Multitasking Future Actions

    What if human beings were able to "predict" future actions and be prepared to respond accordingly in a matter so as to multitask? One can say this similar to the concept of muscle memory. However, this is not the case. Muscle memory is different, for it is the product of motor learning through procedural memory. What I am discussing here is what is known as the "parallel action regulation hypothesis." This hypothesis refers to the concept that actions that are to occur in the near future are sequenced and regulated in parallel, meaning multiple actions can be "readily" activated with decreasing potential. This hypothesis takes the process of serial inhibition and expands on it. I will also discuss serial inhibition through retina ganglion activity.

    In the article "Parallel Regulation of Past, Present, and Future Actions During Sequencing," by Behmer et. al. (2018), the researchers present some of the earliest human data present on the parallel action regulation hypothesis via direct tests. They were able to do so by using transcranial magnetic stimulation (TMS), in that the TMS highlighted the excitation of flexion in the right index finger of a subject while typing. As the subjects continued to type, there was less action potential due to the parallel regulation occurring. It was discovered that a serial inhibition process could be suggested to regulate future actions (in parallel) while sequencing. 

    In the article "Sensitivity to Image Recurrence Across Eye-movement-like Image Transitions Through Local Serial Inhibition in the Retina" by Krishnamoorthy et. al. (2017), the researchers used mouse models to study encoding of stimuli in the retina. They furthered existing research by finding that certain ganglion cells are suppressed in the retina upon viewing various visual patterns, and when a pattern is repeated, they are activated via a sudden spike burst. In other words, "rapid image transitions" lead to a local serial inhibition process in the retina that is regulated via Glycine and GABA inhibition. 

    Both articles show that due to serial inhibition, it is possible to decrease successive action potentials needed to stimulate a response. It may be possible to take the results of the Behmer et. al. study and procure a new study in which decision-making could be studied in such a way so as to see if it is possible to "program" the brain to complete certain actions that would be otherwise conscious in an unconscious manner, due to the parallel sequencing already planning ahead for the completion of said action. The Krishanmoorthy et. al. study only furthers this potential future study by confirming the effects of the serial inhibition process, as well as the parallel action regulation hypothesis.

Citations:

Behmer, Lawrence & Jantzen, Kelly & Martinez, Sarah & Walls, Rachel & Amir-Brownstein, Elisabeth & Jaye, Andrew & Leytze, Mckaila & Lucier, Kathleen & Crump, Matthew. (2018). Parallel Regulation of Past, Present, and Future Actions During Sequencing. Journal of Experimental Psychology: Human Perception and Performance. 44. 10.1037/xhp0000507. 

Krishnamoorthy, V., Weick, M., & Gollisch, T. (2017). Sensitivity to image recurrence across eye-movement-like image transitions through local serial inhibition in the retina. ELife, 6. doi:10.7554/elife.22431

Termination of COVID-19 Effects in Gustation

    A pandemic known as Covid-19 has shut down the world due to the deadly disease it has imposed on 

millions of people. The virus has effected many in different ways. Shortness of breath, fever, sore 

throat, and chills are just some of the symptoms that have been reported. Hundreds of thousands have 

been hospitalized due to the lack of self care they are able to provide, as the virus attacks viciously. 

some of the least severe symptoms of Covid-19 have included the loss of senses such as taste and 

smell. These onsets may be very alarming as innate survivor instincts rely on taste for foods and smells 

for environment detection. Taste is especially important given that humans use this sense to determine 

if foods are edible or not. Without this, eating spoiled foods or inedible items can be deadly. Humans 

rely on their senses to navigate around the world , in which a loss of them can be detrimental to an 

individuals health and well being.

    In the Article, "Sudden onset, acute loss of taste and smell in coronavirus disease 2019 (COVID-19): 

a systematic review" by Panduwawala et al., describes the Early detection and management of COVID-

19. US Centers for Disease Control and Prevention (CDC) recently included sudden loss of taste 

(dysgeusia/ageusia). As it is still unknown why the virus targets gustation in some individuals, it has 

been deemed that sensorineural dysgeusia or anosmia due to neurotropic or neurovirulent SARS-CoV-2 

infection targeting the gustatory or the olfactory systems appears to be the pathological basis for these 

symptoms. As cases progress, clinical trials are implemented in curing the case of sensory loss such as 

gustation through medical oral treatments. This is urgent due to the issues of individuals reporting no 

sensory recovery after infection and recovery.

    In the Article, "Ephrin-B/EphB Signaling Is Required for Normal Innervation of Lingual Gustatory 

Papillae" by Rochlin et al., describes the current studies in the field of gustation. This article targets the 

axons through the intervention of taste buds. it was found the Ephs and Ephrins are utilized as ligands 

and receptors for the gustatory system. It was recently discovered that EphrinB was the priority in 

gustation as it is the main concept to send signals through axons to the brain. This would prioritize any 

interventions or medical advancements towards EphrinB as it is the main gateway.

    In conclusion, Gustation is a very new field in medicine that is not well studied or scientifically 

advanced. Due to the new pandemic and symptoms it entails, the finding in Dr. Rochlin's research may 

be the gateway to medical advancements throughout the field of taste. This may also lead a new 

gateway into the field of chemosensory system, curing not only Covid-19, but other illnesses 

throughout.

References    

Panduwalala, Chamila, et al. " "Sudden onset, acute loss of taste and smell in coronavirus disease 2019 (COVID-19): a systematic review". Int J Oral Sci. 2020;12(1):8.

Treffy R, W, Collins D, Hoshino N, Ton S, Katsevman G, A, Oleksiak M, Runge E, M, Cho D, Russo M, Spec A, Gomulka J, Henkemeyer M, Rochlin M, W: Ephrin-B/EphB Signaling Is Required for Normal Innervation of Lingual Gustatory Papillae. Dev Neurosci 2016;38:124-138. doi: 10.1159/000444748

The Inputs and Outputs of the VTA Hold the Answer to Mechanism Behind Reward Behavior

            Reward behavior is a key topic of focus for both behavior psychologists and neuroscientists. From the neuroscience perspective, reward behavior is initiated by the synaptic activity of certain neurotransmitters in reward-oriented areas of the brain. The central area of focus for reward behavior research is called the ventral tegmental area (VTA), located in the midbrain. The VTA has different inputs from and outputs to cortical areas and the limbic system. Dopamine is the neurotransmitter of focus in the brain’s reward pathway. Studying the neurobiology behind reward processing is crucial for understanding addiction, motivation, and aversion. With a better understanding of the VTA and its function, scientists and pharmacologists will find more efficient ways to tackle the negative consequences of the reward pathway. Although much research has been done on the VTA, more findings are bringing us closer to the full mechanism of reward processing. 

