Neurocognitive Disorders Neurodegenerative Disorders

Disparities in Access and Utilization of Neurological Health Care

You were just diagnosed with a neurological disorder, what’s next? Of course it depends on what disorder exactly, but more often than not these diagnoses are accompanied with a discussion about a prognosis, or long-term timeline of that disorder. Along with that, the healthcare professional will most likely detail a schedule of follow ups and possible treatment options to either treat the symptoms or ease a patient as best as they can into the end stage of the disorder. This aspect of healthcare is crucial  because when creating these timelines, medical professionals are trying to think of the best way to keep a person out of the emergency room and hospital. Ultimately, hoping to keep the person comfortable and not accruing too much debt in medical expenses. Unfortunately this goal is not often met throughout the entire population, as this part of healthcare is riddled with racial and socioeconomic inequalities. 

One large scale study of about 279,103 respondents, looked at three groups in terms of the disparities in access and utilization of neurological health care: Non-Hispanic white, Non-Hispanic black, and Hispanic people. The data showed that black participants were nearly 30% and Hispanic participants nearly 40% less likely to see an outpatient neurologist when compared to the whtie participants. Additionally, this study also found that Non-Hispanic black participants had the highest # of encounters for a neurological diagnosis in terms of Emergency department visits and Hospital inpatient discharges. Leading to an overall per capita cost of care of about 1,485$, which is almost triple the per capita cost for Non-Hispanic white and Hispanic participants. The study goes on to discuss how these racial/ethnic disparities are multifactorial. Two of which can be a distrust in the healthcare system or a low density of neurologists in necessary locations. For example, California has less than half the number of neurologists per 100,000 residents than Massachusetts, despite being more racially and ethnically diverse. (Saadi, 2017). 

The socioeconomic disparity is quite clear on what exactly causes it and it boils down to costs. This may seem like an obvious statement, and you would think that programs such as Medicaid (state/federal program which provides health coverage for low income individuals) and Medicare (federal program which provides health coverage to 65+ year olds or 65 and under individuals with a disability) exist so why is there much of a disparity? In the outpatient setting, practices are not forced to take patients who are on these health care coverage plans. According to MACPAC, about 71% of providers took Medicaid and 85% took Medicare. This is in comparison to about 90% of providers accepting private insurance (Masterson, 2019). Well, this shouldn’t really make that much of a difference, right? The percentage is not 0, so there has to be some provider relatively close to people who will take their insurance, right? One study showed that 1 in every 11 insured adults either delayed medical care or did not seek medical care in 2020 due to costs which include copays and travel (Ortaliza, 2022). This mindset of “someone will take care of this patient” is counterintuitive to what healthcare is supposed to be and continues to push away whole populations of people. 

In spite of the cause of the disparity in access and utilization of neurological healthcare, there should not be any reason for the healthcare system to fall into the same trap as other institutions which are too afraid to change and hide behind a veil of “where do we even begin”. I believe two major aspects that lend to such disparities discussed previously, is that the emergency room is 24/7 and cannot deny a patient any services. This is an issue, not only within the neurological side of medicine, but in all fields. Outpatient hours are not really conducive to people who also work a 9-5, nor are they inclined to accept medicaid. As the insurance side of this problem has been a battle for many years, the extended outpatient hours is a much more feasible goal. Some offices do have late night hours, but these offices are few and far between meaning if such an office is too far out of the way for a patient, they might feel more inclined to go to the emergency room. The main way I could see more practices including late night hours, would be to entice them with tax breaks or other benefits. 



Saadi, A., Himmelstein, D. U., Woolhandler, S., & Mejia, N. I. (2017). Racial disparities in neurologic health care access and utilization in the United States. Neurology, 88(24), 2268–2275. 

Masterson, L. (2019, January 28). Doctors less likely to accept Medicaid than other insurance. Healthcare Dive. 

Ortaliza, J., Fox, L. How does cost affect access to care? (2022, January 14). Peterson-KFF Health System Tracker.

Neurodegenerative Disorders

What is Multiple System Atrophy?

Multiple System Atrophy (MSA) is a progressive, neurodegenerative disorder characterized by the suspension of the standard function of the autonomic nervous system with a presentation of symptoms usually arising in the 50s or 60s of one’s adulthood (Mayo Clinic, 2020). The autonomic division of the nervous system regulates involuntary movements of an organism’s internal organs in response to environmental stimuli such as breathing patterns, heart rate, digestion, and metabolism (Kandola, 2020). An individual with MSA most commonly experiences frequent fluctuations in blood pressure, such as low blood pressure when one stands or sits up (orthostatic hypotension) or high blood pressure when lying down (supine hypertension) (2020). One may additionally experience a loss of urinary or bowel control, dysfunction in body temperature regulation due to reduced sweat production, and difficulty maintaining sexual function with a loss of libido (Mayo Clinic, 2020). 

MSA is divided into two categories: MSA-P, parkinsonian, and MSA-C, cerebellar (MedlinePlus, 2016). The most common form, MSA-P, is grouped by movement abnormalities such as rigid muscles, slow movement, trouble bending arms and legs, and difficulty keeping the body in a sustained, balanced position (2016). MSA-C is defined by cerebellar ataxia in which an individual faces complications with muscle coordination (2016). This may present as speech slurring, trouble focusing one’s eyes, or difficulty swallowing or chewing (Mayo Clinic, 2020). 

