Crossing the Line: How our Brain Keeps Vision Seamless and Why Symmetry is Key.

 Most of us have never thought about the center line of our vision or actively seek it out. You look to your left, you look to your right, and even so the world manages to keep is balance and stay in one piece. In a recent article by MIT News, “How the brain splits up vision without you even noticing”, tells us why. As something moves across your view, the brain quietly passes the information from one hemisphere to the other so there isn’t a noticeable glitch or gap. For example, if runners are running a relay race and one passes the baton to the next runner up, and they match their speed so the baton is handed off cleanly and the race will continue without a hitch. This speaks to how perception works in everyday life, such as walking down a crowded sidewalk, during a sporting event, or even while doom scrolling through reels. 

In our Neuroscience seminar, our reading “The role of vertical mirror symmetry in visual shape detection” by Machilsen et al. (2009) talk about how the left and right side of our vision matching isn’t a design for aesthetic purposes but rather helps our brain find shapes in clutter. In the experiment from the reading, participants were asked to spot outline of shapes made from tiny line fragments with slightly turned little lines that made the outline so the shape was harder to see. Through the multiple conditions, shapes that were symmetric were much easier for the participants to decipher compares to chapes that were symmetric. This shows that symmetry acts as shortcut for when scenes aren’t clear or messy for our brains to outright decipher, so our brains use the other half that is clear or more recognizable to fill in the other half. 

But how do these ideas work together? The article by MIT explains how features slide across our vertical midline and the two hemispheres of our brain work together to keep it a continuous scene. Since vertical symmetry is connected by the midline, our brains are able compute that this half should mirror the other half. Symmetry pops because our brain is designed to create one big picture even with many moving pieces. This also confirms what Dr. Baker, our guest speaker, mentioned in his talk. Our vision is built up of many little pieces that work together to create the big picture. 

References: 
https://www.luc.edu/psychology/people/facultyandstaffdirectory/profiles/bakernicholas.shtml

David Orenstein  |  The Picower Institute for Learning and Memory. (n.d.). How the brain splits up vision without you even noticing. MIT News | Massachusetts Institute of Technology. https://news.mit.edu/2025/how-brain-splits-vision-without-you-even-noticing-0926

Machilsen, B., Pauwels, M., & Wagemans, J. (2009). The role of vertical mirror symmetry in visual shape detection. Journal of Vision, 9(12):11, 1–11, http://journalofvision.org/9/12/11/, doi:10.1167/9.12.11. 

Ultraprocessed Foods Linked to Early Symptoms of Parkinson’s

 In class, we had the opportunity of having Dr. Mary Makarious as one of our guest speakers to talk about a program where she takes participation in to have an explanation towards Parkinson’s. Some early symptoms to detect in suspicion of early Parkinson’s are shaking unexpectedly, unable to sleep, losing sense of smell, not being able to stand properly, slow movement, expressionless face, etc. Parkinson’s disease is a disorder centralized of the nervous system that affects movement which over time unfortunately only gets worse. In a more scientific explanation, the dopamine in your brain stops functioning as the cells stop making it.  Global Parkinson’s Genetics Program (GP2), is made from different researchers around the world that do different research to find a cause for Parkinson’s in a genetic aspect. They give us a broader look into how different populations from around the world come to face this disease differently. 

I have come across an article, “Ultraprocessed Foods Linked to Early Symptoms of Parkinsons’s” which center a recent study on the potential cause on how our food choices can have an impact on brain health. With studies, you are going to have successful and Non successful ones, and this one came out to not prove that foods can be cause of this disease but did help on giving us more insight towards food related to Parkinson’s. This involves refraining from consuming too much processed foods, as those who consume it most have been revealed to be at higher risk of developing symptoms than those who consume less. Not only does it affect Parkinson’s, but it can have other life-threatening health problems like cancer, diabetes, dementia, heart disease, etc. This research developed in China and the US and involved analyzing the diets of their participants over years to find that ultra processed food takes a big toll on neurological diseases.  

Although there is still a long way ahead to find a true cause and even a potential solution to this life-threatening disease, research like the one from Dr. Makarious and the one previously mentioned in the article, all contribute to an effort for answers. Many people living with this disease daily are fighting for their lives, and these researchers are putting in an effort to show that hope has not been lost. 

