 

What Can We Learn From The Grand Strategist, David?

1) Adaptation: make it your greatest asset

While we are making decisions, if it proved successful before, we tend to repeat the same tactics and maneuvers we’ve familiarized ourselves with.

Humans are innately lazy creatures and naturally, we cling to what succeeded before and expect it to continue to do so in the future.

This move will prove ineffective in the long term.

Realize: by doing so, you only create rigid pathways, neural-connections, and habits you are better off not adopting.

I want you to see life as a chess game. As long as you repeat the same moves, you are bound to lose.

Always have the flexibility to adapt to your ever-changing circumstances. If something doesn’t work (e.g., self-actualization efforts or business and career success), then change your actions and thoughts. Start thinking strategically to find options that you haven’t thought of before.

Make adaptability your greatest asset.

As Darwin pointed out,

It is neither the survival of the strongest nor smartest, but the most adaptable.

 

2) Shift the Battlefield 

Close combat? That’s what Goliath wants.

Use your wits: In this circumstance, always use the slingshot, never the sword.

Understand: Never play in a field you are oblivious to. The knowledge of the terrain will give you unimaginable and untold power.

Realize: no one can force you to play a game you suck at. If they attempt such a thing, just politely decline, as David did, lead them into playing in your arena—a field where no one but you holds the cards. A field where you become the god and they become the puppet.

The lure of such power is undeniable, don’t you think?

 

  3) The Phenomenon of the Masked Opposite

Most often in life, people tend to mistake appearance for reality. In your interactions with people, always remember the facade of appearances. No one is as they appear to be.

Everyone sees what you appear to be, few experience what you really are – Nicollo Machiavelli

When you confront your enemies, never be intimidated by their appearances. Instead look at the parts that make up the whole. Once you identified the weakness, attack with all your might. They’ll surely fall swiftly just like Goliath.

Remember: The hypocrital nature of appearances always deceives the naive

If you see an extreme behavior pattern in someone (e.g., superiority, arrogance, extreme shyness, avoidance) you are most often confronted with the phenomenon of the masked opposite—what you see is actually the exact opposite.

For example:

If someone acts particularly arrogant, realize that they are actually trying to mask their insecurity and lack of confidence. Someone who is already confident wouldn’t need to act superior in the first place.

If someone smiles incessantly and laughs at every little thing you say, would you assume they are being natural?

No, of course not. They are only using what I’d like to call “the supreme joker mask”. No one can be extremely happy and euphoric all the time. Therefore, they are only happy when you are around.

Maybe they like you and want you to like them back, maybe they want to get close to you and hurt you or maybe they just want to break the ice, whatever the reason might be, they are wearing a mask that most definitely does not express their actual feelings.

You need to train yourself to see what is underneath the mask. Everyone you meet will wear some sort of mask. And there is a reason for that.

If we openly judged people around us, naturally we’d generate unnecessary offense and malice. Therefore, from an early age, most of us have learned to hide our real thoughts and emotions.

Otherwise, we’d be vulnerable and open to attacks. We’d be left alone and isolated. To prevent such unfavorable situations, we choose to cooperate and hide our less than favorable qualities.

This is really nothing more than our ancestor survival instincts.

Therefore, if one is actually insecure but masking it with arrogance, you need to get them to drop their guards.

They need to lose the control. Do something that will make them panic. Anger them on purpose if necessary.

Anger them on purpose if necessary.

 

Final Words

As final words, I want you to remember David and Goliath’s story every time you find yourself in a less than ideal situation.

– You financially struggle but want to start your own coaching business?

Well, that’s good, because. it is possible to bootstrap an online business by being creative and resourceful.

While wealthy business owners spend billions of dollars on advertisements—mistaking ad-generated customers for long term customers—you’ll find your unique selling proposition and create loyal customers much faster thanks to your creative product, resourceful marketing, and sheer hustle.

Starting a business without capital, especially nowadays, is actually a blessing in disguise.

– You want to write a book but you are not native?

Well, that’s good. As a language learner, your humble determination towards studying grammar, vocabulary, and phrases will enable you to get a better grasp of the nuances where most native writers will get over confident and skip the many important stages of becoming a writer—understanding how narratives work, how readers are captivated, how great writers structure stories.

Your humble and hardworking attitude towards writing will enable you to progress at a faster rate than most native writers.

Can you see the power of this strategy?

Nothing can be a disadvantage for you if you are equipped with the right mindset.

Before we wrap this up, don’t forget to share this article and comment below if you’ve experienced a similar “David and Goliath” situation.

Were you in David’s or Goliath’s position? Do you have any specific stories you would like to ask me about?

I’d love to hear your story. (I reply to almost all comments)

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Antidepressants During Pregnancy Dangerous for the Child?

Depression is sometimes described as a disease of modernity, as sharp changes in lifestyle during the last century or so have given rise to many chronic disorders including or linked to depression. Depression is a state of low mood: the person affected tends to lose interest in previously enjoyable activities. In severe cases, self-harm is also possible. Fortunately, there are many options available today to help treat this condition.

Research studies and statistics show that although pregnant women are less prone to major depression, they are more inclined to minor depressive episodes. The prevalence of depression can be anywhere between 8–16% among pregnant women. There are also higher chances that diagnosis of depression is overlooked in pregnant women.

The treatment of depression is quite challenging in pregnancy, as medical specialists have to weigh the benefits of treatment against the risks for the mother and the health of her unborn baby. Furthermore, the health professional has to take into consideration the risks and benefits of any such therapy to the long-term health of the child. New research seems to indicate that treatment of pregnant women with antidepressant drugs may increase the risk of autism, disturbances in motor function, and mental health problem in children. Some of these issues may become clear later in the life, thus studying this subject remains a challenge for researchers.

Why treat depression in pregnancy?

