Cobbers on the Brain – Page 52 – Student Commentary on the Neurological Sciences

Pandemic Pregnancies and Autism

Posted on November 10, 2020 by / 0 Comment

Pregnancy during the time of a pandemic can turn a beautiful, life changing experience into a scary, life changing experience. Most women while pregnant experience paranoia and worries already about getting sick, but during a pandemic this fear most likely heightens immensely. It has been noted that infection during pregnancy can negatively effect the fetus, especially if the immunological response to the infection reaches the fetuses blood circulation supply. Some responses, such as certain antibodies, can be helpful to building the fetus’s immune system, but others, like cytokines, can harm the fetus’s development. Some studies have found that if the fetus is exposed during time of infection or if the mom has a fever in response to infection, there is a higher risk of autism diagnoses. So, the question remains, how will Covid-19 affect children whose mothers tested positive while pregnant?

What happens during infection?

Image showing the events leading up to cytokine storm and how cytokine storms can affect the body.

Over the past year, scientists have been trying to become more familiar with the novel Covid-19 pandemic that has struck all around the world. It seems to be a bit of a difficult task, although, due to the variety of symptoms and uniqueness of each case. It has been shown in case studies of patients with Covid-19 that those who present with existing conditions (hypertension, diabetes, obesity) have a higher risk of death or longer recovery period with longer lasting symptoms. Depending on the severity of symptoms and infection, patients can experience a multitude of aspects caused by the virus. This includes a vulnerable immune system, implications to the neural system, a correlation to the hyperandrogenic phenotype, or cytokine storms. Here we will focus on the cytokine storm aspect of Covid-19. Cytokines are pro-inflammatory molecules that are activated in response to infection. In normal amounts, cytokines can be extremely important in immune responses, but at too high of an amount, they can become dangerous to the health of the patient. An interesting aspect about cytokines is that specific ones, such as IL-6, are able to cross into the placental blood supply for the fetus causing adverse neurodevelopment problems.

Covid-19 and Autism

Diagram showing the similarities between Covid-19 immune responses and aspects that contribute autism.

With all of the immune responses caused by the Covid-19 virus, there are potentially complications that could be seen in the future with children whose mothers had Covid-19 during their pregnancy. A problem that could possibly be seen is a correlation in Covid-19 patients and those with autism. But, since autism spectrum disorder (ASD) is defined behaviorally, a correlation between Covid-19 during pregnancy and autism may not be determined for years when the children begin to develop social behaviors. Although, there are some similarities between Covid-19 and other viruses that have been seen to increase the risk of autism. Studies have shown that infections that have the ability to induce a cytokine storm, for example influenza, that occur during pregnancy correlate to a higher risk for autism. One study even showed that there were higher levels of cytokines in the amniotic fluid of women whose children develop autism. Noting this correlation raises the awareness that children born to mothers who had Covid-19 while pregnant and had increased cytokine levels may develop autism in their future. Scientists have already started case studies with moms who have tested positive while pregnant and their babies to hopefully have an understanding of what effects this virus has on fetuses. Even if the outcomes won’t come for years, the research will be extremely beneficial for moms and children effected.

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Be Wary of Gut Inflammation!

Posted on November 10, 2020 by / 0 Comment

Knock-knock brain, it’s your partner-in-crime, the “second brain of the body”, me, your gut! I have more inflammation for you, ready or not. Research has only seemed to have just started revealing how interconnected our brain and gut are to each other. Things that happen in your gut impact your brain and vice versa, so if I were to tell you that not taking care of your gut increases the risk of the development of a handful of disorders, would I have your attention? If you have kids, what about looking out for their chances for something called autism spectrum disorder, or ASD?

Taking a Closer Look at ASD

What’s the big deal with inflammation, anyways? It seems to be involved in more and more diseases/disorders as science progresses, but one that continues to stand out is ASD. This is due to the broad range of pathophysiology that all circles back to an ASD diagnosis. Although the main cause of ASD still remains largely unclear, there are still many contributions and/or possibilities that are currently being explored, including:

Neural connectivity
Impaired neural migration
Impaired synaptogenesis
Excitation-inhibition imbalance
Broken mirror theory
Impaired immunity and neuroinflammation
Epigenetics
Single gene mutations

There is good reason to believe that ASD originated from disruptions in more than one of these listed above and that one may very well cause another (or more) to become discombobulated. Instead of going through every point listed above, we will analyze just one of the ideas down below: inflammation, specifically originating from the GI.