Reference:  

Callahan, Alic. Ultraprocessed Foods Linked to Early Symptoms of Parkinson’s. The New York Times (2025). https://www.nytimes.com/2025/05/07/well/eat/ultraprocessed-foods-linked-to-early-symptoms-of-parkinsons.html?smid=url-share 

Understanding the World of Silence

     In the beginning of the semester, Dr. Wei-Ming Yu presented the concepts of Hepsin- which is an important transmembrane serine protease, TMPRSS1, that is crucial for the proper functioning of the cochlea and tectorial membrane. To be better prepared for this presentation, we had to read the article "Critical role of hepsin/TMPRSS1 in hearing and tectorial membrane morphogenesis: Insights from transgenic mouse models" by Yang, Ting-Hua et al. This article first started by introducing that mutations in a type II membrane serine protease in family members are highly associated with a non-syndrome hearing loss although some of those mechanisms are still unclear to be understood.  

First and most importantly, Dr. Yu explained the different mechanisms of how sound is produced by vibrations that create particles in a surrounding medium such as air.  This in turn result in a wave of vibrations that travel through air to the eardrum. When sound enters the ear, a series of hair cells activate in which fluid waves bend hair cells called cilia inside the cochlea. Vibrations travel through the ear canal then press against the eardrum, causing it to oscillate, or move back and forth in a rhythm., The movement of fluid bends the cilia in the cochlea which converts mechanical energy into electrical signals that are processed as sound perception via the brain.

Dr. Yu explained in depth at the molecular level that the proper technique of the tectorial membrane is important for accurate the stimulation of these cilia. This reveals that hepsin/TMPRSS1 plays a key in how we hear sounds. In transgenic mouse models lacking hepsin, the tectorial membrane was abnormally shaped and detached from the hair cell leading to severe hearing impairment. This proved that hepsin is necessary for maintaining the correct composition and structure of the tectorial membrane through processing of some specific extracellular matrix proteins.

In the article “Noise Exposures Causing Hearing Loss Generate Proteotoxic Stress and Activate the Proteostasis Network” by Ramirez et al. describes how exposure to loud sounds damage to the inner ear and imbalances the cochlea. They experienced on rats by exposing them to different levels of sound: moderate, loud and very loud studying the biological effects of noise induced hearing loss. The results were that they found loud levels of sound causes protein in the cochlea to unfold and become damaged. 

Even though both articles are different from one another, they explain concepts at the molecular level of hearing loss providing evidence of how environmental and genetic factors produce sound. 

 

1.     Noise Exposures Causing Hearing Loss Generate Proteotoxic Stress and Activate the Proteostasis Network

Jongkamonwiwat, Nopporn et al. Cell Reports, Volume 33, Issue 8, 108431

2.     Yang, T. H., Hsu, Y. C., Yeh, P., Hung, C. J., Tsai, Y. F., Fang, M. C., Yen, A. C. C., Chen, L. F., Pan, J. Y., Wu, C. C., Liu, T. C., Chung, F. L., Yu, W. M., & Lin, S. W. (2024). Critical role of hepsin/TMPRSS1 in hearing and tectorial membrane morphogenesis: Insights from transgenic mouse models. Hearing research, 453, 109134. https://doi.org/10.1016/j.heares.2024.109134

Parkinson's Disease: The Umbrella of All

Parkinson's disease, also abbreviated to (PD),  is a neurodegenerative disorder that involves genetics and mutations found in a gene, which affects an individual's motor skills, balance, and nervous system, eventually leading to impairments of everyday life. PD is a disease that affects people from all over the world if they have at a concerning rate of increase in cases. There is a lot of research that is being done to try to find out what increases the likelihood of developing PD in the future, allowing people to get the care that they need from rehabilitation to medicine.   

Within the neuroscience seminar class, we had a guest speaker, Mary Makarious, who discussed the Global Parkinson’s Genetics Program that she works with. The point of this program is to collect data information from all over the world to understand PD on a whole new level. This is done by teaching institutions, medical locations, and many more how to look at genetic information from patients and volunteers and break down the data. In doing this, the data that is being collected is revealing specific key factors that lead to this complex disease. With the work that is being done, they have found that there are different key genes in different places that are specific to different groups of people, widely ranging across different demographics. This connects to the question of why there are so many different key gene variations that lead to the one disease, PD.  

