Thursday, January 18, 2018

Fre Will and Witchcraft

Human behavior is a complicated and often unpredictable beast. Societies often create their own social norms and hierarchies by which patrons are expected to follow.
Accusations of witchcraft within a society are more common than one might think in this day and age. Beyond that, a study cited by the Scientific American shows that these accusations seem to arise independently throughout the world, with strange commonalities. As an example, scientists in the study found that societies often accuse "witches" of poisoning food. "Witches" are often women, and the tag of "witchood" is often passed through the female lineage. This tag separated "witches" from the rest of their society, establishing social hierarchy within it.

This strange human behavior of labeling and ostracizing members of a community with a label that often defies logic begs a behavioral neuroscientific question. How does the phenomenon begin?

A seminar given in mid-October at Loyola University Chicago was titled "Subconscious Motivations - Free Will - Did my brain make me do it?" posed the question of free will from a neuroscientific perspective. 

The seminar cited a study that claimed to prove that free will doesn't exist. It claimed that all choices are preceded by an awareness of an urge, which is preceded by a readiness potential. Furthermore, that all of these things are visible as neuronal firings through fMRI.
In the small communities that accuse some women of being witches, this study may indicate that accusations of withchood are predetermined. Or, if you're superstitious, the study hints that "witches" poison food in a predetermined way. Are 13% of women in 'small' communities witches? 

I've always been a fan of Halloween, but for the sake of food safety and my ability to sleep, I'd like to believe that this study falsely defines what a 'choice' is, and therefore falsely defines the way humans interact with one another in groups. While the study that claims to disprove free will is a scientific one, and thus, a scientific discussion needs to be had with regard to it, there is certainly room for a philosophical—or at least psychological—debate. Such a claim is huge, and can surely be viewed as a slippery slope argument that leads to conversation about the legitimacy of witches.
What do you think? Is there a spooky correlation going on in small communities around the world? Can it be explained neuroscientifically?

Scientific American:

Wednesday, December 13, 2017

Alzheimer’s in Mice and Chimps

In Beth Stutzmann’s work she uses AD mice models in hopes to identifying early signs of Alzheimer’s. In one paper she discusses different processes that affect Ca+2 (Ca) signaling and their role in Alzhiemer’s disease. Ca signaling is important due to its role neurotransmitter release. If Ca is blocked release is inhibited because without Ca vesicles are not able to separate from synapsin. Increased Ca within the cell inhibits this process by changing the concentration gradient, now more inside than outside, which reverses the normal flow of Ca upon opening of the voltage-gated Ca channels. This decrease in vesicle release causes a decrease in plasticity which is involved in learning/memory. One way Ca is increased is through Aβ peptide increase because they make more Ca permeable channels on the plasma membrane. Increased Ca through RyR3 mediation leads to more Aβ peptides but also Aβ plaque formation. Increase Aβ can also increase RyR3 expression furthering this relationship. APOE gene codes for production of apolipoprotein E, which function is combining lipids for formation of lipoproteins. One variation of this gene, ɛ4, increases intracellular Ca levels by recruiting the plasma membrane channels and RyR-mediated ER stores. APOE is also thought to regulate the formation of Aβ plaques, ɛ4 being bad at preventing their formation.

In another paper she studies nitric oxide’s role in sustaining synaptic plasticity. Due to the “abnormal synaptic function” that is observable before cognitive deficits are, synaptic plasticity is gaining recognition as a cause to the memory impairments of Alzheimer’s. Since synaptic function is altered before cognitive functions they conclude that there must be something compensating in order to keep cognitive functions normal. In this she looks at suppression of RyR-evoked Ca signaling, causing intracellular to increase since RyR regulates the release of Ca. Stutzmann’s research suggest nitric oxide (NO) as a candidate for the “compensatory mechanisms [that] are recruited to maintain a functionally normal net output of the hippocampal circuit”. Both of these papers contribute to finding early warning signs and possible markers that can be used in the diagnosis of AD.

