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

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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.


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

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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

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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

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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 19th century. In the early days, it was primarily used to treat neuropsychiatric disorders. In the mid-19th century, direct electric current was used for electroconvulsive therapy. By the end of 19th-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.


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

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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.


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?

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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.


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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.

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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?

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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.


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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.

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Excessive Porn Consumption Can Cause Erectile Dysfunction – Myth or Truth?

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There’s a growing trend of healthy young men using medications like Viagra and Cialis, drugs intended for older men and those with health-related erectile dysfunction (ED).

Many of these young men (unknowingly?) use these drugs to treat a condition that is psychological rather than physiological: porn-induced erectile dysfunction (PEID).

Online social groups and websites such as Your Brain on Porn and Reddit’s “no fap” group ( were founded to help men with PIED.

At the same time, studies that checked for a connection between watching porn and erectile dysfunction found no evidence associating the two. If that’s the case, what explains the sharp rise in ED cases in young men in recent years?

In 2012, Swiss researchers used the International Index of Erectile Function (IIEF-5), finding an ED rate of 30% in a cross-section of Swiss men aged 18 to 24. A 2013 Italian study reported that one in four patients who sought help for new-onset ED were younger than 40, with rates of severe ED nearly 10% higher than in men over 40.

We asked Takeesha Roland-Jenkins (MS in psychology and MS in neurology) a professional consultant for the Between Us Clinic, to weigh in. Takeesha is an expert in both psychology and neurology, and she has a unique insight into both the psyche and the brain.

In your opinion, can excessive porn consumption really cause a man to experience erectile dysfunction?

Yes, watching hardcore porn excessively, especially pornography with deviant and violent behavior can cause mental changes that may result in erectile dysfunction.

What happens in a man’s brain when he is exposed to extreme sexual stimuli (such as hardcore pornography) and how does this relate to ED?

Hardcore pornography is often graphic and generally displays deviant, violent, and abnormally kinky behavior. This is not typical for the average sexual encounter and it can create unrealistic mental perceptions of how a man should engage in sexual activity. Furthermore, a man may initially get a thrill from watching what he believes is an exotic encounter, but over time excessive porn watching desensitizes men to intense sexual stimuli and even sexual violence which sometimes occurs in the porn that is being viewed, thereby lowering the ability to engage in true intimacy.

Pornography, in general, causes intense mental stimulation that changes the way the brain views sexual activity and sexual violence in pornography exaggerates the alterations in the brain.

This phenomenon is similar to becoming more tolerant to a certain drug after prolonged use; meaning you eventually need higher and higher doses to experience the same feelings of euphoria. Repeatedly watching hard-core porn can have a similar effect on sexual performance. In other words, watching excessive porn changes the way the brain processes sexual arousal and activity, often leading to desensitization that lowers libido and causes psychological erectile dysfunction.

Some say that men who watch too much porn can develop performance anxiety. Why does anxiety affect the ability to get and maintain an erection?

In addition, because a man’s brain has now become accustomed to getting stimulated at the sight of intense pornographic images, an ordinary encounter will cause the man to wonder if he will be able to perform at a similar level (e.g., for extended periods) as what has been observed in a pornographic video. Therefore, the performance anxiety is still related to the changes that occur in the brain and wondering if he can satisfy his partner in the manner that the brain has become used to. In other words, the anxiety is a direct result of worrying about being able to re-enact the sexual scenes in porn; this unrealistic goal can lead to performance anxiety. Subsequently, a man may get an erection, but after beginning to worry about whether he can perform like the actors in porn, the erection may soften or stop altogether.

So, other than performance anxiety, is there another reason why porn could cause men to experience ED?

The changes that occur in the brain’s ability to lead to an erection contributes more to PIED than performance anxiety. Over time the brain needs increasing levels of stimulation from the pornography in order to initiate an erection. Performance anxiety can unfortunately worsen erectile dysfunction.

Does porn-induced erectile dysfunction cure itself if the man stops watching porn?

Discontinuing pornographic viewing does not automatically cure PIED. Furthermore, drugs such as Viagra or Cialis target the physical aspect of erectile dysfunction, not the psychological aspect. This means that a man will become completely dependent upon such drugs until the brain restores its ability to initiate an erection under ordinary sexual circumstances. A healthy relationship (e.g., marriage) with a patient partner can help a man overcome PIED over time.

What form of treatment would you recommend a man who suffers from PIED?

Beneficial treatment would be in the form of individualized therapy, which may vary in time (e.g., weeks, months) depending on the individual and the degree of PIED. As PIED is often the result of an addiction to pornography, this form of treatment should be viewed as the first step to addiction recovery.

The purpose of therapy is to begin to desensitize the brain to the pornographic images and to address some of the reasons that the addiction to porn more than likely started. Men are also encouraged to reconnect intimately with their partners in order to help the brain restore its ability to initiate sexual arousal during ordinary sexual encounters. Overall, a man must be willing to give himself time to gradually overcome PIED.

*Originally published on


Prause N and Pfaus J. (2015), Viewing Sexual Stimuli Associated with Greater Sexual Responsiveness, Not Erectile Dysfunction. Sexual Medicine, 3: 90–98. doi:10.1002/sm2.58.