As of right now, there is no conclusive reasoning for why MSA occurs in the population; however, it is thought for the cause of the disorder to be a conglomerate of genetic and environmental elements (2020). By examining the brain and spinal cord of those who were impacted by MSA, researchers saw a significant shrinkage of the cerebellum, basal ganglia, and brainstem (Mayo Clinic, 2020). All three structures are crucial in their involvement for motor learning, balance, and coordination of body movements (Johns Hopkins Medicine, n.d.). Affected brain tissue has been revealed for neurons in the brain and spinal cord to be composed of an abnormal amount of alpha-synuclein protein, which form clumps, or inclusions, throughout the nervous system (n.d.). Accumulations of alpha-synuclein protein over nerve cells can block proper cell signaling, leading to a progressive loss of control in coordination and motor functions (n.d.). Studies suggest that variations in the SNCA gene, which encodes for the alpha-synuclein protein, have been associated with a greater risk of MSA (MedlinePlus, 2016). 

Unfortunately, no cure has been found for MSA. Although all individuals with MSA experience varying levels of the disorder throughout their years, the symptoms do not decrease in severity. The progression of the condition leads to a greater degree of difficulty in maintaining daily activities with further secondary complications (Mayo Clinic, 2020). 



Johns Hopkins Medicine. (n.d.). Brain anatomy and how the brain works.

Kandola, A. (2020, January 10). What is the autonomic nervous system? Medical News Today.

Mayo Clinic. (2020, May 21). Multiple system atrophy (MSA).

MedlinePlus. (2016, July 1). Multiple system atrophy. National Library of Medicine.

Neurocognitive Disorders Neurodegenerative Disorders

What is Mild Cognitive Impairment?

“I literally had my phone just a second ago…. Where could it have gone?” Most humans have this exact thought play out countless times with a various number of items throughout their lives. The act of forgetting is one thing all humans do, intentionally or unintentionally, and for the most part, it is a daily occurrence. People don’t often pay much attention to what they forget, because for the things they must remember, they try to put a special mental emphasis on it so that it won’t slip their minds. Still, there’s a section of the population, who no matter how much mental emphasis they place on remembering something, they just can’t. Depending on what exactly they cannot remember, those people may have mild cognitive impairment, MCI, and they may have to seek out professional help to assist them in handling the symptoms that impact their way of life (Mayo Clinic, 2020).  

Mild cognitive impairment, MCI, is classified as the “area between the expected cognitive decline of normal aging and a more serious decline of dementia” (2020). An important note is that people with MCI can stay in this intermediary zone and not progress to dementia (2020).  MCI is characterized by an abnormal increase in issues with memory, language, thinking or judgment and those with MCI are aware and conscious that they have some sort of decline (2020). There really are no other specific symptoms, other than a decline in the areas previously discussed. For individuals with MCI, there is a level of understandable anxiety that stems from this decline because when or if the decline will stop, can be uncertain  (2020).

The main difference between MCI and Alzheimers or other dementia-like disorders is that the decline does not progress to the point where the individual cannot carry out daily activities without additional help (Memory and Aging Center, 2022). People with MCI use written reminders and notes to help pick up the parts of their memory that are lacking (Memory and Aging Center, 2022). Additional help is seen as the need for home health aids or care providers to help someone function in their daily lives, which people with MCI do not need. 

While MCI is associated with aging and usually not extremely intrusive to functioning, it is necessary to seek the help from a medical professional when you or a loved one begin to exhibit some neurological decline. The reason being that there may be an underlying greater cause of MCI-like symptoms that can be more severe in nature if untreated. For example, some of these underlying causes are sleep apnea and a Vitamin B12 deficiency (Hamilton, 2022). For those who may be unfamiliar with sleep apnea, it is defined as the “repeated stop and start of breathing while sleeping” (Mayo Clinic, 2020). Sleep apnea can lead to a similar neurological decline in individuals with MCI.  Luckily, these causes when uncovered are easily treatable, with the use of Continuous positive airway pressure machines, CPAP, for sleep apnea or Vitamin B12 supplementation for the deficiency (Hamilton, 2022). However, another possible cause of MCI-like symptoms is Alzheimer’s disease. Alzherimer’s disease is classified as a “brain disease which causes a continuous decline in thinking, behavioral and social skills that affects a person’s ability to function independently” (Mayo Clinic, 2022). Around a third of the patients who are diagnosed with MCI, will be diagnosed with Alzheimer’s disease later on in life (Hamilton, 2022). One saving grace is that if caught early that someone’s MCI can be attributed to early stage Alzheimer’s disease, there are treatment plans that can try to delay the continued abnormal deterioration of that person’s memory and overall ability to be independent in caring for themselves (Hamilton 2022). 

The act of forgetting is something people of all ages do. The quality of one’s memory varies greatly from person to person, where not much attention is paid if one may have a slightly worse or better memory than another. Fortunately, many people with MCI can function and carry out their daily activities with a reliance on written reminders and notes, but it is important to see a medical professional if one believes they or their loved ones may have MCI. A couple of tests in a medical office will ensure that the MCI is not a symptom for a greater underlying cause. 



Clker-Free-Vector-Images. 2012. “Thinker Thinking Person – Free Vector Graphic on Pixabay.” April 11, 2012.

“Mild Cognitive Impairment – Symptoms and Causes.” 2020. Mayo Clinic. 2020.