In Stutzmann’s presentation of her research she gave some insight as to why science is at a standstill in terms of finding a cure. Two reason she listed were that research is focusing on late AD processes and that studies consistently use/target the same areas. Another challenged mentioned was that unlike diseases such as Huntington’s disease, Alzheimer’s does not have clear identifiable genetic markers. This unknown genetic cause contributes to the issue because the knowledge of what causes this disease genetically would allow us to focus on the chemical aspects of the disease and monitor their levels. This could help in identification and treatment of early stage Alzheimer’s.

In an article on Scientific American (Nature on Aug. 1 2017) by Sara Reardon discussed biological makers, which are thought to contribute in the development of Alzheimer’s, are found in chimpanzees. Specifically, the three markers discussed are plaques, tangles of proteins, and the loss of neurons. The amyloid-β and tau proteins, what causes plaques and tangles respectively, found in chimps are identical to those in humans. They looked at 20 chimps’ brains, examining brain regions that are damaged during AD. Pre-tangles were found in all 20, four had plaques and tangles, and “several of the chimp brains contained amyloid-β”. Regardless of similarities, researchers found no evidence of severe dementia and could not link biological changes to changes that occurred in chimp brains. William Hopkins, co-author, suggest that these markers present the opportunity for dementia to happen. One explanation for this is the idea of a protective factor within chimps. Two theories discussed as possible reasons for this contrast are; the protein markers, amyloid-β and tau, may fold differently in chimpanzees and/or the different behavior of APOE between the two species. Alzheimer’s, a progressive neurodegenerative disorder caused by neuron death, is effected by the protein markers through their suggested contribution in cell degradation. One piece of evidence for different folding of these proteins mentioned within this article is due to finding amyloid-β in the brains studied. Amyloid-β is more commonly found outside of blood vessels in humans, however the presence in brains “suggests that plaques may form in a different way in chimps”. The article specifies the function of APOE as controlling “how amyloid-β aggregates into plaques”, because this is its suggested role in AD development. Within humans the APOE gene has three alleles (ɛ2, ɛ3, ɛ4) but in terms of AD development APOE ɛ4 is the relevant allele. APOE ɛ4 is purposed to increase risk of Alzheimer’s by not being as effective as the other alleles in break-down of the plaques. Essentially the absence of dementia could be from the different folding of proteins, meaning plaques never form, and/or the better functionality of APOE in chimps, a more effective break-down of possible plaques. Prior to these findings humans were thought to be the only primates where plaques and tangles occur simultaneously. Reardon reported that Elizabeth Head, a neuroscientist at the University of Kentucky in Lexington said “Even if chimps never develop the symptoms of Alzheimer's, knowing that they spontaneously develop biological signs of the disease could yield useful information about its early stages and potentially how to prevent it” Mary Ann Raghanti, conductor of the brain analyses, says “If we could identify the things that are similar and different in chimpanzees and humans, we can start to unlock why humans are so uniquely susceptible to this pathology”. From these findings future steps, which Raghanti says are now being done, in their studies include examination of inflammation and neuron loss with age which are two other important factors to AD.

Both these studies discuss the APOE and plaques possible roles in AD. Unlike Stutzmann, Raghanti did not get to observe the brain activity of these chimps which greatly limited her research. I would be interesting to see the role of Ca had with chimp synapses. If two studies such as these were to come together, NO testing in a chimp brain, many strides into the working of these processes could happen. Useful information that could come through further studies of chimpanzees are; potential of identifying a protective factor, determine cause of dementia development, and better caretaking of chimpanzees. However, since 2015 biomedical research on chimps has ended, including MRI scans. This obviously prevents most studies that can been done in relation to AD and chimps but if betterment of chimpanzee life is considered and emphasized maybe there is a chance for exceptions to be made. At least in regards to scans being performed on chimps while they’re alive to get more accurate information on possible degeneration.