GI + Inflammation = ASD?

Although there remains to be no scientific proof of gastrointestinal (GI) inflammation being the solo-contributor or major player of ASD development, there seems to be good reason for a relationship between the gut and brain to exist. Chronic or increased amounts of exposure to cytokines in the brain seem to lead to chronic inflammation and ultimately neuron damage and death. The popular term “leaky gut” may play a role in how inflammation even develops within the brain. The gut-blood barrier is very important inside of the body, which prevents things such as undigested food, toxins, and pathogens from crossing over from the GI tract into blood vessels that can then be carried anywhere within the body via the circulatory system.

Scary, right?!

This will trigger an immune response, and when these invaders reach specific places inside the both, like the brain, will cause an “alarm system” to go off and force cells inside the brain to start attacking the invaders. Changes in some of these protector cells in the brain can ultimately result in neuronal dysfunction, some of the same associations with the mechanisms of ASD.

Fig. 1

There is also an incredible overlap with kids who already have ASD that also suffer from GI issues. This in turn has also been reported to make their ASD symptoms worse. A study examined different groups of children, with one group having ASD and GI issues, and found that this group, compared to the rest, not only had increased levels of cytokines, but also different gut bacteria and increased levels zonulin. All groups with ASD individuals experienced decreased levels of a protein that regulates both neurodevelopment and the immune system.

An Optimistic Closing

As the science field continues to make strides towards opening new doors to answer questions about disorders such as ASD, there is bound to be something relating back to the GI tract. These discoveries will have the ability for early diagnosis/prevention as well as effective treatment options for patients and their family. So, until there is enough evidence, be mindful of your body by keeping your gut happy and healthy!

Health

ASD an Overview

Posted on November 9, 2020 by / 0 Comment

Autism spectrum disorder (ASD) is an umbrella term for a developmental disability that can cause significant social, communication, and behavioral challenges. These individuals typically aren’t distinguishable by appearance but rather exhibit different methods of learning, interaction, and behavior. ASD is described as a spectrum since individuals can exhibit a diverse range of behaviors that vary in severity. High functioning autistic individuals may not be distinguishable from others, they can pursue education, earn a salary, and live independently while low functioning individuals may be nonverbal and require assistance.

ASD is a complex condition with many underlying conditions that influence and contribute to the risk of development. Challenges in studying ASD arise from the complex pathophysiology of the condition which involves neural connectivity, neural migration, excitatory and inhibitory imbalances, increased synapses, lack of mirroring in neurons, neuroimmunity disturbances, epigenetics, and dysfunctional genes, all of which have complex signaling and cross-communication of their own. To keep this article brief, we will only examine a couple of these to observe how they may impact the development of ASD.

Let’s begin by exploring imbalances in Glutamate (primary excitatory neurotransmitter) and GABA (primary inhibitory neurotransmitter). The Excitatory/Inhibitory balance between glutamate and GABA is critical for the proper functioning of neuronal networks and brain functions. It has been found that there are disturbances in glutamatergic and GABA-ergic receptors within ASD patients leading to an Excitatory/Inhibitory imbalance. This results in excessive glutamatergic excitation which may lead to excitotoxicity and cell death, as well as activation of glial cells that stimulate neurotransmission. To summarize, an imbalance in these important chemicals within the brain can lead to overstimulation of the brain and cause damage to neurons which ultimately results in reduced or altered brain function.

Another pathology relates to synaptic pruning. In neurotypical brains, the initial overabundance of dendritic spine formation is selectively pruned to support brain maturation, and this is regulated through a complex process abbreviated as mTOR regulated autophagy. In autism, there is a reduction in developmental dendritic spine pruning resulting in an impairment in mTOR regulated autophagy. Put simply, as we develop from infancy, our neurons make connections with one another some of which (in a healthy brain) are removed to reduce overstimulation and strengthen/reinforce the important pathways. In autistic individuals, this removal of unnecessary neural connections is not performed leading to an overabundance of connections and decreased efficiency in brain processing and communication.