“Mild Cognitive Impairment.” 2022. Memory and Aging Center. 2022.

Hamilton, Jon. “This Form of Memory Loss Is Common — but Most Americans Don’t Know about It.” 2022. March 18, 2022.

“Sleep Apnea – Symptoms and Causes.” 2020. Mayo Clinic. 2020.

“Alzheimer’s Disease – Symptoms and Causes.” 2022. Mayo Clinic. 2022.

Neurodegenerative Disorders

Neurodegenerative Disease of Unknown Source

Over the past year, a cluster of forty-eight cases of a distinct neurodegenerative disease arose in New Brunswick, Canada. The disease runs its course quickly, killing the individual in just a matter of months. In identified cases, there is an even split between women and men, and ages range from as old as 85 to as young as 18 (Murphy, 2021). Symptoms ranged from memory problems and muscle spasms to balance issues, vision deterioration, hallucinations, and extreme weight loss without any other underlying cause. Some individuals also experienced marked changes in behavior and pain in their limbs (Government of New Brunswick, 2021). 

Initially, this phenomenon was assumed to be Creutzfeldt-Jakob disease (CJD). Although CJD can be genetic in origin, some cases are iatrogenic, meaning the disease is transmitted surgically via direct contact with brain or nervous system tissue. It can also be contracted by eating meat from cattle infected by bovine spongiform encephalopathy (BSE), colloquially referred to as “mad cow disease”. Both CJD and BSE belong to a family of diseases called transmissible spongiform encephalopathies (TSEs), which are caused by misfolded proteins called prions. The word “spongiform” is used because the brains acquire numerous holes, taking on sponge-like appearances. CJD can present as symptoms of dizziness, loss of coordination, impaired memory and cognition, vision problems, and hallucinations, which is largely consistent with the New Brunswick cases (US Department of Health). 

To diagnose CJD or rule out any other diseases, physicians typically conduct spinal fluid tests, looking for specific polypeptide markers in the cerebrospinal fluid. However, upon examining spinal tap results, none of the New Brunswick cases had such proteins. Autopsies of the nine deceased individuals in the cluster also revealed no signs of CJD. Since this discovery, scientists have been searching for the source of the New Brunswick outbreak to no avail. Thus, the disease has been termed NBNSUC (New Brunswick Neurological Syndrome of Unknown Cause). 

Substantial evidence has now been accumulated for doctors to reach the consensus that this is a novel condition. While almost all the people studied in the cluster ate seafood like lobster, this is probably trivial and there is no evidence linking the symptoms to any particular food. Now scientists have directed their attention to neurotoxic environmental exposures, which they suspect are the culprit due to the geographical localization of the cases. Eight individuals reported that they may have been exposed to harmful algal blooms (Murphy, 2021). Blue-green algae, or cyanobacteria, are of particular concern, since they are known to produce four types of toxins,and neurotoxins are the rarest. When they do produce neurotoxins, it is often anatoxin-a, but all of them interfere with neuronal functioning at the synapse between nerve cells, causing symptoms like muscular paralysis (Hoff, 2007). However, there is no current evidence indicating the exposures in these cases elicited NBNSUC symptoms. 

Twenty-five individuals have also reported industrial exposures in their home or workplace, and twelve said they had possible indirect exposure to herbicides or pesticides. Interestingly, more than half of those surveyed said they regularly spent time gardening in the two years before the onset of their symptoms, and at least two people handled pesticides directly (Murphy, 2021). It would not be surprising if pesticides were to blame, as there is an abundance of literature supporting their neurotoxicity. Many pesticides are not highly selective, so in addition to targeting the nervous systems of organisms that pose a threat to crops, they can have unintentional effects on people. While insecticides target ion channels and have more of an acute, reversible toxicity, other pesticides have been associated with the development of chronic neurodegenerative disorders like Parkinson’s disease (Costa, 2007). However, since there is no concrete evidence to support this hypothesis either, for now, the root of this remains elusive (Government of New Brunswick, 2021).



Costa, L. G. (2008). Neurotoxicity of pesticides: A brief review. Frontiers in Bioscience, 13(13), 1240. 

Government of New Brunswick, C. (2021). New Brunswick cluster of neurological syndrome of unknown cause. Government of New Brunswick, Canada. 

Hoff, B., Thomson, G., & Graham, K. (2007). Neurotoxic cyanobacterium (blue-green alga) toxicosis in Ontario. The Canadian veterinary journal = La revue veterinaire canadienne. Retrieved from 

Murphy, J. (2021). Doctors investigate Mystery Brain Disease in Canada. BBC News. Retrieved from 

U.S. Department of Health and Human Services. (n.d.). Creutzfeldt-Jakob Disease Fact Sheet. National Institute of Neurological Disorders and Stroke. 

Neurocognitive Disorders Neurodegenerative Disorders Uncategorized

Neurogenesis: Remembering or Forgetting

Neurogenesis refers to the process of developing new nerve cells from multipotent neural stem cells, and it is essential during embryonic and infant brain development. While it also occurs throughout adulthood, it is restricted to specific parts of the brain as we age. These areas include the ventricular-subventricular zone (V-SVZ) and the subgranular zone (SGZ) of the dentate gyrus, a hippocampal structure important for episodic memory formation.  Episodic memories are long-term memories characterized by conscious recollection of past events and experiences.