  1. Chakroborty, Shreaya, and Grace E. Stutzmann. "Early calcium dysregulation in Alzheimer’s disease: setting the stage for synaptic dysfunction." Science China Life Sciences 54.8 (2011): 752-762.
  2. Chakroborty, Shreaya, et al. "Nitric oxide signaling is recruited as a compensatory mechanism for sustaining synaptic plasticity in Alzheimer's disease mice." Journal of Neuroscience 35.17 (2015): 6893-6902.
  3. Reardon, Nature Sara. “Chimpanzees Are First Animal Shown to Develop Telltale Markers of Alzheimer's Disease.” Scientific American, 1 Aug. 2017,

The Opioid Crisis in the Hands of Mary Jane

        It’s time to put our tails between our legs and blaze it, medical marijuana is going to be legal in all states pretty soon. People in 29 states including the U.S. District of Columbia are smoking away their pain without worrying about the cops. Sure, that seems like something that every semi-with it person knows, but when you see the numbers it’s frustrating, for some, blood boiling.

         In 2015 Opioid overdoses were up to 33,000…. THIRTY-THREE THOUSAND. The addiction level is unreal. This is why the work our speaker, Folabomi Oladosu, is so important. Her idea to regulate the people that are prescribed opioids and attempting to cure chronic pain is one way to get us out of this mess. Lifelong addictions to Vicodin and other opioids could also be corrected with the use of marijuana. Scientific American states that “multiple studies have shown that pro-medical marijuana states have reported fewer opiate deaths and there are no deaths related to marijuana overdose on record” (Grover, 2017 & Cohen, 2017). People are testing/creating new medicines that contain THC and CBD extracts, one guy in New York is even trying a chewing gum- neat! Natalie Grover mentions Israel-based Intec and their recent announcement concerning their work on early-stages of testing of THC and CBD extracted painkiller as well.

         Grover quotes California-based Nemu’s CEO Brian Murphy who told Reuters that,” doctors like to be able to write a prescription and know that whatever they wrote is pure and from a blinded, placebo-controlled trial.” To think, there is more confidence in prescribing a Schedule 1 drug than the legal stuff. It’s baffling, it’s dumbfounding, it’s 2017 so when the heck are they going to jump on board? I mean, have they not seen the emotional recking Facebook video of a child who stops seizing because her parent fed her a daily dose of medical Mary Jane? Or even the babies that are born addicted to opioids?

         This whole situation is just some messed up boo-hunky. From a biologist standpoint, it’s frustrating to watch something being done so wrong. Scientific American headlined this article, “medical weed is a popular way to manage chronic pain.” Other than opioid abuse, it has helped cancer patients, those who suffer with seizures, and a less intense but still very serious problem, anxiety disorders. Grover says that there are other non-opioid painkillers under research as we speak, but as a community we are much closer to seeing medical marijuana be a part of our lives sooner than we think (and sooner than some pharmaceutical companies would like).

As depressing as it sounds, this is good news. We are close. Oh, so, close, to more than just hippies and their freedom, but to actual medical breakthroughs on large communities of people.


Grover, N. (2017, June 23). High Hopes Ride on Marijuana Amid Opioid Crisis. Scientific American. Retrieved from

Cohen, R. (2017, Mar 27). Would legalizing medical marijuana help curb the opioid epidemic?. Reuters. Retrieved from