There is a widespread misconception that depression is not as threatening as other medical illnesses. Thus, treating depression is viewed as a matter of choice or even a luxury. Moreover, many patients that are on antidepressant drugs before pregnancy are in the remissive stage. Therefore, their doctors may think of discontinuing the therapy.

However, if a pregnant woman that is vulnerable to depression is not provided with antidepressant therapy, there is a higher risk of preterm birth, low birth weight, substance abuse in pregnancy (e.g., smoking and drinking alcohol), and a significantly higher risk of postpartum depression.

Research has shown that if antidepressants are discontinued for the period of the pregnancy, the relapse rate of major depression is as high as 60–70%. This can have severe consequences for the patient, family, and child. In addition, children born to mothers with untreated depression have higher levels of cortisol, which may have adverse impacts on their health.

Risks of antidepressants

As already mentioned, the use of antidepressants in pregnancy is a complicated issue due to possible dangers. Below are some of the common problems associated with the use of antidepressants during pregnancy.

Persistent pulmonary hypertension

This is a failure of lungs blood vessels to dilate in a child post-birth. Thus, a new-born may have breathing difficulties, a deficit of oxygen in the blood, leading to intubation. In many cases, outcomes may be fatal. This condition is also found to be related to maternal smoking, diabetes, and sepsis. Though the risk of persistent pulmonary hypertension in new-born increases up to six times with the use of antidepressants, at the same time there is a consensus among the medical community that non-use of antidepressants may be even more harmful.

Withdrawal symptoms

This is also called “poor neonatal adaptation.” These symptoms are common when a mother has been exposed to antidepressants during the third trimester of pregnancy. Some of the symptoms characteristic of this syndrome include difficulties in breathing, unstable body temperature, hypo- or hypertonia, irritability, constant crying, and seizures. Therefore, some specialists recommend tapering the dose of antidepressants in the third trimester.

Motor development

By motor development, we mean child’s ability to move around and handle the environment. There are clinical studies that indicate that the use of antidepressants during pregnancy may slow the motor development. A child may start walking later than other kids, or may have other problems related to movements.

Autism spectrum disorders

This is a neurodevelopmental disorder of children. Studies seem to show the modest increase in the risk of autism if a mother is exposed to antidepressants during the first trimester.  However, no link has been found if such treatment has been given before the pregnancy, nor much relationship has been demonstrated if the therapy was initiated in a later phase of pregnancy. Thus, researchers caution that decision of prescribing antidepressants should be taken on a case by case basis by analysing the risks and potential benefits for maternal and child health.

Psychiatric disorders

In one of the large-scale studies, scientists analysed the data of almost one million births, and they found that the use of antidepressants in pregnancy was related to higher risk of developing psychiatric disorders later in life. Nonetheless, at the same time, researchers cautioned against jumping to the quick conclusions because it is a well-known fact that mental disorders have relation to genetics. It means that women prescribed antidepressants during the pregnancy have higher chances of passing to children the genes that may result in psychiatric diseases later in life.

Although antidepressants may increase the risk of specific disorders in the new-born babies or may even have a negative impact later in the life, it does not mean that antidepressants should not be taken during the pregnancy. It is essential that women should not feel guilty about taking such drugs. The medical specialists must be aware of the risks and weigh them against the benefits before they prescribe antidepressants to pregnant women.

References

Casper, R.C., Fleisher, B.E., Lee-Ancajas, J.C., Gilles, A., Gaylor, E., DeBattista, A., Hoyme, H.E., 2003. Follow-up of children of depressed mothers exposed or not exposed to antidepressant drugs during pregnancy. J. Pediatr. 142, 402–408. doi:10.1067/mpd.2003.139

Croen, L.A., Grether, J.K., Yoshida, C.K., Odouli, R., Hendrick, V., 2011. Antidepressant Use During Pregnancy and Childhood Autism Spectrum Disorders. Arch. Gen. Psychiatry 68, 1104–1112. doi:10.1001/archgenpsychiatry.2011.73

Ko, J.Y., Farr, S.L., Dietz, P.M., Robbins, C.L., 2012. Depression and Treatment Among U.S. Pregnant and Nonpregnant Women of Reproductive Age, 2005–2009. J. Womens Health 2002 21, 830–836. doi:10.1089/jwh.2011.3466

Payne, J.L., Meltzer-Brody, S., 2009. Antidepressant Use During Pregnancy: Current Controversies and Treatment Strategies. Clin. Obstet. Gynecol. 52, 469–482. doi:10.1097/GRF.0b013e3181b52e20

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The Most Important Thing We Can Do for Our Brain? Exercise!

If I would have guessed ten years ago what the best way to train the brain would be, I would probably have thought about crossword puzzles, sudoku, or cognitive apps. But then I would be wrong. The best way is physical exercise. During the last decade, neuroscience has shown that physical exercise has extraordinary effects on our brain.

Most people know by now that exercise will improve their mood—but few know that it will boost all of their cognitive abilities—memory, attention, creativity, and how we cope with stress. It all gets better in a way unparalleled by any drug, food-supplement, or cognitive training method.

So what happens in our brain when we move? First. the brain gets more blood. Bloodflow is increased by 20% while walking fast compared to sitting. More blood means more oxygen and nutrients. But increased bloodflow is only the beginning. The rate of neurogenesis—the formation of new brain cells—is increased by exercise. The newly born brain cells are formed in the dentate gyrus, a part of the hippocampus known as the “memory center”, and the effect is substantial. The hippocampus actually grew by 2% when a group of sedentary individuals walked regularly for a year. Typically, the hippocampus shrinks by up to 1% per year from our late twenties onwards, contributing to gradual memory loss as we get older. The exercise-based boost of hippocampal growth not only increases memory but improves mood. Exercise has been shown to be as efficient as antidepressants for mild and moderate depression, useful information in an age where more than one in ten adults are prescribed antidepressants in the US.