            In the study, “Optogenetic excitation in the ventral tegmental area of glutamatergic or cholinergic inputs from the laterodorsal tegmental area drives reward,” Dr. Steidl et. al studied the optogenetic excitation of LDTg cholinergic neurons and LDTg glutamatergic neurons. These two types of neurons are located in VTA, and they control reward processing. The experiment involved only ChAT-IRES-Cre mice that were Cre+, and the mice were all males. Using stereotactic injections, the researchers injected adeno-associated viruses into the mice. They then used a plane procedure to expose the mice to situations with light so that their LDTg neurons can be stimulated when exposed to light. There were two groups of mice, the ChAT-ChR2-eYFP and ChAT-eYFP mice. The researchers used a chamber with light and a chamber without light. They were trying to monitor how long each mouse from each group spent in the light chamber and non-light chamber. Those that spent more time in the light chamber are more rewarded, which means light stimulation is causing synapses at the VTA (ventral tegmental area). Mice with LDTg-cholinergic neurons activated spent longer durations in a light-paired chamber. Mice with LDTg-glutamatergic neurons activated took many visits to the light-paired chamber. So, the researchers determined that both neuronal inputs induced reward-seeking behavior in different ways. The activated glutamatergic neurons caused the mice to replicate the behavior that gave them a rewarding feeling. On the other hand, the activated cholinergic neurons caused the mice to remain longer in a state that gave them a rewarding feeling. The optogenetic activation of these particular neuronal inputs never caused avoidance from the stimulus, which was the light chamber. However, optogenetic methods cannot help discover if these different neuronal inputs are co-activated or selectively activated for various forms of rewards. The researchers concluded that LDTg-glutamatergic neurons are crucial for initial decision making to receive a reward, while LDTg-cholinergic neurons are essential for maintaining rewarding behavior. Both LDTg-cholinergic and glutamatergic neurons are a central element in the reward processing mechanism located in the VTA. 

            In the study, “The Lateral Preoptic Area: A Novel Regulator of Reward Seeking and Neuronal Activity in the Ventral Tegmental Area,” Dr. Gordon-Fennell et. al discovered that the lateral preoptic area (LPO) has both direct and indirection projections to the VTA that can modulate the activity of the VTA. The LPO is an unexplored region within the hypothalamus. By controlling the activity of the VTA, the LPO has control over reward processing. In past studies, LPO was found to be involved in causing preferential behavior and locomotor activity. In this study, the researchers used male Sprague Dawley rats. They tested reward behavior in these rats using operant self-administration of either cocaine or sucrose or reward-seeking behavior of the same two stimuli. The greater the intake or search for stimuli, the stronger the reward behavior as induced by the LPO activation. The LPO region was activated using bicuculline, which is a GABA antagonist and inhibited by using a mix of baclofen and muscimol, which are GABA agonists. The researchers conducted five different experiments in this study. Each experiment studied both self-administration and reward-seeking behavior. The researchers found that when the LPO was stimulated, the reward-seeking behavior of the mice increased. The reward-seeking was examined by removing the stimulus and then seeing if the mice continued to seek the stimulus through their behavior. The researchers also compared the reward-seeking behavior between two different stimuli: cocaine and sucrose. Both stimuli yielded increases in reward-seeking behavior when paired with LPO stimulation even though cocaine is more addictive by nature. LPO activation, however, did not increase the operant self-administration of the mice. When scientists administered punishment to LPO activated mice, the mice's behavior was not altered by the punishment and thus did not avoid the stimulus. This result was not the case for regular mice who avoided the stimulus after punishment. Lastly, the researchers studied the projections of LPO that synapsed in the VTA. Both GABA and glutamate projections from the LPO are located in the VTA. Furthermore, there are indirect pathways by which LPO affects the VTA. This study could not find the exact mechanism of LPO on VTA. However, they found that LPO stimulation causes inhibition of GABA neurons and the enhancement of dopamine neurons in the VTA. This means that the LPO stimulation causes reward behavior. This research study focuses on the LPO, one of many regions in the brain, which modifies the activity of VTA and thus controls reward behavior. 

            Both of these studies looked at neuronal inputs and how the outward behavior changed following neuronal changes. Dr. Steidl and his fellow researchers directly stimulated two different types of neurons located within the VTA to test their effect on reward processing. Likewise, Dr. Gordon-Fennell and his fellow researchers tested the stimulation of LPO on reward behavior and its connection to the reward pathway located in the VTA. The results of both studies added to the puzzle of the reward system mechanism. There are many elements of this complex mechanism. Both studies used different means of stimulation, means of assessing reward behaviors, and locations of interest in the brain. They both concluded that the VTA and the projections that activate it are the keys to understanding reward processing. Many more research projects are being done and need to be analyzed to reach the full picture of the reward processing mechanism. 

Citations

Gordon-Fennell AG, Will RG, Ramachandra V, et al. The Lateral Preoptic Area: A Novel Regulator of    Reward Seeking and Neuronal Activity in the Ventral Tegmental Area. Front Neurosci. 2020;13:1433. Published 2020 Jan 17. doi:10.3389/fnins.2019.01433

Steidl, S., Wang, H., Ordonez, M., Zhang, S., & Morales, M. (2016). Optogenetic excitation in the ventral tegmental area of glutamatergic or cholinergic inputs from the laterodorsal tegmental area drives reward. European Journal of Neuroscience, 45(4), 559-571. doi:10.1111/ejn.13436

Institutionalized Care and The Need for Change to Foster Care

    Orphaned children are among a group of persons that experience moderate to extreme developmental issues. They never receive a beneficial amount of social interaction to prepare them for the world and many end up relying on the state for funds, housing, insurance, and more because their exposure to economic life is nonexistent and they have only been to know their institutionalized life. Zeanah et al. (2006) went to Bucharest, Romania with the idea of an early-intervention program for institutionalized children up to 30 months of age that had met two criteria: 1. had spent at least half of their life in the institution and 2. passed basic health assessments. The experiment was to demonstrate the effects of institutionalization and foster care on a child's development over time. There were two groups, care as usual (remained institutionalized) and those in foster care. The hypotheses consisted of: 1. The development of children raised by a family would be enhanced compared with that of children raised in institutions; 2. The longer children remained in the institutions the more compromised their development would be; 3. The age at which children are placed into foster care may play a role in their development and may play an important role over time. Using the guidelines for a longitudinal study, the researchers developed the understanding that the effects of foster care were far better than those who remained in an institution. They theorized this as the lack of affection would impede on the cognitive and neural development, as well as early child development.

    Recently a book was published, Young People Leaving State Care in China (Shang & Fisher, 2017) and talks about institutionalization in China and the mechanisms of how it works but mainly about the children that come from these state institutions. It is stated in the book that once children are in an institution the only way to get out is to be adopted or to mature and eventually be set into the world without any knowledge of how the world works. As a result, they face serious challenges "to establishing an independent life, employment, housing and social connections when they enter adulthood" (Shang & Fisher, 2017). There is positive and negative feedback on both types of care, state and foster, and how they affected people interviewed in the book by explaining how the positive and negative interactions made each person feel. The positives of foster care were rooted in the reliability of parents to take care of the children. The positives of state institutions were limited to feeling cared for by those they could not form formal relationships with (i.e. other children, staff, caregivers). The negatives of foster care were the effects of lost affectionate relationships and a sense of misplacement due to foster parents giving more affectionate, warming, and tailored care to their birth children. The negatives of the institutions goes on about emotional support, social support, physical abuse, and more. 

    The underlying argument is that if foster caregivers were trained in programs like in the BEIP, then maybe caregivers would be more willing to take on caring for one or two more children. There is government support when fostering, but many people look at that simply as extra spending money. Foster care is a wonderful opportunity to give a child a semi-normal life to allow them to be socially and emotionally engaged. Without those types of interactions, many will fail in modern society because they will be unable to form different types of relationships whether is is friendship, romantic, or professional. Continuing to push for foster care to eliminate institutional care is not simple, but must be taken seriously around the globe.