Mirror neurons have also been found to contribute to the development of ASD. In a healthy brain, the mirror neuron system works to help with learning observed actions and emotions, but in autistic brains, fMRI have shown cortical thinning of regions belonging to the mirror neuron system. This means ASD symptom severity can be correlated to the limited development of the mirror mechanism which may appear in behavioral differences between autistic individuals and others.

Though there are several other contributions we could examine, the final component we will explore is genetic mutations which negatively impact synaptic transmission and synaptic growth. Dysregulation in gene networks forming both the synaptic transmission supporting system and the synaptic growth rate are implicated in the development of ASD, but no specific single gene modulation is sufficient to cause ASD symptom formation. This means more research is needed to elucidate the specific gene-environment & gene-gene interactions giving rise to ASD symptoms. This describes that genes play a significant role in the regulation of neural communication and that issues with this are found in patients with ASD. It’s also understood that it isn’t the dysfunction of a single gene that leads to the development of ASD but rather likely the contributions and combinations of multiple genes and uncovering these genes has yet to be done.

This was a brief overview exploring the very basics of a couple factors out of many that contribute to the complexities of understanding ASD. There remains much research to be done on the subject and a cure has yet to be discovered. Understanding the complex pathophysiology of this condition could provide insight into the dysfunction of countless other conditions and yield future treatment strategies.

Sources

https://pubmed.ncbi.nlm.nih.gov/28499914/

https://www.cdc.gov/ncbddd/autism/facts.html#:~:text=Autism%20spectrum%20disorder%20(ASD)%20is,social%2C%20communication%20and%20behavioral%20challenges.

http://neurochemistry2020.pbworks.com/w/page/141966597/Advances%20in%20understanding%20the%20pathophysiology%20of%20autism%20spectrum%20disorders

Community/Disease

Broken Mirrors: Mirror Neurons and ASD Symptoms

Posted on November 8, 2020 by / 0 Comment

We learn by watching others. As we grow and develop, we learn how to speak, behave, and even think based on our observations of other humans. Much of this learning is dependent on a part of the brain known as the mirror neuron system. But what happens when the mirror breaks? Read on to find out how this system works and how its dysfunction may contribute to symptoms of ASD.

ASD on the Brain

Autism spectrum disorder (ASD) is diagnosed in roughly 1 in 68 children as of 2017. ASD is characterized by a triad of symptoms: 1. impaired social interaction, 2. language difficulties, and 3. stereotypical (repetitive) behavior.

Many theories have been raised to suggest what causes ASD in the brain. As of yet there is no definitive, accepted, all-encompassing theory. However, most prevalent modern theories boil down to four abnormalities on the neuronal (brain cell) level: synapse construction, impaired protein turnover, impaired regulation of protein expression, and structural modification. Let’s define those terms and take a look at how they’re implicated in ASD.

Synapse Construction

Synapses are the spaces between neurons. If one neuron sends a signal to another, the chemicals (known as neurotransmitters) that transmit the signal have to cross over the synapse between them.
In ASD, the brain has many more neurons than expected. Normally, the brain prunes (gets rid of) extra neurons that are not being used. This way the neurons aren’t wasting energy and resources that could instead be used to strengthen connections among neurons that often communicate with one another.
- With the elevated number of neurons in ASD, the connections are not as strong, and there is a lot of extra ‘noise’ from connections that are not necessarily needed.

Impaired Protein Turnover

Learning occurs due to a process known as long-term potentiation (LTP) in the brain that semi-permanently strengthens connections among neurons. In order for LTP to occur, expression (creation) of certain proteins needs to occur. Creation of these proteins is dependent on a signaling pathway known as the mTOR pathway.
- In ASD, there may be an impairment in the mTOR pathway, resulting in interruptions in LTP and learning.
- mTOR is also important in pruning neurons, so impairment in the pathway could impact synapse construction as well.

Impaired Regulation of Protein Expression

As explained above, correct levels of protein expression are essential for all of the brain’s functions. Protein expression is dependent on genes; DNA in genes is ‘read’ and transcribed to make proteins.
Epigenetics is the process of genes being modified by environmental factors. If genes are methylated, methyl molecule groups are added to them, and these block the gene from being read. Methylation is important so that genes coding for development stop being read and transcribed, but too much methylation can silence genes that should be being transcribed into proteins. Epigenetics have been proposed as a factor in causing ASD as environmental factors may impact development.
Hundreds of gene defects have been found to result in autism, but there is no one ‘autism gene’. Some impacted genes have been found to affect synaptic growth while others impact synaptic transmission (communication among neurons). The problem seems to involve the suppressors of these genes being incorrectly expressed.