How about kids? Exercise does wonders to children’s cognitive abilities and their ability to learn. Just 20 minutes of playing increases math and reading test scores. And this isn’t exclusive to tests in the lab, several studies have shown that kids in good shape actually perform better in school. Physical activity even seems to affect IQ! When data from the Swedish military service was analyzed from 1.2 million 18-year old male Swedes a clear pattern emerged—boys in good cardiovascular fitness had higher IQs, a result that was also apparent for identical twins. In a number of identical twins, one brother was in good shape while the other brother was not. The brother in good shape had a higher IQ than his identical twin—even though they, more or less, have identical genes (there can be small differences in identical twins) and have grown up together!

The list goes even further. Exercise can make us more creative. A recent study showed that creativity test results for divergent thinking (“brainstorming”) increased by more than 50% if participants had walked for 45 minutes before the test. The creativity-boost is temporary, we get more creative during 1-2 hours after exercise—probably due to increased blood flow, than we are back to our normal creativity-level. The takeaway message is: if you are stuck with a problem, then go for a walk or jog, and rethink of the problem an hour afterward and increase your chances of coming up with a solution.

But why is exercise so important for the brain? It is not at all obvious from our modern perspective but makes more sense if we look at our history. Our brains are basically the same today as they were 10 000 years ago. It was when our ancestors moved: during hunting, running from predators, and discovering new lands, that they really needed their cognitive abilities. That was when they needed to be attentive and have a memory to remember new experiences. That is why evolution has slowly tailored the brain in such a way that it benefits from exercise and that is why we still benefit from it today as our brains have not grossly changed since our ancestors days on the savanna.

While the human brain is fundamentally unchanged in the past 10 000 or even 20 000 years or so, our lifestyle has changed enormously. Modern sedentary lifestyle deprives many of us from getting enough physical activity, leading to vast consequences not only in terms of obesity and type-2 diabetes but also when it comes to wellbeing and how we function mentally. Exercise is not about sports. It is not about participating in a lifestyle. It is something we need to do for our brain and cognitive abilities since we have evolved for it. Now neuroscience is helping us to rediscover the brain-medicine that we forgot.

References

[1] Eriksson P et al (1998) Neurogenetis in the adult human hippocampous. Nature medicine. 4;1313–1317. doi:10.1038/3305

[2] Alvarexz- Bueno C (2017) The Effect of Physical Activity Interventions on Children’s Cognition and Metacognition: A Systematic Review and Meta-Analysis. J Am Acad Child Adolesc Psychiatry. 56(9):729–738. doi:10.1016/j.jaac.2017.06.012

[3] Åberg, M et al (2009) Cardiovascular fitness is associated with cognition in young adulthood. Proc Natl Acad Sci USA. 106(49):20906–11. doi:10.1073/pnas.0905307106

[4] Oppezzo et al (2014) Give Your Ideas Some Legs: The Positive Effect of Walking on Creative Thinking Journal of Experimental Psychology: Learning, Memory, and Cognition. 40(4):1142–1152. doi:10.1037/a0036577

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One Ring to Rule Them All: Cure-all Drug for Neurodegenerative Conditions Possible

The secret to finding a single drug treatment for neurodegenerative conditions may lie in unfolding the mystery of misfolded proteins. Most of the non-infectious neurodegenerative diseases (like Alzheimer’s and Parkinson’s) are characterized by progressive death of neurons due to the accumulation of misfolded proteins in brain cells.

To understand the pathogenesis of these diseases we have to first understand proteins.  They are essential for building our body structures and functional regulation. Thus, there are thousands of different proteins with various functions. These proteins are made up of only 20 amino acids. These 20 amino acids are like the alphabet in a language, they can create thousands or millions of proteins when used in different combinations. A single misplaced letter in a word results in a spelling error. Similarly, a misplaced amino acid can create the wrong kind of protein. Misplaced words can create a grammatically wrong and incomprehensible sentence. In a similar fashion, misfolded proteins have no structural or functional value.

Another important concept that has to be understood is how prions are involved. From school books, we know that infections are caused by microorganisms like bacteria, fungi, and viruses. All of them have genetic material in the form of nucleic acids (as DNA or RNA, or both), that is essential for the reproduction or multiplication of these microorganisms. But prions, unlike microorganisms, are just protein chains that are infectious. These proteins, after entering the living organism, cause misfolding of proteinaceous infectious particles (PrPs). PrPs are found in all of us, our brain and neurons are especially rich in them. Their role, however, is still poorly understood.

Misfolded PrPs cause encephalopathies. These misfolded proteins are also thought to cause a chain reaction resulting in the misfolding of other proteins. These misfolded proteins propagate further like an infectious microorganism. What causes this chain reaction and propagation is still unclear. These chains of proteins are called prions. They cause Creutzfeldt-Jakob disease (CJD) in humans and bovine spongiform encephalopathy (BSE) in cattle. Prions have a long incubation period, it takes a long time for the disease to appear and progress.

In many neurodegenerative diseases like Alzheimer’s and Parkinson’s, misfolded proteins get progressively accumulated in brain cells, leading to the death of neurons. There is growing evidence that the prion-like process of seeding and templated protein corruption are behind the progression of these diseases.

PrP (healthy prion) is commonly found in our brain cells. However, when a defective prion protein is somehow introduced into the cells, it causes misfolding of newly forming PrP. This process is progressive and propagated like an infectious disease to the other cells. Thus, one of the potential treatment approaches is to block the propagation of this prion-like protein.

Accumulation of these prion-like misfolded, mutant proteins is toxic for cells. The prolonged toxic stress produced in brain cells induces specific death pathways. Understanding how these toxic proteins cause stress for neurons and why the cells die could also help to find new treatment strategies.