As we learn from experiences throughout life, our brains are predominantly developing through the formation of new synaptic connections rather than increasing in number of neurons. In healthy brains, old connections are also pruned over time to ensure proper brain functioning if they are no longer necessary. However, the number of neurons becomes pertinent when we take neurodegenerative conditions such as Alzheimer’s and dementia into consideration, wherein abnormally configured beta amyloid proteins accumulate in the brain. This forms sticky plaques which are thought to contribute to brain atrophy by disrupting synaptic transmission, eventually eliciting cell death. In simpler terms, conditions that involve neuronal cell death highlight the importance of processes that increase the number of neuronal cells. Thus, studying adulthood neurogenesis in brain areas related to memory in order to see what promotes this proliferation may provide insight into how we can maximize brain and memory maintenance. 

Some studies done on mice suggest that exercise, and particularly aerobic exercise results in the incorporation of new neurons into hippocampal pathways. A molecule called brain derived neurotrophic factor, or BDNF, plays an integral role in this process. As exercise duration and intensity increase, so does BDNF concentration. Periodic moderate exercise over prolonged periods of time was determined to be optimal for increasing neurogenesis (Liu, 2018). 

Since exercise and neurogenesis appear to promote brain health, one would assume they protect against episodic memory deterioration as well. However, the opposite is true: neurogenesis also plays a key role in forgetting, and studies involving infantile amnesia showcase this interesting phenomenon. Contrary to Sigmund Freud’s reasoning that we have repressed early childhood memories because they are unacceptable or traumatic, one study posits that the formation of new neuronal cells during infancy is the reason why most of us can’t remember anything from that period of our lives. In the study, both adult and infant mice were trained and then tested to assess the maintenance of their memory. Under baseline conditions, the infants appeared to retain the memory of the training experience for a short time, but that memory was not maintained over a longer duration, as opposed to the adult mice which had no problems with their recall. However, when the adult mice were provided with exercise wheels, increased neurogenesis created weaker, shorter-lasting memories of the training experience (Ackers, 2014).

A group of infant mice were then treated with a drug called temozolomide (TMZ) which is known to prevent neurogenesis by preventing mitotic cell division. Surely enough, blocking neurogenesis in the infant mice resulted in stronger memories, essentially undermining infantile amnesia. Like humans, when mice are born they are unable to remember anything without such a treatment. However, there are similar rodent species that are precocial, meaning they are born more developed. Thus, for instance, when guinea pigs were tested, there was no difference between memory maintenance in adults and infants, as both groups had already completed most of their neurogenesis. Also as expected, exercise decreased their memory maintenance and induced infantile amnesia by promoting neurogenesis. This converging evidence therefore suggests that neurogenesis can also play a role in forgetting under certain conditions. The fact that neurogenesis may be involved in both remembering and forgetting processes may seem counterintuitive, but it does link neurogenesis to infantile amnesia, despite its long-standing association with memory promotion (Ackers, 2014).



Akers, K. G., Martinez-Canabal, A., Restivo, L., Yiu, A. P., De Cristofaro, A., Hsiang, H.-L. (L., et al. (2014). Hippocampal neurogenesis regulates forgetting during adulthood and infancy. Science, 344(6184), 598–602. doi:10.1126/science.1248903 

Josselyn, S. A., & Frankland, P. W. (2012). Infantile amnesia: A neurogenic hypothesis. Learning & Memory, 19(9), 423–433. doi:10.1101/lm.021311.110 

Liu, P. Z., & Nusslock, R. (2018). Exercise-mediated neurogenesis in the hippocampus via BDNF. Frontiers in Neuroscience, 12(7). doi:10.3389/fnins.2018.00052

Neurodegenerative Disorders

The Mediterranean Diet and Age-related Neurodegenerative Disease

The Mediterranean diet is often credited as the ideal model of healthy eating. Multiple studies have proven its effectiveness in preventing a wide array of maladies, including diabetes mellitus, obesity, hypertension, cardiovascular disease, and cognitive disease (Aridi, 2020). Until recently, there was little evidence suggesting that this diet  protects against neurodegenerative disease, but with advances in technology, preliminary research has indicated this may be the case (ScienceDaily, 2021). As we age, we become more susceptible to developing neurodegenerative disorders, which are progressive diseases that impede the functioning of the central nervous system. While they do have a strong genetic component, they are also known to be triggered by environmental factors, such as exposure to certain toxins or viruses (NCI Dictionary). Although many of these factors are out of our control, we are able to decide what we are consuming.

The Mediterranean diet first got attention in the mid-twentieth century when studies confirmed  a significantly decreased amount of cardiovascular disease among Greek and Italian populations as compared to the rest of the world. It is believed that this can be attributed to the variety of fresh plant-based foods they consume, with most meals consisting primarily of vegetables, legumes, and whole grains. Processed foods with synthetic trans fats are substituted for lean meat and olive oil, which contains healthier unsaturated fats. Fish is often consumed as a good source of omega-3-fatty acids and is eaten in place of red meat.  Fresh fruit is also eaten as a substitute for desserts that are high in sugar and fat (Mayo Foundation, 2021).