Structural Modification

Altered synaptic activity due to reasons explained above may cause demands that physically change the synapse’s structure such as altered numbers of ion channel receptors (receptors that react to neurotransmitters to let electrically charged ions into and out of the cell).
Reelin is a gene that plays an important role in organizing the brain and making sure neurons are where they need to be during development. Mutations in the reelin gene have been implicated in ASD.

Phew; that was a (maybe not so) brief overview of neuronal differences that have been found in ASD. Causes of these abnormalities have been theorized, as mentioned in some of the bullet points: genetic and environmental causes have been theorized, as has inflammation. We’re going to look into a recent theory of what might be causing some of those above molecular changes and the symptoms of ASD: the mirror neuron system.

Mirror Neurons

So, what are mirror neurons? First of all, they’re normal neurons with specific functions. Many mirror neurons are located in the motor cortex of the brain, which involves motion, and fire when the body does a specific action. Others are in the somatosensory cortex, which involves pain and sensation, and are activated when touching something or experiencing pain. However, what makes mirror neurons special is that they don’t just activate when you move or feel pain; they also activate the exact same way when you observe another person moving or feeling pain. This ‘mirroring’ activation is important in learning and empathy.

The mirror neuron system has a wide variety of functions when working normally. It develops in infants before they have reached 12 months of age and begins to let them understand others’ actions. As the famous Hebbian theory of neuroscience states, “cells that fire together, wire together”. This means that cells that are activated simultaneously form connections. This is also known as associative learning as it results in the brain forming an association between the two objects or concepts (for example, a glass of water and the feeling of thirst). Language development, which is in some ways a form of associative learning, also involved this system.

Mirror neurons have also been implicated in intention understanding; the deductive understanding not just what a person is doing (drinking a glass of water) but why they are doing it (that person must be thirsty). Mirror neurons are often involved in emotions and empathy as they system allows us to understand and relate to fellow humans. Finally, the mirror neuron system is important in what is known as the theory of mind, being able to imagine what another person is thinking or feeling on a more nuanced level than simple intention understanding.

The ‘Broken Mirror’ in ASD

With that brief introduction, we can see that the mirror neuron system is quite important in many higher-order brain functions like language, learning, and empathy and that issues with the system could result in significant developmental problems. The “broken mirror” mirror neuron theory suggests that an issue in this system is the cause of ASD. The theory posits that problems with dendritic morphogenesis (the shape of a neuron’s dendritic spines, an area that forms the receiving end of the synapse) resulting from synapse-related causes mentioned above are a large factor contributing to ASD.

Evidence for this theory is found in the fact that the mirror neuron system doesn’t activate the same way in ASD as it does in the non-ASD brain. As mentioned above, the mirror neuron system typically activates in the exact same way when you complete an action and when you observe another person complete that same action. In individuals with ASD, the mirror neurons activate when they complete the action, but not to the same extent when observing another person do so. It’s not all-or-nothing; the system typically still activates, and some studies have found that there isn’t a significant difference since there is so much variability, but on average there is less activation in the ASD brain.

When we consider all the functions that the mirror neuron system is responsible for, it makes sense that abnormalities could be blamed for ASD symptoms including difficulty with language, self-identification, imitating others, and intention understanding. The theory remains far from conclusive and more research needs to be done to find the role that the mirror neuron system plays in ASD, but for now, it presents a compelling theory for what could be causing ASD symptoms: a broken mirror.

Disease/Health

The Importance of Autism Spectrum Disorder (ASD)-Friendly Healthcare

Posted on November 5, 2020 by / 0 Comment

What is Autism Spectrum Disorder (ASD)?

Autism Spectrum Disorder (ASD) is a developmental disorder that affects an estimated 18 million people worldwide. This disorder results in disruptions in social, cognitive, and behavioral functioning as individuals with this condition are more likely to have difficulties interacting with peers, communicating with others, and may experience repetitive or obsessive behaviors.

There are numerous molecular mechanisms that contribute to the development of many of the symptoms within ASD, including an excess of neurons and synapses within the brain. This surplus of synapses leads to overstimulation of the senses, resulting in greater sensitivity to light, noise, and tactile stimuli in many individuals with ASD.