With increasing evidence that prion-like mechanisms are behind the progression and propagation of most neurodegenerative disorders, scientists have started looking for methods to stop this propagation. One such method is the use of specific immunotherapy, where researchers are trying to develop vaccines that can cure these disorders, or at least stop disease progression.

Larger proteins in our body contain hundreds or thousands of amino acids in various combinations. These large proteins are folded into specific structures. If a protein is misfolded, it loses its specific structure too. It also loses its properties and becomes toxic for cells. One therapeutic approach aims to develop a vaccine that can activate our immune system (B and T cells) against these defective misfolded proteins so that they are destroyed in a timely manner.

To achieve this aim, scientist have tried two methods. One of them is to create a vaccine that works against very short chains of misfolded proteins called monomers. They exist while these proteins are being assembled. Another approach is to target the fully formed misfolded protein fibrils. However, both of these methods have so far failed to produce the intended results.

Recently, researchers are exploring a new strategy for the development of immunotherapy against these diseases. This strategy targets so-called “oligomers”. The oligomers are molecular intermediates that exist in the process of assembling the prion fibrils. They are not very small like monomers (initial building blocks of prions) and are also not fully formed prion fibrils.

Smaller monomers lack the antigenic properties (associated with protein structures called beta-sheets) of misfolded proteins that are needed for an immune response. Meanwhile, fully formed fibrils are too big to propagate through cell walls. Thus, it is quite possible that these oligomers play a critical role in the disease propagation processes. A vaccine or immunotherapy targeting these oligomers could be more effective in initiating an immune response against the misfolded pathological prions than their smaller or larger counterparts. Moreover, these intermediate oligomers are common to most neurodegenerative disorders, unlike fully formed fibrils that are specific to each disease.

Although this new approach has shown some success in animal models, there are several challenges to using such immunotherapy in humans. In humans, it is not easy to initiate the immune response because of “self-tolerance.” The misfolded proteins are very similar to normal proteins (normal PrPs). Even if this immune tolerance can be overcome, there is a risk of initiating the wrong kind of immune response against normal proteins. This may lead to sterile encephalopathy or another kind of damage. Further, the blood-brain barrier also poses a challenge: it is important that antibodies created by a vaccine are able to reach a good concentration in the brain.

Despite these challenges, the idea of having just a single approach to treat all (or at least most) types of neurodegeneration is clearly exciting. These diseases have lots in common in terms of the molecular mechanisms involved, and it is quite likely that immunotherapy targeting all of them can be developed.

References

Frost, B., Diamond, M.I., 2010. Prion-like Mechanisms in Neurodegenerative Diseases. Nat. Rev. Neurosci. 11, 155–159. doi:10.1038/nrn2786

Goedert, M., Clavaguera, F., Tolnay, M., 2010. The propagation of prion-like protein inclusions in neurodegenerative diseases. Trends Neurosci. 33, 317–325. doi:10.1016/j.tins.2010.04.003

Marciniuk, K., Taschuk, R., Napper, S., 2013. Evidence for Prion-Like Mechanisms in Several Neurodegenerative Diseases: Potential Implications for Immunotherapy. J. Immunol. Res. doi:10.1155/2013/473706

Rao, R.V., Bredesen, D.E., 2004. Misfolded proteins, endoplasmic reticulum stress and neurodegeneration. Curr. Opin. Cell Biol. 16, 653–662. doi:10.1016/j.ceb.2004.09.012

Walker, L.C., Diamond, M.I., Duff, K.E., Hyman, B.T., 2013. Mechanisms of Protein Seeding in Neurodegenerative Diseases. JAMA Neurol. 70, 304–310. doi:10.1001/jamaneurol.2013.1453

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Electrical Brain Stimulation in Treatment of Neurodegenerative Diseases

The early Egyptians and Romans recognized the numbing effect of the electric properties of catfish. In fact, Romans were the first to cultivate electric fishes for pain relieving effect. But since then, not much has changed in the development of electricity based medical treatments. Things only started to change two millennia later with the discovery of electricity and a better understanding of neurophysiology.

Electroconvulsive therapy was born in the middle of the 19^th century. In the early days, it was primarily used to treat neuropsychiatric disorders. In the mid-19^th century, direct electric current was used for electroconvulsive therapy. By the end of 19^th-century, the alternate current was discovered, and its use along with the use of magnetic fields became the subject of experiments not only investigating neuropsychiatric conditions but also other diseases like epilepsy and chronic severe headaches.

Electroconvulsive therapy is still used in the treatment of severe neuropsychiatric conditions like schizophrenia or depression, where suicidal tendencies do not respond to pharmacological agents. Unlike in the old days, now this is a non-invasive treatment usually performed under general anesthesia. The therapy non-selectively resets various centers in the brain and thus has wide-ranging side effects like loss of memory, headaches, and muscle aches.

Considering the widespread side effects of electroconvulsive therapy, the need for more selective stimulation of particular brain centers specific for a particular disease was obvious. The improvements in understanding of brain physiology and surgical techniques gave rise to “deep brain stimulation” (DBS). This is an invasive method where electrodes are surgically placed inside the specific part of the brain that are connected to a small electrical device that generates the stimulation.

At present, DBS has been shown to be effective in the treatment of Parkinson’s disease, epilepsy, obsessive compulsive disorder, and dystonia. It is being studied for applications in treating depression, drug addiction, and other neurodegenerative disorders such as dementia. As the method is invasive and involves the surgical implantation of electrodes inside the brain, it is reserved for cases that fail to respond to pharmacological therapy.

Deep brain stimulation in Parkinson’s disease

Dopamine is a chemical messenger in the brain that plays an important role in physical movement. In Parkinson’s disease, there is a progressive loss of dopamine-producing neurons resulting in motor deficiencies. Thus, the first line therapy for this disease is to give dopamine replacement therapy by prescribing a drug called levodopa.