References

Shang, X., & Fisher, K. (2017). Young people leaving state care in China. Bristol, UK; Chicago, IL, USA: Bristol University Press. doi:10.2307/j.ctt22p7km9

Zeanah, Charles H., Koga, Sebastian F., Simion, Bogdan, Stanescu, Alin, Tabacaru, Cristian L., Fox, Nathan A., Nelson, Charles A., & BEIP Core Group (2006). Ethical considerations in international research collaboration: The Bucharest early intervention project. Infant Mental Health Journal. DOI: 10.1002/imhj.20107.

The Effects of Stress on Skin

     Stress is a reaction that everyone has experienced at some point in their lifetime. Whether it is due to the demands of schoolwork, an important interview, important presentation, etc. Stress can be induced through a variety of outlets and can cause a variety of symptoms, from increased heart rate to an increased appetite. We owe a large part of our body’s stress response to the hormone Cortisol, otherwise known as the “stress hormone”. Cortisol is a significant stress hormone and is responsible for many of our body’s stress responses. 

    Dr. Weinberg examined the neural responses that are caused by acute stress, and in addition, observed any possible relationship between stress and reward-processing. To achieve this, the researchers conducted a study where about participants were divided into both control and stress groups, and from there both groups were required to complete a variety of tasks: the door task, the flanker task, and the MIST task. The difference between the stress and the control groups was that an observer stayed with the stress group for the entire duration of the MIST task, while the observer only stayed for a short period of time in the control condition. This was how they were able to cause differing levels of stress between the two groups. The authors used salivary samples to record cortisol levels, while the EEG was incorporated to measure the reward processing. Based on their results, the researchers discovered that the stress group displayed higher levels of cortisol than the control group and that their cortisol levels lasted longer as well. In addition, they noted that stress affects reward-processing behavior by reducing it. An important takeaway from this study is the evidence that cortisol plays a large role in stress responses. 

    As mentioned previously, cortisol is the primary hormone that is involved in stress and more specifically stress responses, and we can clearly see that through the study conducted by Weinberg et. al (2020) as cortisol levels were higher in those experiencing stress compared to the control group. When it comes down to stress responses, we know that cortisol is responsible for inducing our stress responses, but what about its effects on our skin? An article published by The New York Times titled “This Is Your Skin On Stress” highlights the effects of stress on our skin, and more importantly, the role that cortisol plays in it. The article emphasizes that it is ultimately cortisol's effect on the skin barrier that causes stress-induced blemishes. Our skin barrier is responsible for the maintenance of moisture and the protection against harmful bacteria, and it requires oil, water, and microbiome in order to be sustained. What cortisol does is diminish these three things, harming the skin barrier. In terms of oil, cortisol depletes the production of beneficial oils while simultaneously stimulating the overproduction of sebum, an oil known for causing acne formation. With the changes in oil production, arises the microbiome producing more harmful bacteria as well. Finally, with the changes in the microbiome comes the possibility of free-radical production, and if dehydration could arise if the free-radicals were to attack lipids. Clearly, cortisol causes a domino-effect, from first affecting oil production, to eventually water levels in the skin barrier. A recommended method to combat these effects is not impossible, through activating a relaxed response to stress triggers, we can stimulate the parasympathetic system and reduce cortisol levels and protect your skin from the harmful effects of stress. 

     These works both reveal the notion that cortisol is an important component of stress responses. Dr. Weinberg’s study reveals that cortisol is always present when one is undergoing stress, while the article written by The New York Times exhibits one of the effects cortisol has on our skin as a stress hormone. As these works were able to identify cortisol as a major contributor to stress and stress responses, we are now able to find ways to mitigate the effects of cortisol.

Source:

Defino, J. (2020, December 08). This Is Your Skin on Stress. Retrieved December 10, 2020, from https://www.nytimes.com/2020/12/08/fashion/this-is-your-skin-on-stress.html 

Ethridge, P., Ali, N., Racine, S. E., Pruessner, J., & Weinberg, A. (2020). Risk and resilience in an acute stress paradigm: Evidence from salivary control and time-frequency analysis of the reward positivity.

The Growth Potential of Cerebral Organoids and their Clinical Applications

    Modern clinical approaches in neurological diseases mostly consist of imaging, biomarkers, and cognitive assessment, which often offers poor resolution and are only applicable after the disease has progressed significantly (Logan et al., 2020, p. 1301). Significant development in the exploration of many human congenital or neurodegenerative diseases have been limited by the complexity and ethical restraints of research on the diseased human brain or the usage of embryonic stem cells. In the last decade, neuroscientists have developed cerebral organoids derived from induced pluripotent stem cells (as opposed to embryonic stem cells), providing an effective in vitro 3D model of human brain development and/or disease progression. 

    Lancaster & Knoblich published their protocol titled “Generation of cerebral organoids from human pluripotent stem cells,” (2014) which was the first to detail the formation of 3D cerebral organoids; it emphasized the clinical advantages of the 3D spatial organization of organoids in investigating the “mechanisms of human neurological conditions that have been difficult or impossible to examine in mice and model organisms” (p. 2330). They also noted that its potential was limited, as in all in vitro systems, “the method lacks surrounding embryonic tissues that are important for the interplay of neural and non-neural tissue cross-talk… specifically, [due to] the lack of meninges and the vasculature” (p. 2330). This highlighted the cerebral organoid model’s applicability particularly to congenital brain conditions or diseases that develop over time, such as Zika-derived microcephaly, lissencephaly, brain cancers, fetal alcohol syndrome, Alzheimer’s disease, and Parkinson’s disease.

    In 2018, cerebral organoids were used to model the amyloid beta and tau pathology in Alzheimer’s disease by Gonzalez and colleagues. Unlike 2D cultures, the 3D system was able to mimic in vivo neuropathology of genetic Alzheimer’s disease and Down Syndrome with endogenous levels of protein expression, despite lacking accurate cellular heterogeneity and extracellular matrix organizations, and lack of mature synapse connections and vascularization (Gonzalez et al., 2018, p. 2373). In 2019, Linkous et al. utilized cerebral organoids to model patient-derived glioblastoma, which has a bleak median survival of approximately 15 months from diagnosis (p. 3203). The organoids successfully exhibited stage-specific neural development and demonstrated myelinated axons, dendrodendritic synapses, neurons, and glia (Linkous et al., 2019, p. 3207), the formation and proliferation of infiltrative tumors (Linkous et al., 2019, p. 3208, and the recapitulation of the human pathology overall, including the network of tumor microtubes that facilitate glioblastoma progression (Linkous et al., 2019, p. 3209). In the 2020 article, “Dynamic Characterization of Structural, Molecular, and Electrophysiological Phenotypes of Human-Induced Pluripotent Stem Cell-Derived Cerebral Organoids, and Comparison with Fetal and Adult Gene Profiles,” Logan and colleagues discussed their advancements in “dynamic development, cellular heterogeneity and electrophysiological activity,” (p. 1301) demonstrating, for the first time, in vitro recapitulation of electrophysiological drug response in cerebral organoids. This study also showcases the rapid development of cerebral organoids, as they displayed the system’s ability to exhibit “(1) a heterogeneous gene and protein markers of various brain cells, such as neuron, astrocytes, and vascular cells including endothelial cells and smooth muscle cells, (2) and increased gene expression of brain cell-specific markers over time, and (3) functional electrophysiological properties as evidenced by the neurons with action potential and synapse-like structure, functional response of ion channels to the drug stimulation” (p. 1317). 