Sleep Deprivation and the Severe Physical and Mental Effects

Zaynah Farooq
NEUR 300
Sleep is a necessary part for the functioning of the human body. Without sleep, it is impossible for someone to perform at their fullest potential at daily tasks, let alone higher functioning cognitive tasks. Nowadays, it is not uncommon for people to be severely sleep deprived, and therefore, hindering the quality of the work they do in their daily lives. The more hours of sleep an individual gets, the more they are able to be productive and effective at their daily tasks. Extensive research has been done, examining the effects that sleep deprivation can have on an individual. It has been shown that not only sleeping less can cause sleep deprivation, but also simply offsetting one’s circadian rhythm. This can be done by sleeping at odd hours of the night, being affected by insomnia, and other effects from disorders that may effect regular sleeping patterns. What is common across the board is the agreement that sleep is essential in not only physical health, but a person’s mental health as well. Research done at the Massachusetts Medical Society largely focuses on the effects of sleep deprivation on long haul truck drivers. According to an article by the Huffington Post, sleep debt can cause various reactions in people, like physical and mental decision-making characteristics.

            Loyola University’s Dr. Gail Baura touched on the significance of sleep deprivation in long-haul truck drivers, as she reviewed research done by Dr. Mitler and his lab at Massachusetts Medical Society. The study reviewed 20 male truck drivers and through different methods of monitoring including electrophysiogical and performance, it was possible to estimate the amount of sleep each driver was able to get. The amount of naps and eye rolling movements were also recorded, as well as some tell-tale signs of sleep. While the recommended required amount of sleep is around 7 hours, these drivers were getting around 4.78 hours, much less than the recommended amount.  Dr. Baura spoke about the ways to solve this problem in drivers that are driving under the influence of extreme sleep debt. Often times, long-haul truck drivers are under extreme sleep deprivation. Mitler et al. was able to pinpoint that steady night and steady day drivers had a significance difference in the amount of sleep they got, with the night drivers getting much less sleep. Perhaps using different technologies readily available now will be the solution to lessening the amount of accidents that occur as a result of sleepy driving. Dr. Baura mentioned that detecting unintended lane departure, self-driving cars, and EEGs imbedded in the steering wheel could be effective solutions to this problem. However, within these there are other problems. Eyelid closure detectors detect when a person is falling asleep and is able to alert the driver to wake up. It is possible to use this to perhaps lessen the amounts of accidents occurring by drowsy drivers. Yet, merely electrophysiological technologies or car/truck technologies are not enough to detect full sleepiness in a driver, and researchers still look for a way to properly combat this pressing matter.
            While everyone is aware of the adverse effects of driving while drunk, there is a shocking revelation that most need to be made aware about, an epidemic worse than drinking that affects all. Studies have shown that sleep deprivation can lead to the same negative effects of drunk driving, yet nearly everyone has fallen victim to driving while drowsy.

            Sleep is the time for the body to reset and restore all that was used during the day. Vital needs need to be met in the human body, and the time for this is during the night when a person is sleeping. The brain also uses sleep to clear itself from toxins that accumulate. The much-needed energy used through the day by the body is also restored during sleep. These all factor into the importance of sleep for the human body. The HuffPost article titled “Here’s A Horrifying Picture Of What Sleep Loss Will Do To You” highlights on some of the negative effects of sleep deprivation. Physically, it is possible that due to the body not recharging and eliminating toxins during sleep, the possibility for cancers may increase. Also, the risk for diabetes goes up, while the life expectancy decreases and sperm count goes down. Due to clogged arteries as a result of sleep debt, the risk for cardiovascular impairments may also increase, as well as the quadrupling of the risk of stroke and the increase in risk of obesity. On the other hand, mentally, people are more likely to have depression and also have an accident while driving, as discussed in Dr. Gail Baura’s talk.

            It is no surprise that sleep debt and deprivation have negative effects on the human body. These effects are not only hurting the person experiencing them, but also those around them. It is very important that everyone keeps their circadian rhythm in check and is able to get the recommended amount of sleep nightly.

Mitler, M. M., et. al. (1997) The Sleep of Long-Haul Truck Drivers. Massachusetts     Medical Society, The New England Journal of Medicine, 24 Feb. 2016,

Schocker, Laura. “Here's A Horrifying Picture Of What Sleep Loss Will Do To You.” The Huffington Post,, 8 Jan. 2014,