Inhabitants of the small Greek island of Ikaria adhere the most strictly to this diet, except they eat significantly less meat and fish, replacing them with more vegetables which contain many more antioxidants. Such areas of the world where life expectancy is strikingly higher than in others are referred to as “blue zones,” and Ikaria certainly meets the qualifications, with people living eight to ten years longer than the average American. While the strong social culture of the island and the general active lifestyle there contributes to the overall health of the inhabitants, there is reason to believe their diets also play a key role. In addition to eating healthy, Ikarians drink herbal tea daily, which they make using freshly grown herbs. While they are also excellent sources of antioxidants, they are mild diuretics as well, working to lower blood pressure. This is actually directly related to neurodegenerative disease. According to Johns Hopkins research published in the Journal Neurology, the regular use of diuretics decreased the risk of Alzheimer’s by seventy-five percent, partially accounting for the fact that Ikarians over 85 have less than 10 percent chance of developing Alzheimer’s (Kotifani, 2020).

In Alzheimers and dementia, there is an accumulation of beta amyloid protein in the brain, forming clumps and causing neuronal cell death. The brain will also shrink in volume in a process called atrophy, thus manifesting as symptoms of memory loss, confusion, and disorientation. The German Center for Neurodegenerative Diseases has conducted studies following individuals’ diets over time and investigating the link between Mediterranean-like diets and protection against these physical changes in the brain in some healthy individuals and others that were identified as having a higher risk for these diseases. Magnetic resonance imaging was used to assess differences in brain volume and neuropsychological tests assessed the subjects’ memory and general cognitive abilities. Biomarker levels for beta-amyloid proteins in the cerebrospinal fluid of subjects were also measured. Subjects that more strictly adhered to the Mediterranean diet had consistently less beta-amyloid plaque deposits and performed better on memory tests. Their brains also showed less signs of atrophy and greater brain volume in the hippocampus, a brain structure essential to learning and memory. However, the underlying biological mechanisms at play are still poorly understood and are the focus of new research and longitudinal studies (ScienceDaily, 2021).

One factor contributing to the exceptionally low incidence of neurodegenerative disease in Ikaria and the results observed in atrophy studies is that consuming fresh foods means there are no neurotoxins. The US Food and Drug Administration permits the use of around 3,000 food additives, including some known neurotoxins like aspartame, diacetyl, monosodium glutamate (MSG), and aluminum. These target the central nervous system to reduce neuron functioning and elicit premature cell death. They are associated with a plethora of conditions, ranging from dementia and Alzheimers to anxiety, depression, headaches, and brain fog. Opting for fresh vegetables as opposed to processed food provides natural protection against these issues. However, mercury is a naturally-occurring neurotoxin that’s found in fish, which may contribute to why Ikarians, who avoid consuming too much of it, live even longer and have an even lower incidence of dementia and alzheimers than their other mediterranean counterparts (Alban).

Today, it is important to be aware of the dangers of consuming diets rich in processed foods, especially in the United States where this practice has grown to be so commonplace.  Unfortunately, the health and safety of consumers often takes a backseat to the monetary gain of large companies that have put a price-tag on the public’s health.  As more studies are conducted on the link between the Mediterranean diet and protection against neurodegenerative disease, it is advisable to steer clear of packaged foods with flashy labels, as they are designed by marketers to distract from the preservatives and high fat and sugar content. While it may seem difficult to live like Ikarians and consume what we perceive to be strict diets, they think their habits are just the norm. Thus, Americans should aim to emulate this lifestyle to thereby limit our risk of neurodegenerative disease to the extent that we can.  



Alban, P. (n.d.). 5 neurotoxins found in popular foods. Be Brain Fit. 

Aridi, Y. S., Walker, J. L., Roura, E., & Wright, O. R. L. (2020, April 28). Adherence to the Mediterranean diet and chronic disease in Australia: National Nutrition and    physical activity survey analysis. Nutrients. 

Kotifani, A. (2020, June 3). A Greek island’s ancient secret to avoiding Alzheimer’s. Blue Zones. 

Mayo Foundation for Medical Education and Research. (2021, July 23). Mediterranean diet for heart health. Mayo Clinic. 

NCI Dictionary of Cancer terms. National Cancer Institute. (n.d.)., 

ScienceDaily. (2021, May 6). Alzheimer’s study: A Mediterranean diet might protect against memory loss and dementia. ScienceDaily. from

Neurodegenerative Disorders

Biological Underpinnings of Multiple Sclerosis and Conditions with Similar Presentations

Multiple sclerosis (MS) is a chronic demyelination disease, or an ongoing condition that causes damage to the myelin sheath of nerve cells in the brain and spinal cord.  Myelin coating is important for conducting signals in the form of action potentials and is thus essential to executing many of our basic bodily functions.  

In order for a neuron to fire an action potential, it must first detect an electrical signal that is strong enough.  If this received signal is above the threshold voltage, the action potential will be initiated and channels in a patch of the neuron’s axon will open in response.  The change in channel configuration allows positively charged sodium ions into the nerve cell for a brief period of time in a process known as depolarization.  This makes the inside of the cell very positive compared to the outside.  After that, a section of the membrane will become re-polarized as positive potassium ions leave the cell through channels.  As time progresses, this process of increasing and decreasing charge continues to occur down the length of the cell’s axon without losing its strength. The rate at which these action potentials travel is called conduction velocity.