    As described above, the challenges faced by Gonzalez et al. in their 2017 study had been largely resolved in close future studies, demonstrating cerebral organoids’ rapid growth potential and high utility in the investigation of a broader range of neurological conditions. Conclusively, cerebral organoids will play a critical role in the future of neuroscientific and neuro-medical research. It is, however, imperative to expand on the discourse of ethics around cerebral organoids and their further development to responsibly proceed in this field of research.

Bibliography

Gonzalez, C., Armijo, E., Bravo-Alegria, J., Becerra-Calixto, A., Mays, C. E., & Soto, C. (2018, August 31). Modeling amyloid beta and tau pathology in human cerebral organoids. Molecular Psychiatry, 23(12), 2363-2374. https://doi.org/10.1038/s41380-018-0229-8

Lancaster, M. A., & Knoblich, J. A. (2014, September 4). Generation of cerebral organoids from human pluripotent stem cells. Nature Protocols, 9(10), 2329-2340. https://doi.org/10.1038/nprot.2014.158

Linkous, A., Balamatsias, D., Snuderi, M., Edwards, L., Miyaguchi, K., Milner, T., Reich, B., Cohen-Gould, L., Storaska, A., Nakayama, Y., Schenkein, E., Singhania, R., Cirigliano, S., Magdeldin, T., Lin, Y., Nanjangud, G., Chadalavada, K., Pisapia, D., Liston, C., & Fine, H. A. (2019, March 19). Modeling Patient-Derived Glioblastoma with Cerebral Organoids. Cell Reports, 26(12), 2303-2311. https://doi.org/10.1016/j.celrep.2019.02.063

Logan, S., Arzua, T., Yan, Y., Jiang, C., Liu, X., Yu, L.-K., Liu, Q.-S., & Bai, X. (2020, May 23). Dynamic Characterization of Structural, Molecular, and Electrophysiological Phenotypes of Human-Induced Pluripotent Stem Cell-Derived Cerebral Organoids, and Comparison with Fetal and Adult Gene Profiles. Cells, 9(5), 1301-1323. MDPI. http://dx.doi.org/10.3390/cells9051301

Elevating Online Learning through Gestures

 

When learning at a young age it is easy to become distracted and easily confused by new and intimidating subjects. A way to better engage young learners and have them best obtain the information they are learning can be done through gesturing. In a study done by Elizabeth M. Wakefield et al. called “Learning math by hand: The neural effects of gesture-based instruction in 8-year-old children” they analyzed the affects of gesturing on learning. Their study examined the “neural correlates underlying how children solve mathematical equivalence problems learned with the help of either a speech + gesture strategy, or a speech alone strategy” (Wakefield et al., 2019). This study was one of the first studies to explore “neural mechanisms of learning through gesture” and it was critical for their work that they would be studying differences in how the task was learned rather than how well the task was learned (Wakefield et al., 2019). During their study they used a math-learning paradigm in which they had 7-9 year old’s answer math questions after being placed in a gesture or non-gesture condition of a one-on-one math lesson (Wakefield et al., 2019). After doing this they were able to collect data from performing brain analyses of the participants in an fMRI scan, considering both data from participants within the same training condition and effects of training condition on their ability to process mathematical equivalence problems (Wakefield et al., 2019). What their work found was that learning through gesture leads to lasting and embedded neural trace of motor system (Wakefield et al., 2019). The work of their study provided evidence for the benefit of gesturing in learning of young students and how gesture aided lessons are better for the student to learn and apply to solving individual problems.

Considering the current event of Coronavirus changing most aspects of our normal routines. One thing I have noticed personally as a student and through observation of family and friends is that learning online is hard. Going from strictly in class education to a fully virtual environment has been a tough change for many individuals. One of the reasons for why this new form of learning is so hard is partially due to the lack of interaction between students and teachers including things we would normally experience such as gesturing and visual aids. Online learning for my self has mostly been hearing a teacher talk over a power point, seeing at most the teachers face and either more unfamiliar faces or little black boxes representing my fellow classmates. This learning often lacks the gesturing needed to accompany teacher’s speech in creating engaging and beneficial lectures. A study that investigates the benefits of gesture in videotaped learning is called “The Role of Instructional Gesture in Learning Science Concepts in Undergraduate Students” by Andrea J. Fogarty. This study not only furthers the evidence found in Wakefield et al. study on the benefit of gesturing, but it also applies the work on gesturing to college age students who are learning through a technological environment.

In this study, Fogarty discusses how gesture facilitates learning, discussing the reality that “representational gestures are often spontaneously produced by both instructors and learners while verbally explaining abstract and spatial concepts in science and mathematical problem-solving” (Fogarty, 2018). She also discusses is that “both spontaneous and rehearsed gestures have promoted more learning in comparison to no gestures in both math and science learning” (Fogarty, 2018). What this means is that student and teachers meaning to gesture or not does not affect the benefit it brings, by instinctually gesturing or planning it out does not change the benefit. This also means that often times student and teachers may be gesturing and receiving the benefit of gesturing without knowing it. Could this be a reason why students are feeling that online learning is so much harder? And if so, how can we create a learning system that is best able to enhance the learning environment for students from a virtual system? Well, as we will see the work that Fogarty did in the rest of her study may be helpful for teachers doing online learning and will “encourage instructors to produce representational gestures with their accompanying speech, especially with abstract topics with novice learners” (Fogarty, 2018).

In the study done by Fogarty, she created the videotaped conditions in which a teacher was describing the scientific concept of tectonic plates would be doing a representational gesture (hand gestures as well as pointing and tracing visual aids) , a beat gesture (tapping on the leg in sync with the speech), and no gesture. From her study with 45 undergraduate college students each watching one the videotaped (7 min) lectures then completing a posttest she could see that learning increased in all conditions but were highest from pretest to posttest in the representational gesture condition (Fogarty, 2018). This study presents a lot of evidence for understanding the benefits of gesturing as well as providing instructors with ideas on improving online learning so that it is as effective as possible for students and teachers (Fogarty, 2018). Suggestions such as lecturing “in-person” over the camera versus recording lectures over slides. As well as incorporating more gestures overall to a lecture which will allow students to see you demonstrate and show mechanisms or demonstrations for the information. In one of my classes I had a teacher that said multiple times in a prerecorded lecture where we could not see her face, that if it were a normal class she would be able to show us, or have us do an activity to better conceptualize the information. But, with evidence from Fogarty’s work teachers and school systems can create a better online experience for all students by changing the ways they deliver their lectures and take advantage of the many abilities technology gives us.

In both Wakefield et al. and Fogarty’s studies they provided evidence of gestures increasing learning by making more abstract concepts such as math and science become more concrete to the learner. Both of these studies span a large age group which shows that from a very young age to higher forms of education gesturing is always beneficial for learning more difficult concepts, and should be a focus at all levels of education. During this time when we are nationally and globally facing Covid-19, taking in the evidence and ideas presented in these two studies will help to enhance online learning for all, making an environment foreign to most students as effective and beneficial as possible.

 

Citations

 

Fogarty, Andrea J., (2018). The Role of Instructional Gesture in Learning Science Concepts in Undergraduate Students. BSU Honors Program Theses and Projects. Item 289. https://vc.bridgew.edu/cgi/viewcontent.cgi?article=1273&context=honors_proj.