The problem is, one-third of cases of Parkinson’s disease progress quickly and stop responding to the therapy with levodopa or other pharmacological agents, thus necessitating a treatment like DBS.

For the best results, it is recommended to go for DBS well before the symptoms become debilitating. In the later stages, the effectiveness of DBM tends to be lower.

DBS in Parkinson’s disease involves the application of continuous high-frequency electrical pulses through electrodes implanted in the subthalamic nucleus (STN) in the brain (though sometimes other locations may also be chosen). The STN is demonstrated to be over-activated in Parkinson’s disease. These electrodes are connected to the compatible pulse generating device. The pulse generator uses various pulses to achieve the optimal effect, where the right kind of settings can be chosen for a person by assessing treatment effectiveness.

Continuous DBS was shown to improve motor symptoms in more than two-thirds of patients, as compared to no stimulation or intermitted stimulation.

In one of the clinical studies, bilateral STN DBS was performed on patients that were not responding to the maximum dose of levodopa or to a continuous infusion of apomorphine. DBS showed marked improvement in motor function in 61% of cases. After the procedure, there was a 37.1% decrease in the daily dosage of levodopa in the patients. There was an almost 70% decrease in the need for apomorphine, with some patients not requiring apomorphine at all. Thus, the effectiveness of bilateral STN DBS in advanced Parkinson’s disease is well established.

Although the exact mechanism whereby DBS is effective is still unknown, it is believed to involve overcoming abnormal electrical patterns generated in the basal ganglia.

With the devices and surgical technique being constantly refined,  the effectiveness of this treatment may improve sufficiently enough to be widely used during the early stages of the disease in the future.

Deep brain stimulation in Alzheimer’s disease

In Alzheimer’s disease, DBS is still an experimental treatment. Lots of research with the use of various techniques has been done on animals, some with positive results. In one such study in monkeys, intermittent DBS was used with 60 pulses for 20 seconds with an interval of 40 seconds in between. The experiment demonstrated improvements in the memory of the primates. The experiment also showed deterioration of memory following continuous stimulation. The differences with results in the treatment of Parkinsonism might be explained by the differing pathological mechanisms involved.

After months of intermittent stimulation, the monkeys demonstrated improvements in memory even on discontinuation of stimulation. This lasting effect has not yet been explained. It is quite possible that such intermittent stimulation results in an improved connection between neurons, or higher levels of release of the neurotransmitter acetylcholine.

DBS has certain benefits over drugs, as it stimulates specific areas of the brain, while anticholinergic drugs used to treat Alzheimer’s have widespread non-selective action. Thus, DBM may prove to be a safer treatment option in the future.

It has to be noted that apart from DBS, non-invasive neurostimulation using transcranial magnetic stimulation has also demonstrated promising effects in animal studies.

References

Dubljevi?, V., Saigle, V., Racine, E., 2014. The Rising Tide of tDCS in the Media and Academic Literature. Neuron 82, 731–736. doi:10.1016/j.neuron.2014.05.003.

Elder, G.J., Taylor, J.-P., 2014. Transcranial magnetic stimulation and transcranial direct current stimulation: treatments for cognitive and neuropsychiatric symptoms in the neurodegenerative dementias? Alzheimers Res. Ther. 6, 74. doi:10.1186/s13195-014-0074-1.

Green, A.L., Bittar, R.G., Bain, P., Scott, R.B., Joint, C., Gregory, R., Aziz, T.Z., 2006. STN vs. Pallidal Stimulation in Parkinson Disease: Improvement with Experience and Better Patient Selection: STN vs. Pallidal DBS. Neuromodulation Technol. Neural Interface 9, 21–27. doi:10.1111/j.1525-1403.2006.00038.x.

Hansen, N., 2014. Brain Stimulation for Combating Alzheimer’s Disease. Front. Neurol. 5. doi:10.3389/fneur.2014.00080.

Little, S., Pogosyan, A., Neal, S., Zavala, B., Zrinzo, L., Hariz, M., Foltynie, T., Limousin, P., Ashkan, K., FitzGerald, J., Green, A.L., Aziz, T.Z., Brown, P., 2013. Adaptive deep brain stimulation in advanced Parkinson disease. Ann. Neurol. 74, 449–457. doi:10.1002/ana.23951.

Mallet, L., 2010. Deep Brain Stimulation in Psychiatric Disorders, in: Koob, G.F., Moal, M.L., Thompson, R.F. (Eds.), Encyclopedia of Behavioral Neuroscience. Academic Press, Oxford, pp. 376–381. doi:10.1016/B978-0-08-045396-5.00249-9.

Sharifi, M.S., 2013. Treatment of Neurological and Psychiatric Disorders with Deep Brain Stimulation; Raising Hopes and Future Challenges. Basic Clin. Neurosci. 4, 266–270. PMCID: PMC4202568.

Varma, T.R.K., Fox, S.H., Eldridge, P.R., Littlechild, P., Byrne, P., Forster, A., Marshall, A., Cameron, H., McIver, K., Fletcher, N., Steiger, M., 2003. Deep brain stimulation of the subthalamic nucleus: effectiveness in advanced Parkinson’s disease patients previously reliant on apomorphine. J Neurol Neurosurg Psychiatry 74, 170–174. doi:10.1136/jnnp.74.2.170.

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Detrimental Effects of Bright Screens on Sleep Patterns

We often complain about people around us constantly being glued to their phone. Mobile technology is everywhere these days. When not on the go, we still tend to stare at computer screens both in the office and back at home. For many, this addiction to high-tech devices represents a way to be connected to friends and family. Many others think that these devices isolate us from real interaction with the world around us. One way or another, we do indeed spend too much time with our computers, laptops, tablets, and smartphones.

