Cobbers on the Brain – Page 105 – Student Commentary on the Neurological Sciences

Understanding the Causes for Autism

Posted on May 1, 2017 by / 0 Comment

Autism spectrum Disorder (ASD) is a mental health disorder that is characterized with the difficulty with social skills, repetitive behaviors, and most forms of communication and uniqueness of strengths. Autism is a disease that has many different forms that are in a range of severity, which is why it is called autism spectrum disorder. The different forms of autism are the result of different combinations of genetic and environmental factors. It is currently accepted that ASD is contracted through polygenic inheritance, meaning that there are multiple genes that can contribute to the formation of the disorder. The disorder is usually diagnosed between 14 months and by age 3. Diagnosing ASD can be very difficult because there is no physical medical test such as a blood screening to validate the presence of the disorder. Diagnosing takes two steps of Developmental Screening and Comprehensive Diagnostic Evaluation. These steps include evaluating their behaviors and progression through development. ASD can include associated neurological disorders such as mood disorders and systemic disorders such as immune dysfunction and GI tract problems. The symptoms of autism are usually lifelong but can be managed to reduce symptoms and improve skills and abilities.

https://www.autismspeaks.org/what-autism/symptoms

A review Article in the Frontiers of Psychiatry journal discuses more on the factors linked to ASD. Although the polygenic genetic inheritance is predominately responsible for the development of autism it does explain the whole story. The review article discusses the many different environmental factors such as immune system abnormalities and Zinc deficiency. The picture below expresses all of the difficulties and risk factors of Autism.

Immune system abnormalities are linked to prenatal stress, prenatal viral infection, and parental age at the time of pregnancy. During prenatal stress the mother releases corticotrophins from her adrenal gland, which can pass through the placenta and cross the blood brain barrier causing inflammation in the fetus’ hippocampus. Parental age is associated with the increase rick of autoimmune disorders around the age of 30 years old which can affect the fetus and cause immune system abnormalities.
Zinc deficiencies are said to be caused by prenatal malnutrition, heavy metal poisoning, and maternal diabetes. Zinc is a very important molecule that regulates many different functions in the body and is a structural component in the body. Thus, indicating that a deficiency of Zinc could be related to immune deficiency and increase risk of infections.
Although the causes and rick factors for autism have been displayed, the underlying causes and specific biological abnormalities are k=not well known. Many people throughout the world suffer from Autism. Families struggle with finding and adapting to their family member that suffers from the disorder. I believe that more research and more people should investigate the causes and mechanisms that are responsible for autism spectrum disorder.

Disease/Health

Parkinson’s Disease and How You Can Make a Difference

Posted on May 1, 2017 by / 0 Comment

What is Parkinson’s
Roughly one million people in the US alone are living with Parkinson’s Disease (PD). It is a neurodegenerative disorder that slowly takes away an individuals ability to coordinate muscle movement. Although not directly fatal, the loss of motor control and other non-motor symptoms tremendously reduce quality and expected length of life. Research is ongoing to elucidate the underlying molecular mechanisms that lead to PD. As with many diseases affecting the brain, no cure yet exists. However, some treatments are available to manage symptoms. Raising awareness and public support is a critical component to ensure progress continues towards better outcomes for those living with PD.
Early Signs and Symptoms

Tremor or Shaking
Small Hand Writing
Loss of Smell
Trouble Sleeping
Trouble Moving or Walking
Constipation
Softening of Voice
Dizziness
Muscle Stiffness
Slowing of Movement
Loss of Balance

What Happens In The Brain
The substantia nigra is a structure located in the mid brain that contains dopamine producing neurons involved in controlled/planned movement, reward seeking, and addiction. Symptoms of PD are the result of the progressive malfunction and death of these neurons.
Much of the research done on PD has implicated the hallmark protein alpha-synuclein (a-syn). It has a poorly characterized function, but may be important for synaptic function and dopamine release. In diseased brains abnormally high levels of phosphorylated a-syn create aggregates that generate toxic protein inclusions known as Lewy Bodies. The dysregulated a-syn is a main component of the disease, but whether it is the cause, or result of PD remains a mystery.
The elevated levels of phosphorylated a-syn in diseased brains led researchers to investigate the role that kinase activity plays in the development of PD.
Dysregulation of kinase activity can induce or result in mitochondrial dysfunction, oxidative stress, autophagy, and inflammation. This altered activity can in turn create the high levels of phosphorylated a-syn and increase the likelihood of cell death. It is probable that some of the altered kinase activity initiates the disease pathway and others continue the progression of PD. Determining what causes the altered kinase activity and the role they play in the development and progression could provide future targets for prevention and therapy.