In the article that I found, “α-Synuclein Deposition in Sympathetic Nerve Fibers in Genetic Forms of Parkinson's Disease”, which was published in 2021, goes on a deep dive into why there are so many different genes that are linked to PD. To learn this, they looked at a common denominator, which is α-synuclein, a protein that collects to form Lewy bodies within the brain and nerve cells, which happens in PD, to see how this interacts with the varying genes that lead to parkinsons. To create an experiment to show this, they colled skin biopsies samples from 65 participants; 30 of the participants with PD gene mutations, 19 participants that has no inherit gene or family that has had PD before them but yet still have PD, and lastly 16 participants who did not have PD or any signs of developing the disease. In these samples, it has the sympathetic nerves, which were then put through immunofluorescence microscopy to tag the α-synuclei and nerve fibers marked with tyrosine hydroxylase. Once calculated,d they were able to see how much the other overlapped using the colocalization index.  The results from this experiment showed that the participants who had the mutation gene SNCA, LRRK2, and GBA, and those who did not have a previous mutation, showed high amounts of α-synuclein that collected in the nerve fibers.  What was interesting was that the participants with PD with the mutation of PRKN had very small to practically no amount of α-synuclein. This then leads to the conclusion that the reason for this even happening is because PD is not just one specific disease, but instead it is an umbrella for all the different issues that happen within the body within the nerves and brain, leading to the symptoms that are known as PD. 

The research that took place for the articles really shows the importance of how research can further our understanding of PD. With the knowledge that is gained, it will allow people all over the world to get a proper diagnosis of the disease early on. Another important key to note is the fact that with continuing research on PD, we will be able to better create solutions, such as care and treatment for all of the different symptoms of PD. 

 

References: 

Tackling a Disease on a Global Scale, the Global Parkinson’s Genetics Program, GP2: A New Generation of Opportunities: The American Journal of Human Genetics, www.cell.com/ajhg/fulltext/S0002-9297(25)00284-8 . Accessed 11 Oct. 2025. 

 α-Synuclein Deposition in Sympathetic Nerve Fibers in Genetic Forms of Parkinson’s Disease. Movement Disorders, vol. 36, no. 10, 2021, pp. 2346–2357, https://doi.org/10.1002/mds.28667. Accessed 11 Oct. 2025.https://movementdisorders.onlinelibrary.wiley.com/doi/epdf/10.1002/mds.28667

Fighting Back: Silent Engrams and Alzheimer's Disease Research

Memory is a very widely known and recognized cognitive function. Despite this common knowledge of its existence, how memory actually works behind the scenes has been widely debated for decades. Dr. Stephanie Grella presented a talk at Loyola University Chicago about engrams, a theory gaining more traction in recent years that suggests the physicality of a memory in the brain. Something that particularly struck me was the discussion of silent engrams. Silent engrams are memories that are no longer retrievable by natural means (Josselyn & Tonegawa). Scientists have experimented with this concept by messing around with optogenetics and disrupting the normal consolidation process using protein inhibitors (commonly known to cause amnesia). They found that administering anisomycin, a protein inhibitor, would block the formation of memories. In this context, scientists were fear-conditioning mice and after administering anisomycin, mice would show little fear response. However, reactivating the associated neurons using optogenetics was sufficient to bring back the memory. 

This concept has been used in the study of Alzheimer's Disease (AD). AD is a neurodegenerative disease that mainly affects the elderly by slowly eating away at their brain. Studies have been surrounding this disease for years, desperate to find a cure or specific causes. Silent engrams have been used to study AD, with it being used as a possible explanation for the early stages of AD. Transgenic mice used for studying AD and expressed genes that were associated with the onset of the disease underwent an optogenetic treatment to reactivate an area of the brain associated with memory (Josselyn & Tonegawa). Miraculously, these mice essentially got their memories back. This has been compared to reports of humans in early-stage AD having enhanced memory retrieval if specific retrieval cues are used. This is a very promising step in figuring out how to combat AD, and with more research on engrams, perhaps a medicinal solution is not entirely out of reach.