Apart from changing the way we communicate (for better or worse), all these devices have one more thing in common: bright screens. These light emitting screens can seriously affect our sleeping pattern. Moreover, the blue light (of a wavelength of ~470 nm) that is emitted by these devices is particularly harmful to normal sleep.

These days, an increasingly large number of people report problems with sleeping. Many people can’t fall asleep in the evening and then do not feel refreshed the next morning when they have to go to work. Lots of people complain about disturbed shallow sleeping and frequent awakenings at night. With normal sleeping hours often affected, people sleep less at night and if they can, compensate for this lack of sleep with daytime naps.

Disturbed sleep patterns are often linked to a diminished ability to focus on work, lack of motivation, and a generally low mood. This may lead to conflicts and stress at the workplace resulting, in some cases, in anxiety and depression. There are long-term negative consequences for other organs and systems of the body too. For instance, the link between chronically bad sleep and cardiovascular problems is well documented. Sleeping pattern disturbances also contribute to excessive body weight. It is estimated that around half of all Americans suffer from chronic stress at moderate or severe levels. Disturbingly, this number is growing in recent years.

Apart from many social and psychological factors, the growing level of stress in the general population can also be linked to the growing and excessive use of computers and smartphones. Exposure to bright screens in the evening hours is particularly harmful.

Our circadian rhythm (the sleep-wake pattern) is regulated by our exposure to light. There are several components of this system that are particularly important. First, we have specific cells in our eye retina that function as detectors of the duration and intensity of light. These cells, called intrinsically photosensitive retinal ganglion cells (ipRGCs), are particularly sensitive to short wavelength blue light.

Light-exposed ipRGC cells send signals to the suprachiasmatic nucleus in the brain. This region is responsible for setting the body clock, achieved by regulating the production of the hormone melatonin in the pineal gland. Melatonin plays a role in the adjusting mechanism: it synchronizes the body’s circadian rhythms with the real-life cycle of day and night experienced by the body. The problem is, this system can be easily fooled by prolonged exposure to artificial light. When you stare at your laptop screen late in the evening, you are also sending a signal to your brain that you are currently experiencing daytime. Your body will try to adjust accordingly to help you take advantage of daytime hours—it will reduce your desire to sleep. And once the screen is off, you don’t feel like sleeping anymore…

Recently published experimental data demonstrated that just two hours of evening exposure to bright computer screens emitting blue light decreases sleep duration and, more importantly, dramatically reduces its quality. People exposed to computer screens were awakening during the night much more often compared to those who did not use computers in the evening. The data also demonstrated that both the type of light emitted by the screens and its intensity is important for nighttime sleep quality. The screens with low brightness were less disturbing for sleep quality, and the screens emitting red light did not affect nighttime sleep at all.

Exposure to blue light-emitting bright screens in the morning is actually a positive thing: it can help to readjust the body to the correct time of the day. In fact, morning exposure to blue light is even used in a number of bright light therapy methods aimed at normalizing the circadian cycle, particularly in elderly people who often experience sleep-wake pattern disturbances.

It is quite unlikely that after reading this article anyone will immediately give up the habit of late-night internet browsing or chatting with friends via social networks before going to sleep. There are, however, several simple methods to reduce evening exposure to blue light emitted by screens. First, you can reduce the brightness of your screen. You can also change the background color while reading some types of documents. Text with white letters on a black background definitely reduces light exposure. If you anticipate working with documents in the evening, it might be a good idea to print them out. Paper is certainly much friendlier to the eyes. It is also possible to cover your computer screens with special filters that block out blue light. These small changes won’t require any major changes to your habits and routine but will help you to regain a normal sleep-wake pattern and bolster feeling refreshed the next day.

References

Arendt J. (2006) Melatonin and human rhythms. Chronobiol Int. 23(1-2): 21-37. DOI: 10.1080/07420520500464361.

Figueiro, M.G., Wood, B., Plitnick, B. et al. (2011) The impact of light from computer monitors on melatonin levels in college students. Neuro Endocrinol Lett. 32(2):158-63. PMID: 21552190.

Skene DJ, Arendt J. (2006) Human circadian rhythms: physiological and therapeutic relevance of light and melatonin. Ann Clin Biochem. 43(Pt 5): 344-53. DOI: 10.1258/000456306778520142.

Wright HR, Lack LC, Kennaway DJ. (2004) Differential effects of light wavelength in phase advancing the melatonin rhythm. J Pineal Res. 36(2): 140-4. DOI: 10.1046/j.1600-079X.2003.00108.x.

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Toxoplasma Gondii: Common Brain Parasite Behind Brain Disorders?

Most people have never heard of the brain parasite called Toxoplasma gondii. We tend to think that creatures of such kind belong to the realm of exotic tropical diseases affecting people somewhere in miasmatic swamps of equatorial jungles. However, toxoplasma infection is remarkably common: it is believed that one in every three persons around the world have it. And not only in tropical regions, the prevalence of this infection in France is estimated at 84%! In fact, T. gondii is one of the most common parasites in the developed world. The majority of people reading this article have it in their brains.

If the infection is so common, why is it hardly ever mentioned? The reason is simple. As horrible as it sounds to have a parasite living in your brain, the infection with Toxoplasma gondii is asymptomatic and doesn’t seem to affect us in any obvious way. The initial exposure to the parasite may cause some flu-like symptoms, but very soon the infection enters latent stages and does not manifest itself. It can, however, become dangerous in people with weakened immune system, such as those with HIV/AIDS.

The parasite has a rather curious life cycle. It can live in almost any warm-blooded animal, but its major hosts are cats and other felines. In their bodies, the parasite can sexually reproduce giving rise to new generations of offspring. In other animals, as well as in humans, Toxoplasma gondii can only reproduce asexually. Thus, feline species are the definite hosts of T. gondii, while humans can only be intermediate hosts.