What You Can Do
Supporting organizations such as the National Parkinson’s Foundation, American Parkinson’s Disease Association (APDA), and The Michael J. Fox Foundation, is crucial to support those affected and move research forward. These websites have great information regarding the disease and on how anyone can contribute. This includes tips on how to get involved with community fundraising, organize your own fundraising event, and more. They also have wonderful resources to provide support in any way possible to caregivers, families, and individuals currently dealing with PD. I encourage you to visit the websites to find out how you can find support, get involved, and raise awareness for Parkinson’s Disease.

Disease/Health

Alzheimers Disease-and How to Minimize Your Risk

Posted on April 30, 2017 by / 0 Comment

Alzheimer’s disease (AD) is a progressive and irreversible brain disorder affecting about 5 million Americans according to the Centers for Disease and Control (CDC). This equates to about one person developing the disease every 66 seconds. It is also the 6^th leading cause of death right behind strokes, accidents, chronic lung disease, cancer, and heart disease.

What is Alzheimer’s?
Put simply it is the progressive death of brain cells leading to a gradual decline in cognitive function and brain shrinkage. Beta-amyloid plaques and hyper-phosphorylated tau proteins are the culprits driving neuronal cell death. They contribute to the formation of toxic neurofibrillary tangles (NFT’s) associated with the disease. However, why these proteins build up, become hyper-phosphorylated, and generate NFT’s is not well understood. Research has pointed to the dysregulation of the PI3k/Akt/mTOR (PI3) pathway as a potential player in the etiology of AD.
The PI3 pathway is an intercellular signaling mechanism important for several physiological functions such as cell cycle regulation. Dysregulation of this pathway occurs in some individuals with age and has been shown to have down-stream effects leading to the disease. Losing the ability to properly regulate this pathway promotes beta-amyloid formation and a reduced ability to get rid of it. The increased beta-amyloid levels in turn upregulate the level of PI3k signaling creating a vicious cycle. On top of that, it also increases the activity of the kinase responsible for phosphorylating tau. Which is a protein that helps stabilize the membrane of neurons.
The overactive PI3k signaling also increases levels of FOXO, a transcription factor important for proper protein metabolism, stress responses, and DNA repair. The hyper-phosphorylated tau and beta-amyloid plaques eventually lead to the trademark NFT’s and toxic cellular environments. These mechanisms progress to the point of cell death and lead to the associated dementia.

What are the Symptoms?
The symptoms present themselves as a slow decline in cognitive abilities. The first things typically noticed are forgetfulness and confusion. At first mild forgetfulness and confusion are noticed which progresses to more severe memory loss, especially with regards to recent memories. Besides memory, marked declines in thinking, reasoning, planning, and making proper judgments are present themselves. Emotional effects such as depression, mood swings, wandering, and delusions are also experienced. These things can also hurt the ability to properly care for current health problems. It can also make the individual susceptible to things such as falls, malnutrition, and bed sores. Eventually living assistance for all aspects of daily care is necessary.
Who is at Risk?
Aging is the main risk factor for about 95% of AD cases. One in nine people over the age of 65 have AD and it is present in nearly one-third of people over 85. Family history is another strong risk factor if you have a parent, brother, or sister with the disease. Most researchers agree that a combination of genetics, environmental factors, and unhealthy lifestyle contribute to AD risk.
How To Minimize Your Risk
A healthy life style is generally your best defense against any human affliction. This is also the best known way to avoid AD and other types of dementia. Research has found that strategies to promote healthy aging also lower AD risk. This includes things such as adequate sleep, proper diet, exercising (both body and mind), and avoiding tobacco.

Some current studies are finding benefits to brain training video games as a way to increase/maintain cognitive function and lower AD risk. Ongoing research such as this is promising and moving the field forward. However, much more needs to be done for finding a cure, improving treatments, and preventing the disease.