Health Disparities in those with ASD

Individuals with Autism Spectrum Disorder, compared to adults without ASD are twice as likely to develop:

Diabetes
High Blood Pressure and Cardiovascular Diseases
Gastrointestinal Disorders
Psychological Disorders (e.g. Schizophrenia, Depression)
Neurodegenerative Disorders (e.g. Parkinson’s Disease)

On average, individuals with ASD have a life expectancy that ranges from 20 to 36 years shorter than those without the disorder. Additionally, the suicide rate of a person with ASD is 9 times greater than the general population.

Although having ASD indeed increases vulnerability to various health conditions due to physiological consequences of the disorder, many other factors contribute to the greater risk of comorbidity. A prominent factor is the degree to which ASD individuals have access to affordable health care as a result of socioeconomic status. Studies have shown that children with ASD have both greater healthcare costs and needs, yet they maintain poorer access to affordable healthcare than children without the disorder.

Additionally, both children and adults with ASD may be deterred from pursuing healthcare due to an extreme deficit in accommodations for patients with ASD in both inpatient and outpatient settings. As mentioned above, many of those with ASD experience an overstimulation of the senses as a result of excess neural connections. Since healthcare settings are filled with bright lights, countless noises and beeping sounds, and other intense sensory stimuli, ASD individuals may avoid essential services due to this overwhelming characteristic of the healthcare environment. This aspect demonstrates the need for the development of ASD-friendly healthcare initiatives that make the healthcare experience more individualized and comfortable for each patient with ASD.

ASD-Friendly Healthcare

Many of the following strategies have already been introduced in various healthcare settings across the nation, including Boston Medical Center in Massachusetts.

These strategies include:

increased access to and affordability of healthcare services that are geared towards ASD patients
education and training of healthcare personnel to increase awareness of how they can treat their patients with ASD with highest level of respect and compassion
individualized care plans, in which the patient with ASD fills out an autism support checklist (ASC) that collects patient preferences regarding preferred communication style, triggers, sensory sensitivities, and other considerations of the patient
providing ASD patients with information that will detail exactly what their healthcare appointment will entail in order to decrease anxiety before and during the appointment
specific rooms that have reduced fluorescent lighting and fewer noises
alternative communication methods (e.g. communication picture cards, whiteboards, tablets, etc.)
a “sensory toolbox” that the patient can use to increase level of comfort during the visit. In this toolbox there might be noise-cancelling headphones, sunglasses, fidget toys, communication cards, and other helpful objects.

Autism and Gynecology: A primary example for the need of ASD-friendly healthcare

Reproductive health procedures and examinations can be quite overwhelming and uncomfortable for any patient. This level of discomfort can be amplified in those with ASD, as overstimulation of the senses and a detrimental lack of accommodations accompany these appointments. This unfortunate reality contributes to many women with ASD avoiding these appointments, putting them at a much higher risk for countless genitourinary complications, including cervical cancer that would be detected via pap smears.

This area of medicine therefore demonstrates a large need for numerous strategies and accommodations to make gynecologic appointments more comfortable for patients with ASD. These strategies include:

thoroughly explain the procedure steps, how long the procedure may take, and how this procedure contributes to the maintain of their reproductive health
provide charts, pictures, and anatomical models that can further explain the procedure
reducing the amount of time the patient is undressed
ask/warn the patient before touching them
continue to ask them throughout the procedure if they are comfortable/feeling okay
come up with a word or sign that signals they need a break from the procedure

Looking Ahead

Individuals with ASD are at much greater risk for developing cardiovascular diseases, gastrointestinal disorders, and other conditions than those without ASD. However, they are often deterred from seeking out services that will reduce the risk of comorbidity due to the overwhelming and uncomfortable environment within healthcare settings. As awareness increases regarding the initiatives pursued by healthcare settings across the nation in the hopes of accommodating ASD patients, more inpatient and outpatient settings will hopefully adopt some of these same strategies.

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Decoding Autism Using Dogs

Posted on November 5, 2020 by / 0 Comment

Autism affects 1 in 68 people, according to the CDC’s autism monitoring network. Chances are that you probably know someone with Autism, and have seen its effects firsthand. Autism has been called a uniquely human disorder, as in it may be one of the only disorders that is solely found in humans. For me, this brought up the question: are there animals that have autism? And if not, then why is it just humans that we see the disorder in?