The presence of myelin is the reason why we can have such thin nerve cells and still rapidly transmit signals.  Normally, the larger the diameter of our neurons, the higher the conduction velocity, or the faster the signal travels. However, myelin increases conduction velocity and causes a change in the way action potentials propagate. The myelin sheath doesn’t cover the entirety of the axon, but rather is broken up at points called nodes where the ion channels are concentrated.  Thus, the action potentials travel quickly through the myelinated internodes, essentially jumping from node to node in a process known as saltatory conduction. When there has been demyelination, the action potential has no issue traveling from a demyelinated section to a myelinated one, but it will have difficulty reaching the section that’s demyelinated, causing many complications.

In MS, the central nervous system (the brain and spinal cord) is specifically targeted.  Rather than impacting the myelin itself, the immune system destroys cells called oligodendrocytes which are responsible for synthesizing the myelin.  Thus, once they are destroyed by inflammation, symptoms begin to manifest.  Individuals may experience a loss of energy, vision, and motor control, and the severity is subject to fluctuation over time through periods of remission and relapse (Multiple Sclerosis…).  

When someone experiences MS-like symptoms and goes through remission in the absence of subsequent flare-ups, it is simply referred to as Clinically Isolated Syndrome (CIS).  As the name suggests, these are single isolated episodes, typically characterized by neurological symptoms that persist over 24 hours.  These may evolve into full-fledged MS down the line, but this is not guaranteed (Clinically Isolated…).  Acute Disseminated Encephalomyelitis (ADEM) is very similar in this sense, but it is most common in children after the onset of severe viral or bacterial infection whereas CIS is not usually associated with fever or infection (Moawad, 2019).

However, these are not the only conditions that involve demyelination.  For instance, Neuromyelitis Optica Spectrum Disorder (NMOSD) involves other cells called astrocytes which support the neuron and provide the lipids necessary to make myelin.  Despite the distinct pathology, myelin production is also being hampered in this case, thus producing effects that resemble the response to oligodendrocyte destruction.  Even deficiency in vitamin B12 can mimic the signs of MS, causing fatigue and numbness in the limbs due to its role in the breakdown of fatty acids which is necessary to get these lipid building blocks (Orenstein).

From a purely scientific standpoint, these diseases can be fascinating, as they showcase the complexity of myelin production and its integral role in basic physiological functioning.  However, the nuances of each of these conditions and the devastating impacts they have is heartbreaking when applied to real people and situations.  Trying to get a clear diagnosis and to understand what’s happening in one’s own body can be an unnerving experience.  Thus, to combat the added stress and confusion, it is imperative that there is dialogue about the biological underpinnings of demyelinating diseases so that the general public is informed about the symptoms to look out for.


Clinically isolated syndrome (CIS). National Multiple Sclerosis Society. (n.d.). Retrieved from 

Heidi Moawad, M. D. (2019, December 1). Adem can cause temporary weakness or paralysis. Verywell Health. Retrieved October 10, 2021, from 

MediLexicon International. (n.d.). Multiple sclerosis (MS): Types, symptoms, and causes. Medical News Today. Retrieved October 10, 2021, from 

MS and MOG antibody disease. Cleveland Clinic. (n.d.). Retrieved October 10, 2021, from 

Orenstein, B. W., Gleason, T., Dunleavy, B. P., Bostick, M., & Sen, M. (n.d.). 16 conditions commonly mistaken for multiple sclerosis: Everyday Health. Retrieved October 10, 2021, from

Neurodegenerative Disorders

Racial Disparities Seen in Prevalence of Alzheimer’s Disease

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by compromised memory, thinking, and behavioral patterns. It is believed that Alzheimer’s is a result of aggregations of beta-amyloid protein fragments between neurons as well as neurofibrillary tangles inside neurons that result from accumulations of tau protein. These protein accumulations grow to effectively disrupt communication and signaling between neurons (“What happens to the brain in Alzheimer’s disease?,” 2017). The nature of these biological markers surrounding Alzheimer’s often leads to symptoms of cognitive impairment to appear much later in one’s life than the true start of the disease. Current research still cannot explain what conclusively causes these harmful protein aggregations; however, the biggest risk for Alzheimer’s has been linked to aging.

While the discussion surrounding this disease has generally been restricted to genetic and biological associations, recent data suggests communities of color are disproportionately impacted in the risk of developing and obtaining a diagnosis for Alzheimer’s. Compared to white individuals, African Americans are twice more likely to develop Alzheimer’s, and Hispanics are one and one-half times more likely to have Alzheimer’s (Alzheimer’s Association, 2020). Despite the higher prevalence rate of Alzheimer’s, these respective groups are still less likely to be given a timely diagnosis in earlier stages which inevitably restricts potential treatment options contingent on early intervention. It is reported for the age of initial symptoms to be, on average, 6.8 years earlier in Hispanic individuals than the average age of initial symptoms in white individuals (Alzheimer’s Prevention Initiative, 2012). With an earlier onset of initial symptoms and a delayed awareness of the proper diagnosis, one can see how the gap of accessing correct treatment may worsen the prognosis of the Alzheimer’s condition. The racial and ethnic disparities that are seen in Alzheimer’s data may suggest how socioeconomic factors play into the development of this disease in certain groups.