Disease/Health

Being Happy With Alzheimer’s

Posted on April 30, 2017 by / 0 Comment

My grandmother had Alzheimer’s disease for as long as I remember being around her—we lived overseas so I really only saw her for two months out of the year (so I don’t have that many memories of her in the first place), but the most recent ones were definitely ones in which she didn’t really know who I was. She’d refer to my sister as I as “dear” and say “oh it’s YOU!!” very excitedly.
We lucked out—my grandma was the sweetest person ever, even when she didn’t know who we were. My mom referred to her as “my cute mommy” and held back tears whenever it really struck her that her own mother didn’t recognize her. But my grandmother was truly a joy to be around—she’d walk up to baby dolls and treat them like real babies, and pet little dogs or cats that were on greeting cards that she’d read over and over again (and be surprised by what they said each time!).

Grandma had also developed diabetes—which could get her in to some trouble because she’d sneak cookies whenever she could! My mom would catch her and say “Mom, you can’t eat that, you’re diabetic!” to which grandma would respond, “I AM?!” She made for some cute stories, and at least all of my memories of her are positive ones.
Not everyone is that lucky. Many people that get Alzheimer’s become aggressive, and are not really very pleasant to be around. There are tons of medications that people can take to treat some of the symptoms of the disease, but I wonder if we should be adding happy pills to the mix.
Alzheimer’s is one of those diseases where we don’t really treat the cause, we mostly only treat the symptoms; probably because many things can go wrong in the brain which can kick-start the disease. Basically what happens is a combination of things which lead to protein aggregation and plaque buildups in the brain, which cause brain cell death and overall brain shrinkage.
Some of the things that can cause these plaque buildups include:

An increased activity of the PI3K pathway (a pathway which helps to regulate the cell lifecycle)
An increased resistance to insulin (an important part in the PI3K pathway)
An increased activity of mTOR (a pathway related to brain synapse growth)

Alzheimer’s disease can be really difficult not only for those whom have the disease, but also for those that interact with people with Alzheimer’s. I think that we should we at least try to make their memory-less existence bliss, and make life more enjoyable for their fearless caretakers.

Community/Disease/Health

Clearance of Beta-Amyloid Plaques in Alzheimer’s Disease: The Key to the Cure?

Posted on April 30, 2017 by / 0 Comment

Alzheimer’s Disease (AD) is a very debilitating disease that destroys memory and other proper cognitive functions. It can be really hard on families and friends of the patient. It is also tough because there is no known specific cause of AD, although there are some genes that have been found to show some susceptibility to the disease. It is also unfortunate because there is no cure for AD, and most treatments cannot reverse the memory loss and dementia seen with the disorder. The buildup of β-amyloid plaques and neurofibrillary tangles in the brain, along with other protein aggregations, such as tau, are some of the main biomarkers of the disease.

Aging has been identified as a risk factor for AD. The PI3-K(phosphoinositide 3-kinase)/Akt signaling pathway regulates healthy aging and longevity. Its main activators are insulin and IGF-1 (insulin-like growth factor-1). In AD, this pathway is continuously activated, which leads to desensitization and removal of some of the normal insulin/IGF-1 responses in the brain, as well as AD pathology and cognitive decline. Insulin/IGF-1 binds to the receptor tyrosine kinase, which activates PI3-K. PI3-K cleaves PIP₂ into PI3. PIP₂ binds Atk, which can then go on to phosphorylate things, such as FOXO, GSK3β, and mTOR. The first two are decreased with activation of the pathway, and the latter is increased. Without the normal transcription levels of FOXO, the brain loses some of its defenses against stress and inflammation. mTOR is increased, and it will uncouple the insulin receptor substrate from the insulin receptor, which leads to the insulin resistance seen in AD. It will also increase protein translation at synapses, such as tau and APP (which gets cleaved into Aβ), which may contribute to the proteins aggregations seen in the disease as well. The over-active kinases seen with over-activation of the pathway also contributes to the hyperphosphorylation of tau seen in tau protein aggregations. The over-active PI3-K/Akt pathway leads to Aβ aggregation as well, developing into the β-amyloid plaques and neurofibrillary tangles. These plaques and protein aggregations also contribute to the development of one another and are what are thought to mainly contribute to the pathology of AD as the normal functions of neuronal polarity, synaptic plasticity, learning, memory, metabolic function, and proteostasis are thrown off. They block the normal movement of other molecules important for carrying out these processes from being able to enter the nucleus as well.