Wakefield, E. M., Congdon, E. L., Novack, M. A., Goldin-Meadow, S., James, K. H., (2019). Learning math by hand: The neural effects of gesture-based instruction in 8-year-old children. Attention, Perception, & Psychophysics. https://doi.org/10.3758/s13414-019-01755-y.

 

Addiction and the Neural Signaling Pathways of Reward

      Dopamine is a neurotransmitter that has had much research connecting its role in the reward processing of addiction.  According to an article written for Promises Behavioral Health, an addiction recovery blog, dopamine has been deemed the “feel-good chemical,” playing a major role in mood, motivational drive, desire, pleasure, and satiety (Promises Behavioral Health, 2020). In actuality, substance abuse can alter the neural signaling pathways of various neurotransmitters, particularly to the motivation and reward centers of the brain. Repeated exposure to these substances can lead to cravings of more “reward,” resulting in addiction (Promises Behavioral Health, 2020).

In this article, the authors described the effect some commonly abused substances have on the circuitry of the brain and the subsequent effects on behavior. Alcohol affects neurotransmitters GABA, glutamate, serotonin, dopamine, as well as endorphins and can cause either sedative or excitatory effects. Marijuana affects the levels of dopamine and anandamide (a neurotransmitter that plays a role in the regulation of mood, memory, pain, appetite, cognition, and emotions), and can lead to feelings of euphoria, relaxation, and heightened visual and auditory perceptions. Amphetamines increase energy and excitation by affecting dopamine and some glutamate receptors in the brain. Cocaine, a drug that is commonly implicated into many studies investigating the neural circuitry of addiction, raises dopamine levels in the brain and often leads to dependency and continued cravings for the drug. It also affects serotonin and norepinephrine levels, resulting in increased energy and confidence (Promises Behavioral Health, 2020.

The ventral tegmental area (VTA) of the midbrain, a major structure in the reward circuit in the brain, is a hub of dopaminergic pathways innervating other limbic and cortical structures in the brain. The VTA receives inputs from the laterodorsal tegmental nucleus (LDTg), which has differing populations of cholinergic, glutamatergic, and GABAergic neurons (Woolf &Butcher, 1986; Oakman et al., 1995; Geisler & Zahm, 2005; Lammel et al., 2012; Watabe-Uchida et al., 2012). Some of these LDTg neurons that input into the VTA form synapses with neurons that project to the nucleus accumbens (NAc), another important structure in the reward circuit (Omelchenko & Sesack, 2005). In the study conducted by Steidl and colleagues, “Optogenetic excitation in the ventral tegmental area of glutamatergic or cholinergic inputs from the laterodorsal tegmental area drives reward,” the researchers focused on LDTg-cholinergic and glutamatergic neurons to investigate their role in regulating VTA dopaminergic neurons and how their activation effects behavior. In order to induce excitatory input into the VTA, they performed optogenetics in Cre-transgenic mice to stimulate either LDTg-cholinergic or glutamatergic neurons and evaluated the motivational and reward effects this had on mice in two versions of a chamber preference paradigm. They found that selective excitation of both LDTg-cholinergic and glutamatergic neurons play roles in the reward system, although these roles differ. VTA stimulation of LDTg-glutamatergic neurons resulted in increased entry into the light-paired chamber, but only for short periods of time, while VTA stimulation of LDTg-cholinergic neurons also resulted in increased entry into the light-paired chamber (though not as significantly often as LDTg-glutamatergic stimulation) in addition to longer stay in the chamber, showing place preference for the light-paired chamber. This indicates that LDTg-glutamatergic activity might be more important for simply reinforcing initial entry into the chamber whereas LDTg-cholinergic activity might be more important for the actual rewarding effects of staying in the chamber (Steidl et al., 2016). With future directions in mind, the researchers speculated that excitation of LDTg-glutamatergic neurons to the VTA might induce short and rapid increased dopamine levels in the NAc, leading to the behavioral inclinations seen in the increased entry into the light-paired chamber and shorter stays, while excitation of the LDTg-cholinergic neurons to the VTA might have more enduring effects on increasing NAc dopamine levels that led to longer stays in the light-paired chamber (Steidel et al., 2016).

 One could speculate that LDTg-glutamatergic activity may have a role in ‘wanting’ effects towards a reward, while LDTg-cholinergic activity may have a role in the actual ‘pleasure’ of having the reward. These neural pathways may be of use to incorporate into more research for treatments of addiction. Having insight into how these neural inputs regulate dopamine levels in the reward circuits in the brain may bring rise to new ways to help recovering addicts deal with cravings, even possibly curbing the rewarding effects they receive from their drug of choice.

 

 

References

Addiction and Dopamine Neurotransmitters: How Addiction Works. Promises Behavioral Health. (2020, February 25). https://www.promisesbehavioralhealth.com/addiction-recovery-blog/addiction-lights-brain-dopamine-neurotransmitters-101/.

Geisler, S. & Zahm, D.S. (2005). Afferents of the ventral tegmental area in the rat – anatomical substratum for integrative functions. J. Comp. Neurol., 490, 270–294.

Lammel, S., Lim, B.K., Ran, C., Huang, K.W., Betley, M.J., Tye, K.M.,Deisseroth, K. & Malenka, R.C. (2012). Input-specific control of reward and aversion in the ventral tegmental area. Nature, 491, 212–217.

Oakman, S.A., Faris, P.L., Kerr, P.E., Cozzari, C. & Hartman, B.K. (1995). Distribution of pontomesencephalic cholinergic neurons projecting to substantia nigra differs significantly from those projecting to ventral tegmental area. J. Neurosci., 15, 5859–5869.

Omelchenko, N. & Sesack, S.R. (2005). Laterodorsal tegmental projections toidentified cell populations in the rat ventral tegmental area. J. Comp. Neurol., 483, 217–235.

Steidl, S., Wang, H., Ordonez, M., Zhang, S., & Morales, M. (2016). Optogenetic excitation in the ventral tegmental area of glutamatergic or cholinergic inputs from the laterodorsal tegmental area drives reward. European Journal of Neuroscience, 45(4), 559–571. https://doi.org/10.1111/ejn.13436.

 Watabe-Uchida, M., Zhu, L., Ogawa, S.K., Vamanaro, A. & Uchida, N. (2012). Whole-brain mapping of direct inputs to midbrain dopamine neurons. Neuron, 74, 858–873.

Woolf, N.J & Butcher, L.L. (1986). Cholinergic systems in the rat brain: III. Projections from the pontomesencephalic tegmentum to the thalamus, tectum, basal ganglia, and basal forebrain. Brain Res. Bull., 16, 603-637

 

The impact of stress on our lives and how mindfulness might be the answer.

How can stress disrupt your life, and what impacts does it have on your body? And most importantly, what can be done to fix it? We’ve all experienced stress at some point in our lives, rather it was during an important sporting event or an important presentation, we’ve all been there before. Awareness for mental health has been on the rise in recent years, you might have noticed it as well, schools, companies, and even the government, all have been trying to sensitize the general population on mental health disorders, and how to prevent or manage them better. In fact, according to a 2019 article on mental awareness by Forbes, “funding in mental health startups has more than tripled over the past five years.” With this rise in publications, advertisement, and funding, you might be asking yourselves, is are behavioral healthcare system meeting the need? Well, according to data collected by AbleTo, the company specialized in virtual consultations with therapists and coaches showed that our behavioral healthcare system lacks in value, quality of care, and access but is pretty good in awareness and innovation, as we said before. So is there a better alternative to our behavioral healthcare that might be cheap, accessible, and actually be efficient?