Socioeconomic factors have been linked to neurocognitive disorders and cognitive function as individuals with more access to educational and occupational resources are more likely to have normal cognitive function throughout adulthood. It is typically seen that higher educational resources are quite beneficial for memory-based function in elders which ties back to the prevalence of Alzheimer’s disease between different groups of varying socioeconomic backgrounds (Racial and Ethnic Disparities in Alzheimer’s Disease: A Literature Review, 2014). Research conducted by Amy Kind, a physician-scientist in the Division of Geriatrics and Gerontology of the University of Wisconsin, focused on analyzing the prevalence of Alzheimer’s biomarkers and baseline cognition in terms of a socioeconomic context. Kind pooled her cohort of participants, late-to-middle-aged adults with a parental history of Alzheimer’s, from the Wisconsin Registry for Alzheimer’s Prevention (WRAP) study. Through the American Community Survey and Census data, neighborhood and socioeconomic quantifications were created to compile a metric, Area Deprivation Index (ADI) which accounts for poverty, education, housing, and employment indicators to predict health-disparity related outcomes (Kind et al., 2017, p.195). All participants were thereby ranked into deciles of neighborhood disadvantage using ADI and measured for their baseline cognitive function and levels of Aβ42 and P­tau181 in their cerebrospinal fluid. Results had shown those living in more disadvantaged neighborhoods were associated with a lower baseline of cognitive outcome and function in areas of memory and speed despite being controlled for age and education. Although Aβ42 levels did not vary considerably within the different neighborhood deciles, it was noted that those in the most disadvantaged neighborhoods measured disproportionately higher levels of phosphorylated tau in their cerebrospinal fluid with an average of 11.61 P-tau units higher than those in the lesser disadvantaged neighborhoods (Kind et al., 2017, p.196). With these observed differences in biomarker levels and cognitive performance, one may say that socioeconomic and neighborhood disadvantage may be correlated to a higher risk of developing Alzheimer’s.

For the majority of Alzheimer’s research, there has been a dominant bias of acquiring information and data from largely white participants which unfortunately has created a lack of understanding of how this disease can first appear or develop in different groups of people. A 2019 study conducted by John C. Morris, a neurologist and professor at Washington University in St. Louis, measured the differences in Alzheimer’s disease manifestations in African American and white individuals. 1,255 participants of ages 43 or more, based in the St. Louis area, volunteered in studies conducted at Knight Alzheimer Disease Research Center. This cohort aimed to be a representative sample proportional to the different backgrounds within St. Louis. Biological data was extracted from the participants through different testing such as PET scans, MRI scans, or spinal taps to detect and measure amyloid protein buildup, levels of Alzheimer’s biomarkers, and signs of brain shrinkage or damage (Bhandari, 2019). Although PET and MRI scans did not show significant differences between African American and white individuals, it has been seen African Americans who exhibited mild to very mild signs of Alzheimer’s measured lower than threshold levels of expected tau. As stated previously, tau protein accumulations inside neurons create disruptions in how neurons communicate. Larger tau levels signify a greater likelihood of cognitive decline. Therefore, normal and high levels of tau may have been previously misrepresented and could have caused misdiagnoses in African Americans (Bhandari, 2019).

Socioeconomic and racial inequalities continue to create disparities in the prevalence of diseases such as Alzheimer’s. In future research, hopefully, such neurodegenerative disorders can be analyzed carefully into both biological and social factors to create a more health-equitable future.



Alzheimer’s Association. (2020, March). Race, Ethnicity, and Alzheimer’s. Alzheimer’s Disease & Dementia Help.

Alzheimer’s Prevention Initiative. (2012). Alzheimer’s Disease Facts and Figures. Alzheimer’s Prevention Registry.

Bhandari, T. (2019, January 21). Racial differences in Alzheimer’s disease unveiled. Washington University School of Medicine in St. Louis.

Kind, A. J., Bendlin, B. B., Kim, A. J., Koscik, R. L., Buckingham, W. R., Gleason, C. E., Blennow, K., Zetterberg, H., Carlsson, C. M., & Johnson, S. C. (2017). Neighborhood socioeconomic contextual disadvantage, baseline cognition and Alzheimer’s disease BIOMARKERS in the Wisconsin registry for Alzheimer’s prevention (Wrap) study. Alzheimer’s & Dementia, 13(75), 195-196.

Racial and Ethnic Disparities in Alzheimer’s Disease: A Literature Review. (2014, January 31). Racial and ethnic disparities in Alzheimer’s disease: A literature review. ASPE.

What happens to the brain in Alzheimer’s disease? (2017, May 16). National Institute on Aging.

Neurocognitive Disorders Neurodegenerative Disorders

What is Parkinson’s Disorder?

Parkinson’s disorder is a neurodegenerative disorder that primarily affects movement. However, this neurodegenerative disorder is rare in young adults, and normally appears in adults aged 60 or older. Symptoms of Parkinson’s disorder often occur gradually, and different symptoms may appear in different people. Regardless, these symptoms progressively worsen overtime. Symptoms of Parkinson’s disorder may include tremors that usually occur or begin in the limb area or fingers and hands, slowed movement, also called bradykinesia, rigid or stiff muscles, impaired posture and balance, loss of automatic or unconscious movements, changes in speech, and difficulty writing. Early signs and symptoms of Parkinson’s disorder may go unnoticed since they can be mild to detect, and symptoms usually begin on one side of the body and continue to worsen on that side, even after symptoms begin to affect both sides (Parkinson’s disease – Symptoms and causes). 