Clearance of the β-amyloid plaques seems to be a great solution to curing AD, as that is what is thought to be one of the main culprits of the disease pathology. Currently the main treatment options are acetylcholinesterase inhibitors and NMDA receptor antagonists. There have been some studies to find things that could clear the plaques and the Aβ protein precursor. I found a couple things that have been tried, but mostly these studies have only been done in animal models, namely mice, and not in humans yet.
Possible Treatments for Clearing Aβ:
1.     Rosemary extract – rosmarinic acid is an antioxidant, antiviral, antibacterial, and anti-inflammatory. Protects form oxidative stress and is thought to inhibit the formation of Aβ and destabilize and dissolve beta-amyloid fibrils that have already formed. It also has calming effects.
2.     Ginkgo biloba extract – an antioxidant, neutralize free radicles, help resist damaging effects of Aβ
3.     Red ginseng extract – regenerate brain axons and synapses, reduce inflammation by Aβ and promotes microglial phagocytosis of Aβ

4.     EPPS (4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid) is a zwitterionic organic chemical buffering agent) – known to bind to amyloid-beta aggregations and break them down into single-unit proteins. In mice had better results when taken orally

5.     THC – reduced amyloid-beta protein levels and helped eliminate the inflammatory response from them helping nerve cells survive

6.     Granulocyte-macrophage colony-stimulating factor (GM-CSF) – expose old microglial cells to this and conditioned media of young macrophages helped induce microglial proliferation and reduced Aβ levels

7.     Acucanumab – a monoclonal antibody that targets aggregated Aβ, reduces soluble and insoluble Aβ in a dose-dependent manner

All in all, finding a cure for AD will take a lot more research and experimental trials. Hopefully, though, some day there will be a break through and will save many people from the unfortunate symptoms of the disease.

Disease/Health

Understanding the Fog of Alzheimer’s Disease

Posted on April 30, 2017 by / 0 Comment

Understanding the Fog of Alzheimer’s Disease
It is inevitable that we all grow old. There is nothing we can do to reverse the cruel effects of time. One of the most common effects of old age is Alzheimer’s disease. This horrible disease causes more than just one person to suffer from its effects. Family and friends of the patient have to deal with their loved one not remembering details about them or even that they exist. But what causes our loved ones to lose their memories? Researchers are not sure where the disease originates exactly, but there is knowledge about what happens once the disease develops.

Some people have heard of the plaques and tangles involved in Alzheimer’s but they may not know what they actually do within the brain. This figure depicts the problems in the neurons of Alzheimer’s disease. The right side shows how a normal brain should work. Insulin in the brain binds to the insulin receptors which activates a pathway called PI3K/Akt. The activation of Akt leads to several important cell functions. In Alzheimer’s, plaques made of built up Aβ have the ability to remove insulin receptors from the cell membrane and tangles of phosphorylated tau protein lead to cell death. Because the receptors are being taken out of the membrane, Akt is not able to inhibit the activation of GSK3β, so more tau is phosphorylated and more tangles are produced.

http://journal.frontiersin.org/article/10.3389/fnins.2015.00204/full

Another lesser known way the cell function is altered in Alzheimer’s is with two proteins called FOXO and mTOR. FOXO is a transcription factor and mTOR plays a key role in the PI3K/Akt pathway. When we age, our cells are generally undergoing some elevated levels of stress. In order to correct the cell’s function from the stress, FOXO needs to have high activity and mTOR needs low activity. In Alzheimer’s, FOXO levels are low and mTOR levels are high so the response to the stress is not reversed.

http://www.sciencedirect.com/science/article/pii/S053155651300065X

It is unclear where in this system the Alzheimer’s begins, but it is clear that once it begins, there is a snowball effect making the disease become worse with time. At the time, there are no medications that prevent or cure Alzheimer’s, but there are some to help the symptoms. Hopefully with further research, a source of the disease will be found or an early diagnosis system will be discovered with an early treatment to prevent symptoms. In my opinion, Alzheimer’s is one of the most awful diseases. Even though it doesn’t have many physical symptoms, the loss of memory is hard for not only the patient but also for the family and friends.

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Concussions-Not Only a Concern for the NFL

Posted on April 27, 2017 by / 0 Comment

Concussions are a common injury that alters cognitive function. According the the CDC affects 1.3 million people a year in the US alone. They can have very serious health implications even though medically described as a “mild” traumatic brain injury (mTBI).
A high prevalence of concussions from sports related injuries and media can give the impression that only athletes are at risk. The recent movie “Concussion” even depicts the struggle the NFL and its players are facing due to the frequent and inherently violent collisions players sustain. However, concussions are also common with many non-sports related impacts such as falls and car crashes.