Other research surrounding AD has also been undertaken. Another focus besides engrams is hippocampal neurogenesis and how to maximize it. Studies have shown that neurogenesis occurs into adulthood, however it is difficult to study specifically in humans. However, in rodents and primates, hippocampal neurogenesis tends to decrease with age, along with cognition (Lazarov et. al). Scientists have found that growing within an enriched environment and partaking in physical activity is able to retain these levels of neurogenesis from young mice to old mice. Despite this being somewhat difficult to fully apply to human subjects in a scientific setting, it shows promise in how we can potentially make certain lifestyle choices to avoid AD. In the future, more work surrounding this will hopefully allow us to bring a scientific backing for ways on how people can fight back against AD.

References:

Lazarov, O., Gupta, M., Kumar, P., Morrissey, Z., & Phan, T. (2024). Memory circuits in dementia: The engram, hippocampal neurogenesis and Alzheimer's disease. Progress in neurobiology, 236, 102601. https://doi.org/10.1016/j.pneurobio.2024.102601

Josselyn, S. A., & Tonegawa, S. (2020). Memory engrams: Recalling the past and imagining the future. Science (New York, N.Y.), 367(6473), eaaw4325. https://doi.org/10.1126/science.aaw4325

Hepsin-Induced Hearing Restorability and Schizophrenia

After hearing Dr. Wei-Meng Yu’s speech on hepsin, a protein that plays a huge role in normal auditory capabilities, I was tempted to continue researching neurological topics and disorders that could tie into the research results found by Dr. Yu and his colleagues. Dr. Yu and his colleagues discovered that injecting hepsin from humans restored some hearing in mice with a gene that knocked out hepsin activation causing hearing loss (Yu et al., 2024). They also discovered that injecting human hepsin into these partially deaf mice caused some reformation of the tectorial membrane, a structure in the ear that allows for hearing.  It made me wonder if the results found could be of any aid in auditory hallucinations and auditory prediction. In other words, I wonder if introduction of hepsin could help people with schizophrenia, given schizophrenics usually have some type of hearing loss. 

In the article published by Alice Saperstein, Shanique Meyler, and Alice Medalia, the frequency of hearing loss amongst schizophrenic patients was discussed. Through their research, it was determined that patients with schizophrenia had a higher hearing threshold compared to other research subjects of their same age and gender (Saperstein et al., 2022). A higher hearing threshold indicated that these schizophrenic patients needed a noise/sound to be higher in volume in order to be analyzed or at the very least detected. The average hearing threshold for those with schizophrenia was 17.48.3 dB while those with normal hearing had a lower threshold of 14.16.4dB (Saperstein et al., 2022). This difference in threshold allowed the researchers to label the hearing loss in schizophrenics as mild. 

Malformation of the tectorial membrane (TM) causes vibrations to not be converted into neural signals well enough and the loss of those signals causes hearing loss in general. Because the TM works with vibrations of sounds, it can directly be linked to the high hearing threshold that schizophrenic patients have. Based on the research results concluded by Dr. Yu and his colleagues, hepsin could help reform the tectorial membrane and help improve hearing loss. Therefore, if schizophrenic patients could have hepsin introduced into their system, it could potentially help reform the tectorial membrane. In this case, the vibrations would not have to be as loud for them to hear (due to their high hearing threshold) and they would be able to hear at a lower threshold. Doing so could help with the sound overstimulation in these patients' brains and potentially minimize the effect of auditory hallucinations because they wouldn’t need to hear loud things in order to actually hear. In a recent study, researcher Ghazavi and her colleagues determined that patients with schizophrenia were more sensitive to noises than others. Based on results, schizophrenics with auditory hallucinations were even more sensitive to higher noises than schizophrenics with no auditory hallucinations (Ghazavi et al., 2023). This emphasizes the idea that hepsin could potentially help schizophrenic patients with auditory hallucinations in minimizing the effect of their hallucinations. 