Typically, Parkinson’s disorder occurs in stages ranging from one to five. Stage one consists of mild symptoms that do not interfere with daily activities as much, and these include tremors or other movement symptoms that typically occur on one side of the body. Additionally, stage one consists of changes in posture, facial expressions, and walking that are often mild. Stage two consists of worsened tremors, rigidity in muscles, and movement symptoms that affect both sides of the body. During stage two, daily tasks start to become more difficult to perform and take longer to do so. Stage three consists of a loss of balance, bradykinesia, and an increase in falls. Throughout stage three, the individual can still live independently and perform tasks independently. However, symptoms tend to make daily tasks such as dressing and eating a bit more difficult. Stage four consists of limiting and severe symptoms to an extent where the individual may require a walker, and the individual needs assistance with daily activities of living, so the individual cannot live independently. Lastly, stage five consists of stiffness in the legs that make it impossible to stand or walk, hallucinations or delusions, and the individual may be bedridden or require a wheelchair. Stage five normally requires consistent nursing care (Treatment).

Parkinson’s disorder is caused by the gradual breakdown or death of neurons, which are known to produce a chemical neurotransmitter called dopamine. This decrease in dopamine levels results in abnormal brain activity that leads to impaired movement as well as the non-motor symptoms of Parkinson’s disorder (Parkinson’s disease – Symptoms and causes). The specific neurons that are lost are called dopaminergic neurons (Tysnes and Storstein, 2017). Although the exact cause of this loss in neurons is unknown, there are many factors that seem to play a role in their loss, including genetic mutations, exposure to environmental toxins, the presence of lewy bodies, and alpha-synuclein found in lewy bodies (Parkinson’s disease – Symptoms and causes). Researchers believe that clumps called lewy bodies, especially those filled with the protein alpha synuclein, are markers of Parksinson’s disorder (Tysnes and Storstein, 2017)

The cure for Parkinson’s disorder is unfortunately unknown. Additionally, treatment for Parkinson’s varies based on the symptoms the individual experiences. For instance, some people may benefit and alleviate some symptoms through lifestyle changes such as exercise and more rest, whereas others may be recommended medication or surgical therapy (Treatment). Luckily, advances in Parkinson’s research are being made and may improve future course of treatments. 



Tysnes, O. and Storstein, A., 2017. Epidemiology of Parkinson’s disease. Journal of Neural Transmission, 124(8), pp.901-905.

Mayo Clinic. n.d. Parkinson’s disease – Symptoms and causes. [online] Available at: <> [Accessed 26 April 2021].

Parkinson’s Foundation. n.d. Treatment. [online] Available at: <> [Accessed 26 April 2021].

Neurocognitive Disorders Neurodegenerative Disorders

A Neurocognitive Rarity: Explaining Creutzfeldt-Jakob Disease

When thinking about neurocognitive diseases, the most common examples that arise are usually dementia, Alzheimer’s disease, and cognitive dysfunction brought upon by traumatic brain injury. A more unknown neurocognitive affliction is Creutzfeldt-Jakob Disease, a disease in which there are only about 350 known cases in the United States per year, and affects about one in a million people per year worldwide, making it pretty rare (National Institute of Neurological Disorders and Stroke, n.d). Though rare, the disease works rapidly and degenerates brain capability to be fatal in a relatively short amount of time (National Institute of Neurological Disorders and Stroke, n.d). 

Creutzfeldt-Jakob Disease is more common in the age range of sixty years old and above and is so severe that almost seventy percent of those afflicted die within the span of a year (National Institute of Neurological Disorders and Stroke, n.d). This destruction is caused by “prions which are misfolded prion proteins that build up in the brain and cause other prion proteins to misfold as well,” (NHS Choices, n.d.). In an article in Global Genes, a woman writes of her husband who was at first misdiagnosed with severe onset Alzheimer’s, and later found out that he was in fact battling Creutzfeldt-Jakob Disease. She says “I do believe there is hope, hope for all affected by these rare diseases but we must be diligent, passionate and willing to do anything we can to help those affected and their families,” after sharing her family’s story of caring for her husband.

With stories like that and with the quick statistics one can find on the disease, Creutzfeldt-Jakob Disease seems daunting and catastrophic. And while research on the disease is still in its infancy and there is no cure to date, scientists are working on how to combat and learn more about this disastrous disease. In News for Medical and Life Sciences, it was reported from a scientific journal that “National Institutes of Health scientists have used human skin cells to create what they believe is the first cerebral organoid system, or “mini-brain,” for studying sporadic Creutzfeldt-Jakob disease,” and with research like this, they expect to be able to find more ways to examine and create new therapeutics to treat Creutzfeldt-Jakob disease (Ives, 2019). The NIH also shared that “Researchers are examining and characterizing the prions associated with CJD and trying to discover factors that influence prion infectivity and transmission, and how the disorder damages the brain” (National Institute of Neurological Disorders and Stroke, n.d). New scientific strategies like this could open up many more methods of learning about neurodegenerative diseases. 



“Creutzfeldt-Jakob Disease Fact Sheet.” National Institute of Neurological Disorders and Stroke, U.S. Department of Health and Human Services, 

NHS Choices, NHS, “A Shattered Life: The Last Days With Creutzfeldt-Jakob Disease.” Global Genes, 16 June 2016, 

Ives, Reviewed by James. “Scientists Create ‘Mini-Brain’ for Studying Sporadic Creutzfeldt-Jakob Disease.” News, 16 June 2019, zfeldt-Jakob-disease.aspx.