The oocysts produced in cats get excreted with feces and spread in the environment. This is where they can be picked up by rats and mice. In these animals, the parasite eventually reaches the brain, and here is where something really unusual happens. The parasite modifies the behavior of the rodents, making them less afraid of the smell of cats.

In addition, the brain infection affects the motor ability of animals, thereby making them easier prey for cats. These behavioral changes are achieved by introducing some epigenetic modifications affecting key neurons regulating the above behavioral characteristics. The behavioral modification of the host increases the chances of the parasite getting into the body of cats, and thus increases the chances of its reproductive success.

The important question is: does the infection with Toxoplasma gondii change human behavior as well? It appears that the answer to this question is yes. The results of psychological testing published in 2007 demonstrated gender-dependent changes in the behavior of humans affected by toxoplasmosis. Infected men had a tendency to disregard rule and were more expedient, suspicious, and jealous. Infected women, however, were more warmhearted, conscientious, and moralistic. The gender differences are related to different levels of testosterone in men and women.

Motor functions also appear to be affected in infected people. One study demonstrated a 2.65 times higher chance of traffic accidents among people with latent toxoplasmosis. The antibodies to the parasite were detected more often among drivers who were involved in traffic accidents, as compared to the statistical average.

Furthermore, a number of reports demonstrated a correlation between toxoplasmosis and the incidence of schizophrenia and bipolar disorder. Several studies have shown that the risk of attempted suicide is also higher among people affected by latent T. gondii infection. Correlation does not necessarily imply that the infection is the causative factor of neurological disorders, but it is likely to be a risk factor in the development of these conditions.

It is important to mention here that not all researchers believe that T. gondii infection really affects human behavior or the risk of diseases to any significant degree. Some recently published studies indicate that these risks are very small, and the previously published correlations with various behavioral changes are not as significant as we might think.

However, the most recent publication on this subject sounds the alarm again. Scientists used comprehensive systems analysis to look at the range of biomarkers generated by various parasites and to assess their impact in a large cohort of subjects. The data point to a correlation between toxoplasmosis and several neurodegenerative conditions including Alzheimer’s and Parkinson’s disease. The T. gandii infection was also positively correlated with epilepsy and a number of cancers. The scientists not only identified correlations, they also described the biochemical pathways that may actually lead to the increased risk of developing these conditions. They concluded that toxoplasmosis is a risk factor for many neurological disorders, and thus this infection has to be taken into consideration when developing strategies for preventing or delaying the onset of various brain diseases.

Can something be done to cure or at least prevent T. gondii infection? Unfortunately, not much. There are no drugs or vaccines to treat this infection. There is a number of simple strategies to decrease the risk of infection among healthy people. They include avoiding the consumption of raw or undercooked meat (among humans, this is the most common way of getting infected), as well as general basic food handling safety practices.

References

Berdoy, M; Webster, J; Macdonald, D (2000) Fatal attraction in rats infected with Toxoplasma gondii. Proceedings of the Royal Society B: Biological Sciences. 267 (1452): 1591–1594. doi:10.1098/rspb.2000.1182.

Flegr, J (2007) Effects of Toxoplasma on Human Behavior. Schizophrenia Bulletin. 33 (3): 757–760. doi:10.1093/schbul/sbl074.

Flegr, J; Havlícek, J; Kodym, P; Malý, M; Smahel, Z (2002) Increased risk of traffic accidents in subjects with latent toxoplasmosis: a retrospective case-control study. BMC Infectious Fiseases. 2: 11. doi:10.1186/1471-2334-2-11.

Kocazeybek, B; Oner, Y; Turksoy, R; Babur, C; Cakan, H; Sahip, N; Unal, A; Ozaslan, A; Kilic, S; Saribas, S; Aslan, M; Taylan, A; Koc, S; Dirican, A; Uner, H; Oz, V; Ertekin, C; Kucukbasmaci, O; Torun, M (2009) Higher prevalence of toxoplasmosis in victims of traffic accidents suggest increased risk of traffic accident in Toxoplasma-infected inhabitants of Istanbul and its suburbs. Forensic Science International. 187 (1–3): 103–108. doi:10.1016/j.forsciint.2009.03.007.

Torrey, EF; Bartko, JJ; Lun, ZR; Yolken, RH (2007) Antibodies to Toxoplasma gondii in patients with schizophrenia: a meta-analysis. Schizophrenia bulletin. 33 (3): 729–36. doi:10.1093/schbul/sbl050.

Arling, TA; Yolken, RH; Lapidus, M; Langenberg, P; Dickerson, FB; Zimmerman, SA; Balis, T; Cabassa, JA; Scrandis, DA; Tonelli, LH; Postolache, TT (2009) Toxoplasma gondii antibody titers and history of suicide attempts in patients with recurrent mood disorders. The Journal of Nervous and Mental Disease. 197 (12): 905–8. doi:10.1097/nmd.0b013e3181c29a23.

Sugden, K; Moffitt, TE; Pinto, L; Poulton, R; Williams, BS; Caspi, A (2016) Is Toxoplasma Gondii Infection Related to Brain and Behavior Impairments in Humans? Evidence from a Population-Representative Birth Cohort. PLOS ONE. 11 (2): e0148435. doi:10.1371/journal.pone.0148435.

Huân M. Ngô, Ying Zhou, Hernan Lorenzi, Kai Wang, Taek-Kyun Kim, Yong Zhou, Kamal El Bissati, Ernest Mui, Laura Fraczek, Seesandra V. Rajagopala, Craig W. Roberts, Fiona L. Henriquez, Alexandre Montpetit, Jenefer M. Blackwell, Sarra E. Jamieson, Kelsey Wheeler, Ian J. Begeman, Carlos Naranjo-Galvis, Ney Alliey-Rodriguez, Roderick G. Davis, Liliana Soroceanu, Charles Cobbs, Dennis A. Steindler, Kenneth Boyer, A. Gwendolyn Noble, Charles N. Swisher, Peter T. Heydemann, Peter Rabiah, Shawn Withers, Patricia Soteropoulos, Leroy Hood, Rima McLeod. Toxoplasma Modulates Signature Pathways of Human Epilepsy, Neurodegeneration & Cancer. Scientific Reports, 2017; 7 (1) doi: 10.1038/s41598-017-10675-6

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Can Deadly Zika Virus Cure Brain Cancer?