References

Ghazavi, Z., Davarinejad, O., Jasimi, F., Mohammadian, Y., & Sadeghi, K. (2023). Noise Sensitivity in patients with Schizophrenia. Noise and Health, 25(117). https://journals.lww.com/nohe/fulltext/2023/25170/noise_sensitivity_in_patients_with_schizophrenia.2.aspx

Saperstein, A., Meyler, S., & Medalia, A. (2022). Hearing Loss Among People with Schizophrenia: Implications for Clinical Practice. Psychiatry Online, 74(5). https://psychiatryonline.org/doi/full/10.1176/appi.ps.20220226

Yu, W.M., Yang, T.H., Hsu, Y.C., Yeh. P., Hung, C.J., Tsai, Y.F., Fang, M.C., Yen, A.C.C., Chen, L.F., Pan, J. Y., Wu, C.C., Liu, T.C., Chong, F.L., & Lin, S.W. (2024). Critical Role of Hepsin/TMPRSS1 in hearing and tectorial membrane morphogenesis: Insights from transgenic mouse models. Science Direct, 453. https://www.sciencedirect.com/science/article/abs/pii/S0378595524001874?via%3Dihub

From Memory to Medicine: The Power of Engrams in Understanding the Brain

     When I was taking PSYC 382, which is taught by Dr. Stephanie Grella, she lectured on memory engrams. I was deeply fascinated by her when she explained how a memory engram works and by her passion for this topic. Recently, Dr. Grella lectured on a much deeper level as to how memory engrams work. I now have the ability to write about a topic similar to memory engrams which has intrigued me for so long. An engram is a physical substrate (brain cells) that were changed when a memory was formed allowing that memory to be stored and retrieved when that memory is needed. Scientists only theorized if engrams even existed and now after years of research we are now not only able to study them but also able to use them to help people going through numerous diseases. 

Dr. Grella asked us to read “Memory engrams: Recalling the past and imagining the future” written by Sheena A. Josselyn and Susumu Tonegawa before her lecture where she taught us about engrams on a much deeper scale. Throughout this paper Sheena and Susumu explain how memories are physically stored and retrieved in the brain (an engram) by manipulating engram cells. Researchers used optogenetics and chemogenetics to control engram cells and to manipulate them. They used optogenetics by inserting a specific light activated protein into neurons when a mouse was actively forming a memory. After the mouse was moved to a different place light was shined on those specific neurons which made the mouse experience the same memory as when those specific light proteins were inserted. On the other hand, they were also able to turn memories off completely by silencing the neurons associated with a specific memory. This research article helped prove that engrams not only exist but then they can be manipulated. With this research, we may see in the near future ways to combat specific diseases such as PTSD, Dementia, Amnesia, and even addiction. 

In a study done by Christine A Denny et al. titled “From Engrams to Pathologies of the Brain” Denny et al.  talks about how understanding memory engrams can help us tackle brain disorders such as previously mentioned PTSD, Dementia, Amnesia, and even addiction. Denny et al. talks about research methods used to study engrams like optogenetics and chemogenetics mentioned earlier. What is also explained is how diseases affect engram formation. Two such diseases being Alzheimer’s disease (AD) and Depression. Denny et al. explains how in AD memories are not destroyed but rather they become silent engrams. Silent engrams are engrams that have weakened connections with other brain regions which leads to normal cues being unable to recall the memory needed. Denny et al. cites other studies that reactivated these lost memories in mice with AD. This goes to show that people with AD may have a chance to regain important memories that were once lost. Next, Denny et al. informs us on how depression focuses on how dysfunctional engrams in dopaminergic areas could contribute to these depressive symptoms. Specifically in the ventral tegmental area which is known for housing dopaminergic neurons has been shown to have a decreased rate of action potentials. Next, Optogenetics was used in mice with depression and activated neurons in the VTA. This reversed the depression-like symptoms in the mice. More research needs to be done, however engrams do seem to have potential as they could help with disorders of the brain. 

Overall, both of these articles have shown how far neuroscience and specifically research entailing engrams has gone. Engrams started off as a theory by Richard Sermon and now has been proven and could hold great potential for the future of treatment for neurological conditions. Josselyn and Tonegawa’s research shows how engrams can be identified and manipulated to turn on and off memories. Similarly, Denny et al. informs us on how we can use our knowledge on engrams to tackle complex neurological diseases. Together, these studies show that the future of engram research has a promising future for tackling disorders of the brain.  