Scientists went looking for any animals that might display some of the behavioral characteristics that are typical of Autism Spectrum Disorder (ASD) individuals. The problem with this is, how do you know if you’ve found autism? Autism can unfortunately still be somewhat difficult to diagnose from a very young age, and so if we as humans have issues diagnosing it within ourselves, it could be even more difficult to actually pin down when observing an animal.

Researchers also specifically looked at several different species such as dogs, cats, and monkeys, which have more similarities with humans than some animals would. Although most of the animals they looked at had inconclusive symptoms, they did discover similarities in a breed of dog called Bull Terriers, which they found to display some of the (dog equivalent) behaviors that can be diagnosed as autism in humans. I say “dog equivalent” because some of the staple behaviors of ASD are very difficult to distinguish in animals that can’t talk, such as imparied social interaction and not being able to communicate properly, which in humans can manifest as an inability to formulate speech or something similar.

These Bull Terriers were found to avoid other people and dogs at a rate that was higher than most other breeds. Another common behavior found in autism is performing repetitive or ritualistic behaviors, and these dogs would also chase their tails for an abnormal amount of time. I know this sounds strange, as in, “so what, the dog is just chasing their tail, they do that”. But if you think about it, if you saw a dog that was chasing its tail for over twenty seconds, (count that out and imagine it if you need to) it stops being cute and playful and starts becoming a little worrisome. These dogs would also have outbursts of anger, another behavior found in autism. This is along with all of these behaviors being found in predominantly male Bull Terriers, which is how also the case with human ASD.

Now, behaviors by themselves don’t signify autism, so researchers needed some sort of biomarker that they could actually measure to see if physiology of these dogs also matched some of the physiological effects found in humans with ASD. Specifically, they looked at Neurotensin (NT) and Corticotropin-releasing hormone (CRH) levels in Bull Terriers, as they have been found to be elevated in humans with autism. What they found was that the results (levels) in dogs were similar to that of humans, which is an amazing piece of evidence that links up not just the behavioral aspect of autism with animals, but also potentially the physiological side of things too.

But why does it matter that some Bull Terriers might have the dog-equivalent of autism?

To be able to more effectively learn about, treat, and live with autism (or almost any disorder for that matter), scientists use animal models to be able to figure out things about how these disorders operate. Using animals as test subjects (for the advancement of science), we can further understand how autism might arise genetically, or how to treat its symptoms once it does come about. One of the main goals with treating autism is to try give the individual as normal of a life as they can live, and so using this breed of terrier to try figure that out could improve the lives of countless people with ASD (including the dogs too!). Knowledge is power in the world of science and medicine, so being able to aid with a disorder that has plagued so many would be a worthy achievement.

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Control What We Can Control

Posted on November 5, 2020 by / 0 Comment

Our world is often dealt with unfortunate diseases that are very harmful and untreatable. Alzheimer’s is a good example of one of those particular diseases. Alzheimer’s is the number one form of dementia and is a growing disease. Through extensive research and continuation of knowledge, scientist have still not been able to come up with a treatment. Although research is in process to find a cure, there are prevention steps one can take to help their odds from preventing the disease.

Prevention of Alzheimer’s disease is not an easy task and, for some it may be impossible to achieve. However, living a healthy lifestyle can always prove to be beneficial especially when it comes to Alzheimer’s. One area of a healthy lifestyle that should be focused on is their diet. As an American, I am constantly reminded of having a better diet because implications may take place if it is unhealthy. I am guilty of not really listening to those saying this. For much of America we do not realize this until it is too late. So how does a healthy diet relate to Alzheimer’s? In class we recently discussed the correlation between Type II Diabetes and Alzheimer disease. We know that a bad diet and obesity is a main risk factor for Diabetes. To no surprise, findings also indicate Diabetes is a risk factor for Alzheimer.

When one thinks of Type II Diabetes, obesity is often a term that comes to mind. Fat cells cause inflammation which is a problem that often occurs in the brain during Alzheimer’s. Inflammation of the brain can be caused by fat cells which brings us back to our diet. We also see insulin resistance as a pre cursor for Alzheimer’s which relates identically to Diabetes. While knowing these implications, the human population continues to have increasement in obesity problems.