I will attempt to answer this question using research conducted by Dr. Weinberg: “Risk and Resilience in an Acute Stress Paradigm: Evidence From Salivary Cortisol and Time-Frequency Analysis of the Reward Positivity” and research by Dr. Cernasov: “Attenuated Default Mode Network Functional Connectivity is Associated With Improvement in Depressive Symptoms Following Mindfulness-Based Cognitive Therapy in a Transdiagnostic Anhedonic Sample”

Dr. Weiberg’s research builds on the growing scientific belief that stress is associated with the brain’s response to rewards, thus this association is believed to be responsible for the development of some mental illness such as depression or PTSD for example. This research focuses on attempting to determine what associations can be made between stress and reward sensitivity in the brain? To answer this question, the researchers examined the association between hypothalamic-pituitary-adrenal-axis stress response and event-related potentials sensitive to the receipt of reward-related feedback. The study included 100 male participants, the participants were randomly divided between stress and control groups. The research exposed participants to an acute psychosocial stressor and examined its impact on a sensitive measure of neural processing of rewards, they also examined “potential buffering effects of increased neural response to reward on hypothalamic-pituitary-adrenal axis response to the stressor.” This research showed that delta power, which is a brain wave that is believed to generate from the Thalamus and plays a role in suspending external awareness during deep meditation and sleep, this brainwave was particularly enhanced after reward-related feedback. They also showed that this Delta brain frequency was responsible for a reduction in reward-related neural activity after stress, the researchers also studied the impact of stress on cortisol levels and showed that “baseline reward sensitivity in the delta frequency was associated with a reduced cortisol response when exposed to stress”. Dr. Weinberg’s research showed that “stress and the brain’s reward circuitry may have a bidirectional relationship that underlies pathways of risk and resilience for pathology” Furthermore it is believed that stress-induced anhedonia would be associated with reductions in both positive and negative reactivity. It is believed that chronic stress levels could be detrimental to our health due to prolonged exposure to elevated levels of glucocorticoids, which could lead to dendritic atrophy and reductions in neurogenesis. People who suffer from impairments to neural structures involved in reward processing could be more prone to stress, while also showing higher levels of cortisol during stress. 

So now that we have explored some of the neurobiological evidence of the impact of stress on our body, what can we do to fix it? As we said previously, mental health awareness has been on the rise but our behavioral healthcare is starting to show its limits, so let us go back to our original question, is there a better alternative to our behavioral healthcare that might be cheap, accessible, and actually be efficient? If I told you that I found a solution to managing stress in your life and avoiding stress-induced anhedonia, and if I told you that it can be 100% free of charge, no it's not a scam and yes it has been proven to be very efficient in most cases. This practice is called mindfulness, and Dr. Cernasov’s study highlights the scientific benefits of this increasingly popular practice. Mindfulness has been shown to impact neural networks involved in sustained attention, such as the the frontoparietal network, it can also impact networks involved in self-reflective thought, such as the default-mode network. This study used 56 adults with clinically significant anhedonia were randomly assigned to 15 weeks of Mindfulness-Based Cognitive Therapy (MBCT) or Behavioral Activation Therapy for Anhedonia (BATA). The research showed that Mindfulness-Based Cognitive Therapy reduced connectivity of the default-mode network compared to the other form of therapy. So in other words, mindfulness works.

Mindfulness can be practiced at no cost and is maybe the easiest method to use at home when trying to manage stress, you can gain back control over your life one meditation at a time. Mindfulness can be practiced through various activities such as yoga or even just meditation. We have seen what some of the harmful effects stress can have on our brain, most of the time these are dynamic changes but sometimes they can become lifelong if chronic stress is left untreated for too long. Mindfulness just might be the answer to our daily mental wellbeing. 

Mindfulness is a great practice that I highly recommend, it does not work for everyone, some people might get better help seeking professional care but others might benefit more from this experience.

Detecting Alzheimer's Before it's too Late: BDNF and Hippocampal Texture to the Rescue?

  Over the years the world has seen a substantial increase in Alzheimer's disease (AD)., plaguing the elderly of all demographics, and undoubtedly becoming one of the most pressing future public health crises. The ultimate cause of AD is a part of neuroscience that is still evolving and bridled in heated debates. However, it is relatively well understood that AD is characterized by cortical thinning, hippocampal atrophy, enlargement of ventricles, etc. that lead to loss of executive function, memory and language decline, etc. Moreover, the molecular underpinnings of AD are further associated with the accumulation of β-amyloid plaques, p-Tau tangles, whose accumulation leads to an increase of inflammation mediated by astrocytes and microglia, which then mediate an increase of more β-amyloid plaques, p-Tau tangles. It soon becomes clear how this vicious cycle can wreak havoc on the human brain, leading to AD. Despite this understanding of some of the molecular mechanisms at play it is nearly impossible to detect AD early enough to administer clinically significant treatment. However, recently published studies have utilized various biomarkers such as brain-derived neurotrophic factor (BDNF), as well as hippocampal texture in hopes of detecting AD early enough.

The article “Serum pro-BDNF levels Correlate with Phospho-Tau Staining in Alzheimer’s Disease”, published by Krishna Bharani and colleagues in the Journal of Neurobiology of Aging aimed to link the levels of pro-BDNF in serum and in the brain to the onset and progression of AD. To clarify, Pro-BDNF is the precursor molecule to mBDNF. The researchers were able to establish a brain bank, where they obtained brains from AD patients (n=19) and brains from healthy patients (n=12). Here they looked at four regions of interest: the dorsolateral prefrontal cortex (BA46), the hippocampus, and the entorhinal cortex. More specifically when looking at the hippocampus, the researchers examined the levels of β-amyloid plaques, tangles, NeuN, GFAP, pTau tangles, and the concentration of the BDNF receptors TrkB and p75NTR. It should be noted that the TrkB receptor is typically associated with the promotion of neuronal survival, while p75NTR is associated with the instigation of apoptosis. After completing ELISA and western blot assays it becomes apparent that the hippocampus of the AD brains had significantly more β-amyloid plaques and tangles, which should not come by as too much of a surprise; however, what the researchers did note was that the AD brain had higher   p75NTR receptor expression rates than that of the control brains. Furthermore, TrkB was much lower in the AD brains, as compared to the control brains. Since BDNF levels in AD brains were measured to be lower, it is logical that TrkB would be in a lower concentration, as well. The study also found that serum pro-BDNF levels were negatively correlated to hippocampal BDNF, possibly because pro-BDNF is primarily produced to be sent to the brain and mitigate damage. Moreover, serum pro-BDNF was found to be positively correlated to hippocampal-tau. This plethora of evidence suggests a relationship between BDNF and its receptors to the progression of AD.