References 

1. Josselyn, S. A., & Tonegawa, S. (2020). Memory engrams: Recalling the past and imagining the future. Science, 367(6473), eaaw4325. https://doi.org/10.1126/science.aaw4325

2. Denny, C. A., Kheirbek, M. A., Alba, E. L., Tanaka, K. F., Brachman, R. A., Laughman, K. B., Tomm, N. K., Turi, G. F., Losonczy, A., & Hen, R. (2017). From engrams to pathologies of the brain. Frontiers in Neural Circuits, 11, 23. https://doi.org/10.3389/fncir.2017.00023

Alzheimer's and the Possible Reconstruction of Engrams

In our Neuroscience Seminar this semester, we had the privilege of learning about the research that Dr. Stephanie Grella has been doing with Engrams, it focuses on how memories can change over a duration of time in positive and negative ways. Dr. Grella discusses the ways that memories are malleable, meaning they can be distorted or changed with time. She has been able to research this using mice and stress models, this tests their mental state while they are experiencing anxiety and can target the specific areas that are involved in Psychiatric related disorders. Dr. Grella emphasized her interest in Post Traumatic Stress disorder, or known as PTSD, putting the mice in different anxiety inducing environments can cause them to experience similar neuronal reactions to PTSD. The reason PTSD is an important Psychiatric disorder when it comes to studying Engrams is because memory updating can look different to those who suffer with PTSD.  

When describing what an Engram is it can be very complex, however, Dr. Grella referred to an article written by Dr. Sheena A. Johnson and Dr. Susumu Tonegawa, “Memory engrams: Recalling the past and imagining the future”. This article explains not only how an engram is defined, but all the research and scientists that led to the discovery of an engram. In the article an engram is defined as the storage and recollection of memories, an engram can be formed by persistent chemical or physical changes to neurons from an experience in an individual’s life. The recollection of the memory improves if specific cues from the experience are reactivated. Research has proven that synaptic strength and neuronal connection can effect the formation of memories, if these factors are enhanced, memory formation can be refined. The question of whether an engram can be rebuilt after being deconstructed is what sparked my interest in further learning about engrams, but specifically how it can correlate to the Neurodegenerative Alzheimer’s Disease.  

In an article written by Dr. Freddy Jeanneteau, “Stress and the risk of Alzheimer dementia: Can deconstructed engrams be rebuilt?” The topic of Alzheimer’s specifically interests me because it is a very common neurodegenerative disease and if researchers can discover how to reconstruct engrams, this could lead to an immense impact on the treatment or cure of Alzheimer's. Dr. Jeanneteau discusses how the neuronal connectivity is important for memories, he suggests that if a functional connectivity can be promoted then it could have the ability to replace the function of the lost one. The article explains that the more frequently an engram synapses, the stronger the memory functions and the easier it is for the memory to be recalled. Dr. Jeanneteau was able to research that the engram synapses that are closer to amyloid plaques, have shown less neuronal connectivity. This related to patients that suffer with Alzheimer’s Disease, they were shown to have a high number of silent neurons next to plaques, and an increased excitation to inhibition ratio. This provides beneficial information for the future of treating Alzheimer’s disease.  

Although Dr. Grella researches the Psychiatric disorder of PTSD and Dr. Jeanneteua researches Alzheimer’s Disease, they both are interested in engrams and how they can be effected. The research being done around engrams can further relate to many more neurodegenerative diseases and psychiatric disorders. This can lead to treatments and cures for certain disorders and diseases that are very prominent in today’s world, but they are difficult to research due to the complexity of understanding the neuroscience behind why these occur.  

 

References: 

Jeanneteau, Freddy. “Review for ‘stress and the risk of alzheimer dementia: Can deconstructed engrams be rebuilt?’” Stress and the Risk of Alzheimer Dementia: Can Deconstructed Engrams Be Rebuilt?, 25 Jan. 2023, https://doi.org/10.1111/jne.13235/v2/review1. 

Josselyn, Sheena A., and Susumu Tonegawa. “Memory engrams: Recalling the past and imagining the future.” Science, vol. 367, no. 6473, 3 Jan. 2020, https://doi.org/10.1126/science.aaw4325.