Seeing how Alzheimer’s may relate to our diet, we continue to put most of our focus towards a vaccine. Unfortunately, there is not enough effort put towards the controllable. We know that a bad diet can cause Inflammation. Inflammation is present in Alzheimer’s and leads to Amyloid Beta (AB) plaque formation which is ultimately the wrong in Alzheimer’s. AB formation comes from a chain of events brought upon by insulin resistance and inflammation.

As you can see inflammation is not a good thing. Although it may be unknown whether a diet would have helpedcertain indiviuduals with the formation of their Alzheimer’s, it is safe to say that it would not hurt. The world needs to start focusing on what we can control. Yes, progress is being made towards medications but why not provide more education on a healthy living. We know the harm that bad nutrition and obesity plays into our lives. Knowing this information, we still struggle to change. As the human body, we all need to become better educated within these certain controllables and then perhaps we can put a halt to the devastating disease that Alzheimers is.

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An Unlikely Pairing between The brain and Body

Posted on November 4, 2020 by / 0 Comment

What are some unlikely pairings that you have come across in your life? One that comes to my mind right away are sour cream and onion chips. These are two things individually I cannot stand on their own, but together it’s brilliant. Or I think about my teammate who was an English and Math major. These two things just simply should not go together, common sense would tell us the brain cannot be good at both those things. More surprising than either of these to me, is the connection between type 2 diabetes and Alzheimer’s disease (AD). This is a pairing, on the surface, that also seems as if it could not be. Research suggests, however, a deep connection between the two conditions exist that impacts millions around the globe.

Insulin in The Brain

When you think insulin, the first thing that generally comes to mind is blood sugar. However, Insulin also plays a significant role in brain functioning. There are specialized receptors in the brain that insulin binds to that can regulate genes, help protect the brain, facilitate neuronal grow and survival, while also assisting in neuroplasticity. Knowing what insulin does in the brain, and that there is a deficiency in Type 2 diabetes, a picture that brings the two together begins to take shape. Not enough insulin, or an inability of Insulin to bind to its receptors, means major problems within the brain. The figure below gives a nice overview of the myriad of issues that can take place, and you can see the list above is by no means exhaustive. The signaling cascades within neurons are disrupted meaning neurons do not properly develop, and they can even die. Insulin signaling also contributes to the continuation of amyloid plaques and neurofibrillary tangles that are two classic markers of AD. Furthermore, cells that die off and do not function properly, contributes to some of the typical symptoms that are seen in AD. These include the memory difficulties and confusion occurring because of cell death and the build up of plaques and tangles.

If insulin is the problem, why not just give Insulin?

Some fascinating studies have been conducted examining Insulin as a treatment for AD. These studies have shown remarkable measures of cognitive improvement after administering either a nasal or IV dose of insulin. It makes sense that if there’s not enough insulin in both type 2 diabetes and AD, giving insulin could be an effective treatment. This turns out to be the case but there is a catch. Insulin can improve cognitive functioning in patients with AD, but also can do the same for healthy, neurotypical individuals. The symptom improvement is good news, but there is little evidence that it can stop the formation of the plaques and tangles, as well as ultimately cell death. With many having Type 2 diabetes already on Insulin, it can be very difficult for researchers to piece apart what cognitive improvements can be attributed to insulin as opposed to outside causes. Like many things with AD, the data remains unclear.

Bringing it Together

The relationship between AD and type 2 diabetes is very complex to say the least. However, in both diseases’ insulin seems to be a major player. Not enough insulin, and insulin resistance means problems for both the brain and body. This unlikely coupling is perhaps one of the most important looking ahead to how we can alleviate suffering around the globe.

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A Hope For The Future

Posted on November 4, 2020 by / 0 Comment

With the continued progression of science and technology, it is becoming evident that concussions are much more common than many had thought of. Although concussions have been around for a long time, society is much more aware of them in todays day in age. An example of this is with America’s National Football League. If you were to look back into the early 2000’s, the NFL safety precautions were little not nothing. Helmet equipment was a hard piece of plastic with foam cushion in the inside. Players could lower helmets and hit with their head. Fast forwarding to today’s game, helmets are made with advanced technology allowing separation and gel-based cushion to prevent concussions. Rules are in place to discipline players who hit with their head and designated employees are in place to identify signs of concussions. Although advancements have not taken away concussions, they have made it easier to identify one.