With a better understanding of the molecular mechanisms behind AD, as well as some novel evidence pointing to the potential of using biomarkers to detect AD earlier on, we can better appreciate the complexity of this neurological disorder. As it so happens a recent study published by Lauge Sørensen and colleagues, “Early Detection of Alzheimer’s Disease Using MRI Hippocampal Texture” highlights another means to detect AD before characteristic onset. Sørensen et al. recognized that the hippocampus has notable atrophy throughout AD; however, they grew curious as to whether the texture has any association to early cognitive loss. They hypothesized that the accumulation of β-amyloid plaques and neurofibrillary tangles would reach a point in which they could be observed by MRI and that their detection would be early enough before serious atrophy. The researchers also wanted to determine if the MRI marker based on texture would be able to detect conversion from mild cognitive impairment (MCI) to AD. Furthermore, the texture was also tested to see if it reflected changes in hippocampal glucose metabolism by using fluorodeoxyglucose-positron emission tomography (FDG-PET). The experiment posed by the researchers utilized data obtained from the ADNI and AIBL database, which includes information on aging, biomedical imaging, etc. Hippocampus was given a bilateral hippocampal score that was computed by combining a texture descriptor and a support vector machine. From this, the researchers concluded that the ADNI -based results and obtained texture scores make the hippocampal texture a potential new biomarker in early tracking of AD, as it was successful in predicting MCI to AD progression. Finally, the metabolic rate of glucose within the hippocampus showed a significant correlation between texture and decreased glucose uptake. These results are extremely noteworthy as they are measurements that can allude to a decline in cerebral health much sooner than say tissue atrophy. 

Both Bharani et al. and Sørensen et al. aimed to gain a better understanding of Alzheimer's pathology and elucidate on measurable biomarkers that could help detect AD early in its progression. As the hippocampus is one of the main structures to atrophy, in AD, both researcher teams placed heavy emphasis on it and were able to elucidate both molecular and physical mechanisms that were at play.

 

 

 

Work Cited 

 

Bharani, K. L., Ledreux, A., Gilmore, A., Carroll, S. L., & Granholm, A.-C. (2020). Serum pro-BDNF levels correlate with phospho-tau staining in Alzheimer’s disease. Neurobiology of Aging, 87, 49–59. https://doi.org/10.1016/j.neurobiolaging.2019.11.010

Sørensen, L., Igel, C., Liv Hansen, N., Osler, M., Lauritzen, M., Rostrup, E., & Nielsen, M. (2015). Early detection of Alzheimer’s disease using MRI hippocampal texture. Human Brain Mapping, 37(3), 1148–1161. https://doi.org/10.1002/hbm.23091

The Positives Of The Bucharest Early Intervention Project

 The Positives Of The Bucharest Early Intervention Project 

The Bucharest Early Intervention Project (BEIP) is one of the most significant neuroscientific research endeavors in the last few decades. From its onset, the project faced a significant amount of criticism in regards to its ethics, despite passing the IRB process in the U.S. and obtaining approval from Romanian officials. The main contention with the project lies in its usage of vulnerable children for research purposes. Although the investigators did not necessarily put children at an increased risk due to their involvement in the project, many people find it objectionable that children were knowingly left in an unfavorable environment. Critics argue that the researchers possessed the ability to help the children, but they chose not to. In his presentation, Dr. Joe Vukov addressed the complex ethical controversies with this project. Arguments exist for both sides, and no common consensus exists on the ethics behind the BEIP. Although this project potentially faces ethical issues, it is undeniable that the results from this research have added significantly to the field of child development. It is vital to acknowledge the new insights from this research, and utilize them to improve the conditions under which children are raised. 

Dr. Vukov’s talk paralleled certain points presented in the article “Ethical Considerations In International Research Collaboration: The Bucharest Early Intervention Project,” but he added other key ethical points as well. First, it is important to understand the context behind the project. Due to policies under Communist rule, Romanian families were forced to produce as many children as possible. This resulted in widespread child abandonment in the country, and state run orphanages took these children under their care. Romanians held the common belief that the state possessed the ability to raise these children properly. After the overthrow of Communist rule in 1989, institutionalization still remained the predominant form of housing for these children, despite stories covering the social deprivation and appalling conditions common in the orphanages. In the early 2000s, researchers from the BEIP chose Romania as the site to investigate insitutionalization’s effect on brain structure and behavior in children, as well as the child’s ability to recover from these detrimental effects after transfer to foster care. In addition to these goals, the researchers also hoped to provide concrete research in support for foster care, to influence Romanian officials to shift to this form of child care. The study was longitudinal, utilizing a randomized control trial method. The study placed 136 institutionalized children into two groups: a care as usual group in which children maintained their current living circumstances, and a second group where they were transferred to foster care. Later, the investigators added a control group consisting of never institutionalized children. The researchers analyzed all the children at regular intervals until they reached 54 months of age. Altogether, the study gathered a significant sum of data on the effect of social deprivation on child development. The research also proved the benefits of foster care over institutionalization, and demonstrated how transitioning children to foster care carried the potential to correct the negative effects of institutionalization. The bulk of Dr. Vukov’s talk analyzed the arguments for and against the ethics behind the BEIP. The study technically followed all the written ethical guidelines in research. The study placed participants randomly into each group. Researchers obtained consent by contacting the birth parents for the foster care group, and Romanian officials also approved the project. Regarding the risks/benefits for the participants, the care as usual group faced no negative consequences from this research, while the foster care group potentially received improved care. The investigators also supported their usage of randomized control trials, arguing that this method gave the best results, and therefore helped to improve the future conditions of children to the most extent. Dr. Vukov then proceeded to explain the arguments against the BEIT, centering his analysis on the idea that the researchers did not respect the care as usual group’s “status as people”. The investigators did not follow Immanuel Kant’s idea of treating people as an end. Although the investigators possessed good intentions and provided beneficial research, they utilized the institutionalized children as a means to this goal. Second, the researchers did not follow the Golden rule: “Do unto others as you would have them do unto you”. Lastly, the researchers left the children in the care as usual group in a bad environment, when they potentially had the ability to improve their living conditions. Considering these ethical drawbacks, it appears that although this research followed ethical guidelines, it still violated other morals. Dr. Vukov argues that this reveals flaws in current research ethics, and that they require reworking to ensure that morality is fully enforced in research.

After close to two decades after the initiation of the BEIP, scholars continue to debate the ethics behind the project. Although no answer may ever materialize for this issue, it is clear that this research provided immense insight into child development. The article “IQ at Age 12 Following a History of Institutional Care: Findings From the Bucharest Early Intervention Project,” demonstrates how the project still produces important data into the late 2010s. In particular, this study analyzed the impact of foster care intervention when participants of the BEIP reached 12 years of age. Approximately 107 children participated, from which approximately half belonged to the care as usual group, and the other half were part of the foster care group. The researchers also included 72 never institutionalized 12 years olds in the study. The investigators found that the foster care group received a significantly higher IQ score compared to the care as usual group. The foster care group also got a significantly higher Verbal Comprehension IQ subscale score. Furthermore, the data indicated a negative correlation between the percent time spent in institutional care and IQ score of children at 12 years of age. The study showed a few surprising findings. For instance, the researchers wanted to see if the age of placement into foster care (ranging from 20-26 months) affected a child’s IQ at age 12. They found that placement age did not have a significant effect on IQ. In addition, some children in the foster care group did not remain with the same caregiver throughout their childhood. Yet, they still received similar IQ scores as children who remained in the same foster home. Furthermore, the researcher found that the never institutionalized children still scored significantly higher on the IQ test compared to the foster care group. This included significantly higher scores on the Working Memory, Perceptual Reasoning, Processing Speed, and Verbal Comprehension IQ subscales. This shows that although the foster care intervention did improve the cognitive and behavioral performance of children, these children still did not fully recover to match the performance of never institutionalized children. 