Landripet I and Štulhofer A. (2015), Is Pornography Use Associated with Sexual Difficulties and Dysfunctions among Younger Heterosexual Men?. The Journal of Sexual Medicine, 12: 1136–1139. doi:10.1111/jsm.12853.

Park BY, Wilson G, Berger J, Berger J, Christman M, Reina B, Bishop F, Klam WP, Doan AP. Is Internet Pornography Causing Sexual Dysfunctions? A Review with Clinical Reports. Lane SD, ed. Behavioral Sciences. 2016;6(3):17. doi:10.3390/bs6030017.

Image via geralt/Pixabay.

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In and Out of the Abyss: Depression After Brain Surgery

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Once again I was on the phone to my friend, sobbing. She’d put up with my tears every day since I left the hospital. Two or three daily meltdowns were the norm.

Many of my tears were over things that would have merely irritated me before: misplaced scissors, dirty socks in the middle of the living room, a brief computer glitch.

I have cavernous angiomas, tangles of malformed blood vessels, scattered throughout my brain. Two of them—one larger than a golf ball in my right parietal lobe, and the other, smaller, in my brain stem—had bled, and I underwent brain surgeries to remove them.

The bleeds and surgeries led to side effects including loss of balance, vertigo, nystagmus, trouble with sensory overload, and a number of cognitive deficits. My emotions also seemed volatile. I expected that my emotions would settle down as my brain healed. They didn’t.

After putting up with about a month’s worth of meltdowns, my friend spoke up. “I think you need meds.”

I was shocked. The possibility of psychiatric medication had not occurred to me. The people I knew who needed it had major issues: a cousin whose mother had died when she was ten years old, a friend who had been suicidal, a student with bipolar disorder. I wasn’t depressed. I just got really upset too easily. I was just fragile, and, given what I’d been through, that was understandable.

I wasn’t in denial over my emotional state. Aware of my extreme vulnerability, I’d been proactive: I’d started seeing a psychotherapist regularly within days of my return home from the hospital. I had things under control.

I knew that brain injury can cause chemical imbalances, which can lead to clinical depression. In one account I read, a patient lamented not having gone on antidepressants sooner. Feeling fortunate that I wasn’t in that bad of shape, I sympathized with those who were.

I didn’t need meds.

Over the next few weeks, as the tears flowed more often and more freely, my friend grew more insistent. I continued to resist, explaining away my vulnerabilities. It was normal to grieve over losses. I blamed really bad days on my menstrual cycle.

But as the severity and frequency of my meltdowns increased, I had more trouble rationalizing.

I spiraled into the abyss and finally reached the bottom. I felt desolate. I knew I was a burden on everyone around me and that my life wasn’t much of a life. Suicide seemed logical, perhaps the only solution.

I kept my suicidal thoughts secret—I didn’t want my friend or my therapist to try to talk me out of it.
Weeks later, when I began to emerge from the abyss, I kept my silence because I felt ashamed, and later still, I added guilt to the shame—I had betrayed the trust of both my friend and my therapist.

I tried to rationalize my lie-by-omission: I told myself that I could never really take my life, that I didn’t have it in me.

But in some corner of my mind there must have been doubt mixed with the rationalization because a few days later I decided to discuss antidepressants with my therapist. She agreed with my friend: it was time to consider meds.

Until the brain bleeds, I was averse to pill popping. I took painkillers for my migraines and antibiotics for bacterial infections—no other medications. After the bleeds, I started taking blood-pressure meds (Verapamil) to cut back on the chances of another bleed and anti-seizure meds (Lamictal). I was concerned about messing with my body chemistry, and worried about drug interactions—I wanted to avoid medications that listed seizures as a possible side effect. Given my concerns, my therapist sent me to a psychiatrist who specialized in psychopharmaceuticals.

I wasn’t sure whether there was a viable solution within my comfort zone, but the answer turned out to be straightforward: the psychiatrist suggested simply increasing my daily dose of Lamictal. Anti-seizure meds not only prevent seizures; they also act as mood stabilizers and are often used to combat depression and bipolar disorder.

My psychiatrist conferred with my neurologist, who, concerned about adverse reactions to the Lamictal, was firm about capping my daily dose at 600 milligrams. My psychiatrist, determining that my depression was severe, decided to increase the dose directly from the 400 milligrams I was on to 600 milligrams, instead of ramping up in increments, which is the standard procedure.

I responded well to the increase. Feeling like myself once again, I realized just how badly off I’d been. Like my cousin, my student, and my friend, I too had major issues. Except that I really wasn’t like them—my issues were temporary. Once my brain healed, my depression would be over, and I’d be able to get off the meds.

It took a good four years and a couple of trial runs with lowered dosages before I managed to fully shrug off that piece of denial.

A decade later, I’m still on antidepressants, for good reason.

This depression isn’t “situational.” Good friends and therapy help me survive, but they aren’t enough. The bleeds and surgeries changed my neurochemistry. These changes are real, and they’re here to stay. The meds are here to stay, too.

Image via 5arah/Pixabay.

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