Being able to identify a concussion is important because certain procedures need to be put in place to not make the current concussion worse. As we continue to improve the identification, we continue to lack in the treatment. Over the years, researchers have not successfully been able to treat a concussion and its future impact as a traumatic brain injury (TBI). There are multiple targets of research at the moment and one specific drug gives a promising outlook.

A neuroprotective drug, P7C3-A20, has been a hot topic in the world of traumatic brain injury. This drug was recently used in mice models that simulated TBI in middle age humans. A concussive state was put upon the mice and one year later they were given this P7C3-A20 compound. After one month of administration of this drug showed immediate affects with cognitive function. They stopped administration of the drug for some mice and checked results four months later. It showed the same results giving hope that repairment might be taking place. They continued the experiment and eventually found out that this compound was stopping chronic neurodegeneration and even showed signs of cell repairment.

An interesting aspect of this study related to a class discussion on what is going wrong in the brain. When a traumatic brain injury event occurs, our brain undergoes a calcium influx and sequestration in the mitochondria. With administration of the P7C3-A20, it was shown that cells were being protected of this calcium influx. P7C3-A20 showed increasement of proliferation in the sub granular zone of the dentate gyrus. The drug also showed to protect and repair endothelial cells. All these positive outbreaks of the compound administered have provided researchers with hope. TBI has and continues to affect much of our population and leaves a gloomy feeling when there is truly nothing, we can do about it. Within the next few years, we can expect human based trials and, researchers are confident that we could perhaps have a solution to one of the world’s unsolved mysteries.

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Unexpected and At Fault? Insulin Resistance and Alzheimer’s

Posted on November 4, 2020 by / 0 Comment

So first, what exactly is a ganglioside? A ganglioside is a complex lipid that is found in the grey matter of a human brain. These lipids are found to play a major role in brain function, and development, as well as with ‘brain remodeling’ later in a persons life. Seeing as gangliosides are important for brain activity and retention of synaptic plasticity, it only makes sense that an improper regulation of them can cause problems, and it does.

Take for example, in the development of Alzheimer’s, and β amyloid plaques. If the ganglioside GM1 becomes clustered in a plasma membrane microdomain, it can undergo a conformational change and become a binding site for these Aβ oligomers, further promoting aggregation of AβO’s into synaptoxic Aβ plaques. While that is somewhat understood for the ganglioside GM1, an accelerated degradation of the ganglioside GM2 can actually reduce the binding of Aβ on GM1, and is capable of rescuing the cognitive decline caused by GM1 and the Aβ plaques.

Interestingly enough, an unexpected enemy may be at work relating to the modulation of these gangliosides. Diabetes is shown to accelerate the development of these plaques as well as promote the accumulation of the GM1 clusters themselves and in turn, Aβ aggregates. Additionally, there are thoughts that Aβ can be the catalyst behind insulin resistance via interference in the ganglioside metabolism. This interference can cause an increase in GM3 in the plasma membrane, which fits in with another finding that high GM3 results in insulin resistance as well.

For a link between ganglioside regulation and diabetes itself at the surface level, we need to look no further than a dinner plate. A healthy diet we already know is key to not develop diabetes in many people, however it is believed that ganglioside expression in tissues is affected by deficiencies in nutrients, or in foods that do not provide ganglioside synthesis components. For example, breast milk is a very rich source of sialic acid, which happens to be a building block to a major ganglioside in terms of brain development, GM3. Infants who are not breast fed, have a much lower ganglioside content in the frontal cortex of the brain than their breast fed counterparts.

In the end, there is a dualistic relationship between these diseases, and after further research, it is clear the co-morbidity is by no means unrelated. The same plaques that are the hallmark of Alzheimer’s disease have the capability to trigger insulin resistance through both the inhibition of the IR/S to mTOR pathways, as well as via activation of the TNF-alpha receptor which leads to inflammation. On the flip side, as stated above, insulin resistance and diabetes can accelerate the accumulation of GM1 clusters, and in turn the accelerated accumulation of Aβ oligomers into Aβ plaques. The connections between these two diseases are a connection I never had expected to see, and in the future, it’s intriguing to think about how two “unrelated” diseases may be “causes” of each other in the future.