Not long ago, Zika virus was dominating headlines. A new infection was hardly ever heard about before then, yet is now affecting hundreds of thousands of people in Latin America, causing disfiguration and microcephalia in new-born babies. Microcephalia is caused by severe delayed and abnormal development of the brain, resulting in the range of intellectual disability, dwarfism, poor motor functions and speech. With no cure or even preventive vaccination available, many women in the most affected regions were reportedly considering postponing any planned pregnancies.

The virus was actually discovered back in 1947 in Zika forest in Uganda (and this is where its name comes from). The pathogen is related to better known viruses causing dengue and yellow fever. The disease is spread predominantly by one type of mosquito and was a rare occurrence until the epidemics of 2015–2016, when in Brazil alone well over 100,000 cases were reported. The disease caused particular concern as it coincided with the run-up to the 2016 Olympic games in Rio de Janeiro.

Apart from mosquitoes, the virus can be spread through sexual contact and from mother to child during pregnancy or at delivery. The latter way of transmission is a particular concern: while adults suffer only very mild symptoms (fever and rush), children infected during pregnancy suffer major brain damage. The reason for this is that viral infection delays brain development.

Further research identified a more specific reason: Zika virus specifically targets neural progenitor cells, the cells responsible for production of other neurons. This is what makes the virus very dangerous for the developing fetus. Neuron progenitor cells are abundant in the developing fetal brain. However, only a few are left in the brain of adults. In adults with completely formed brain, Zika virus infection causes only mild symptoms, if any (Zika fever). But the specificity with which the virus targets neural progenitor cells gave researchers an idea that might revolutionize the treatment of one of the deadliest types of brain cancer—glioblastoma.

Glioblastoma is one of the most difficult types of cancer to treat, with patients rarely surviving even one year after diagnosis. Unfortunately, this is also one of the most common types of brain cancer. Approximately 12,000 people are diagnosed with glioblastoma in the US alone. The quick return of the disease even after aggressive surgery is caused by the survival of a few glioblastoma stem cells. Many  types of cancer like glioblastoma grow due to the existence of cancer stem cells that give rise to other tumor cells. The glioblastoma stem cells remain almost unaffected by all radio- and chemotherapy regiments currently used to treat this malignancy, even though these therapeutic approaches do kill other cells in the tumor. They also successfully avoid detection and elimination by the immune system, allowing the regrowth of cancer in a short period of time after surgery, replenishing the cancer cells eliminated by therapy.

Researchers noted that glioblastoma stem cells are, in many ways, very similar to normal neural progenitor cells. Therefore, infecting a person with glioblastoma with Zika virus might help in treating the disease by eliminating the stem cells. This was a core idea that researchers initially tested on cancer cells from tumors obtained from surgeries. It turned out that the virus does indeed kill cancer stem cells, leaving other cancer cells almost unaffected.

To further make sure that the virus doesn’t affect the normal cells of the brain, scientists have performed experiments on brain tissues from patients with epilepsy. The tests did not detect any damage to these cells due to viral infection.

The findings suggest that combining traditional chemotherapy with treatment with Zika virus may help to eliminate stem and non-stem cancer cells. Such an outcome will most certainly be beneficial for the patients.

To test the idea further, scientists injected Zika virus directly into the brain of mice with brain tumors. In all animals infected with the disease, tumor growth slowed down significantly and the animals survived longer.

The researchers suggest that Zika virus can be injected into the brain of a glioblastoma patient at the time of surgery. The subsequent chemotherapy will remove any remaining cancer cells that survived surgery, and Zika virus will kill the residual glioblastoma stem cells. The published findings also suggest that the virus can be further engineered to be more easily eliminated from normal healthy brain cells using the patient’s immune system. Less harmful strains of the virus have already been developed to this end and have demonstrated some success in animal experiments.

It remains to be seen if a successful therapeutic approach to treat deadly glioblastoma can be developed using Zika virus. The path to future use of Zika-based treatment in hospitals will likely be long. The original results, however, are very encouraging. This new approach is another fascinating example of a growing number of new innovative tools that are currently being developed to treat a variety of cancers.

References

Bleeker, Fonnet E, Molenaar, Remco J; Leenstra, Sieger (2012) Recent advances in the molecular understanding of glioblastoma. Journal of Neuro-Oncology. 108 (1): 11–27. PMC3337398.

Lathia J, Mack SC, Mulkearns-Hubert EE, Valentim CLL, Rich JN (2015). Cancer stem cells in glioblastoma. Genes & Development, 29(12), 1203–1217. doi:10.1101/gad.261982.115.

Rasmussen, Sonja A, Jamieson, Denise J, Honein, Margaret A, Petersen, Lyle R (2016) Zika Virus and Birth Defects — Reviewing the Evidence for Causality. New England Journal of Medicine. 374 (20): 1981–7. doi:10.1056/NEJMsr1604338.

Zhu Z, Gorman MJ, McKenzie LD, Chai JN, Hubert CG, Prager BC, Fernandez E, Richner JM, Zhang R, Shan C, Wang X, Shi P, Diamond MS, Rich JN, Chheda MG. Zika virus has oncolytic activity against glioblastoma stem cells. The Journal of Experimental Medicine, Sept. 5, 2017 doi:10.1084/jem.20171093.

Image via NeuPaddy/Pixabay.

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