The study above directly demonstrates the long lasting impact of the BEIP. Even though the BEIP is ethically controversial, it produced, and continues to produce important data. Given the researchers’ unique opportunity to control for many extraneous variables, they provide concrete evidence against institutionalization as a form of child care. As highlighted by the impaired performance on the IQ test by institutionalized children, the social deprivation these children faced during childhood continues to hurt them into adolescence. In addition to this, the results point out that lots of work still needs to be done to improve child care. Although the children in foster care fared better compared to institutionalized children, their performance still fell short of never institutionalized children. This provides an incentive to increase the quality of foster care, to ensure children in this situation have a more enriching environment during crucial developmental years. 

Works Cited

Almas AN, Degnan KA, Nelson CA, Zeanah CH, Fox NA. IQ at age 12 following a history of institutional care: Findings from the Bucharest Early Intervention Project. Dev Psychol. 2016 Nov;52(11):1858-1866. doi: 10.1037/dev0000167. Epub 2016 Oct 6. PMID: 27709994; PMCID: PMC5083169. 

Zeanah CH, Koga SF, Simion B, Stanescu A, Tabacaru CL, Fox NA, Nelson CA; BEIP CORE GROUP. Ethical considerations in international research collaboration: The Bucharest early intervention project. Infant Ment Health J. 2006 Nov;27(6):559-576. doi: 10.1002/imhj.20107. PMID: 28640378. 

Deep Brain Stimulation for Treatment of Parkinson’s Disease: Benefits and Neuropsychological Outcomes

              Parkinson’s Disease is a life-debilitating motor-neuron disease that afflicts nearly sixty-thousand Americans [as of 2020]. It impedes everyday life and causes symptoms such as “brain freezes… muscle spasms and struggling to talk,” as shared by Bill Ragle, a finance professor at Cedarville University with Parkinson’s Disease (Johnson, Professor with Parkinson’s Disease Makes a Comeback). Currently, there are no cures for Parkinson’s Disease but current research involving deep brain stimulation has shown to help slow its onset. Bill Ragle is one of the new patients for this new technology. In treatment of Parkinson’s, Deep Brain Stimulation aids in reducing involuntary movements, prevents struggling with speech, and improves ability to walk. Although impressive, researchers are still investigating potential risks, such as neuropsychological effects. 

             In the research article “Neuropsychological outcomes from constant current deep brain stimulation for Parkinson’s Disease,” researchers compared neuropsychological effects of deep brain stimulation to electrode placement alone. One hundred-thirty-six patients with Parkinson’s Disease were evaluated after undergoing bilateral subthalamic device implant surgery. Patients were randomly assigned between three groups: 1. Stimulation immediately post-surgery 2. Stimulation beginning three months post-surgery 3. Control Group. Stimulation in this experiment defines the activation of the implantation devices. Three neuropsychological tests were given pre-surgery, three months post, and one-year post to assess the neurobehavioral safety of this treatment. Before surgery, all patients underwent an initial neuropsychological evaluation, no later than one week prior to the day of surgery. These initial evaluations were used as reference points to indicate that all patients did not have an already-existing cognitive impairment or depression before receiving the implants. The tests observed “overall level of cognitive function, attention and working memory, verbal fluency [tests], depression, and measures of intelligence… Wechsler Abbreviated Scale of Intelligence [WASI] and the Boston Naming Test were administered at baseline to facilitate dementia screening” (Troster, et al., Neuropsychological outcomes from constant current deep brain stimulation for Parkinson’s Disease). 

             Within-groups t-tests showed a degradation in verbal fluency; the experimental group also displayed increased levels of delayed story-recall. Despite this, overall statistical analyses of the data indicate that there is no significant difference between neuropsychological test scores, as compared to the baseline [score]. These research findings agreed with the already-existing research on this topic—that deep-brain stimulation does not negatively impact cognitive abilities. Although both groups showed depreciated verbal fluency skills, the experimental groups had a more sever effect. Such micro-cognitive impairments may be corrected with brain stimulation to other areas; further research is necessary. Additionally, further research is needed to investigate whether baseline neuropsychological-, patient-, and disease-related variables considered in tandem… [may be able to] predict the risk of overall cognitive decline” in patients (Troster, et al.). Both topics are worth-looking into, as these may be able to improve deep brain stimulation devices. 

            This experiment reveals the neurobehavioral safety of deep brain stimulation as a form of treatment in patients with Parkinson’s Disease. The constant, bilateral current had little overall impact in cognitive performance, with only slight [negative] changes in verbal fluency. This form of treatment is currently the best in treating Parkinson’s patients’ motor symptoms, as well as the best alleviator of Parkinson’s medication [long-term-use of levodopa] side effects, such as dyskinesia. This study also revealed the potential for decline in cognitive-performance, mainly verbal fluency but also memory, attention and executive functioning. These side effects may affect between twenty-five to fifty percent of patients with deep brain stimulating implantation devices. Regardless, the high-level of improvement in motor functioning and control in Parkinson’s patients leaves little worry about [potential] these micro-effects. These implantation devices to stop “involuntary movements, struggles with talking and walking,” as Bill Ragle has experienced, are very exciting in the ever-expanding Parkinson’s research field (Johnson). 

           This newly developing form of treatment allows doctors of neuromuscular disease patients to “control the shape, range, direction and position of electrical lead stimulation,” providing more precise care (Fortune Business Insights). Deep brain stimulation implantation devices are becoming a more desirable form of treatment, due to its personalized style, as well as its impressive success in alleviating symptoms, such as those experienced by people with Parkinson’s. This study’s findings were congruent with previous research on such devices and concluded that they do not pose cognitive impairments, though they may cause some cognitive slowing. The many potential uses of such devices leaves much room for excitation in the neuroscience field, indicating further studies should be conducted. 

                                                                   Works Consulted 

Insights, F. (2020, December 02). Deep Brain Stimulation Devices Market to Register an Excellent CAGR

            of 11.6% by 2026; Increasing Prevalence of Neurological Disorders to Accelerate Market

            Revenue, says Fortune Business Insights™. Retrieved December 9, 2020, from

            https://www.globenewswire.com/news-release/2020/12/02/2138065/0/en/Deep-Brain-Stimulation-

            Devices-Market-to-Register-an-Excellent-CAGR-of-11- 6-by-2026-Increasing-Prevalence-of-

            Neurological-Disorders-to-Accelerate-Market-Revenue-says-Fortune-Busine.html Johnson, T. (2020, December 8). 

Professor with Parkinson's Disease Makes a Comeback. Retrieved December 9, 2020, from

            https://spectrumnews1.com/oh/columbus/news/2020/11/30/professor-with-parkinson-s-disease-

            makes-a-comeback 

Troster, A. I., PhD, Jancovic, J., MD, Tagliati, M., MD, Peichel, D., BS, & Okun, M. S., MD. (2016,

            October 18). Neuropsychological Outcomes from Constant Current Deep Brain Stimulation for

            Parkinson's Disease. Retrieved December 9, 2020, from

            https://onlinelibrary.wiley.com/doi/10.1002/mds.26827