Knowledge of the underlying physiological mechanisms is limited, but progress is being made. Currently, sleep and rest are the only treatment for individuals who sustained a mTBI. A greater understanding of the injury at the cellular/molecular is needed to improve prevention, therapy, and long term cognitive effects of repeated concussions.
Concussions are caused by an impact that usually involves a whiplash motion where the brain bounces, twists, and stretches. Symptoms can vary for each individual injury, but can include headache, nausea, lethargy, memory loss, dizziness, and emotional changes. These effects can take weeks to resolve with proper care.

I have personal experience from a high school football injury during a homecoming game. I was defending a pass play in which I leaped for the ball while another player took out my legs. I went head-first to the ground with a forceful impact. Following the play, I had memory loss of the few hours after and only know what happened due to the game film.
The following weeks were filled with dizziness and lethargy. I felt like I could not escape a fog like being extremely sleep deprived. Occasionally I would go to another room in the house to do something specific and completely forget what I was trying to accomplish when I got there. I attempted to return to play the following week and was not allowed regardless of how important my sixteen-year-old self-believed it to be. At the time, I did not realize the magnitude of the risk that returning posed to my health.
The post-concussive brain is susceptible to a second impact which may result in prolonged healing time and permanent damage. Often no visual evidence like a bruise is evident and can create a sense that nothing is in fact wrong. Some individuals believe this and do not rest and return to potentially dangerous activity soon after the initial injury. This can be deadly mistake; second impact syndrome can occur if another significant impact is received before the brain is healed. Extreme and rapid swelling occurs and the brain losses control over cerebral blood flow eventually leading to severe cerebral edema.
Ongoing research works to elucidate the physiological mechanisms and long term effects underlying these mTBI’s. A better understanding could provide more effective prevention, detection, and therapy for the millions of affected individuals a year. Researchers have discovered that damage to the neurons creates ionic fluxes and unsystematic release of the excitatory neurotransmitter glutamate. This disrupts the cellular environment creating stress, impaired axonal transport, and improper signaling in the brain. Making connections between the hard science and symptoms will lead to improved prevention, therapy, and long term outcomes of mTBI.
Simply being conscious to the reality of concussions is simple step that everyone can do to make informed decisions in the event of a possible mTBI.

Community/Disease/Health

Zinc and the Immune System: The Secrets of Autism Spectrum Disorder?

Posted on April 26, 2017 by / 0 Comment

Autism Spectrum Disorder (ASD) is a disease that affects about 1 in 68 children in the United States, according to an ADDM Network Survey from 2012. ASD includes disorders like Asperger’s, Autism, Pervasive Developmental Disorder, and Childhood Disintegrative Disorder, that all have slightly different levels of cognitive and learning impairment, variations in behaviors, and other symptoms. There are two main types of behaviors in children with ASD, although not all people will display all the symptoms, and some may exhibit several of them. The first is restrictive or repetitive behaviors, the second is social communication/interaction behaviors. Sometimes diagnosis can be tough because it is difficult to discern, for example, if a child falls in the lower-functioning end of Asperger’s, or the higher-functioning end of Autism, as they fall on a spectrum. Even with some of the impairments that these children have, they often have great strengths and abilities in one subject or aspect of their lives, such as math, music, or other things.

The prevalence of ASD in the United States is increasing. Some argue that this could be due just to higher numbers of diagnoses as awareness has risen. There is no specific cause that has been identified for ASD, but there are genetic factors that are thought to be responsible for ASD occurrence, although they are not able to account for all cases. There appears to be some environmental factors that also contribute to the number of cases of ASD or increase the risk for it, especially if some of those autism-related genes are present.

The article that we read in class identified two main environmental factors that are thought to contribute to cases of ASD – zinc deficiency and dysfunctional immune system. It is thought that they contribute to dysfunctional excitatory signaling as they inhibit correct structure and development of synapses and their receptors and cause some dysfunctional kinase signaling. Many of the genes implicated in ASD either need zinc or are involved in zinc homeostasis in the body. Low levels of maternal zinc in pregnancy can cause immune system dysfunction, which can make the fetus more susceptible to infections while in utero. This can in turn cause some developmental problems in the child and their brain.

As mentioned, zinc deficiency contributes to immune system abnormalities. Obviously this can make the child more susceptible to diseases, but inflammation can have detrimental effects on the body when it goes on for too long. It can damage developing cells and contributes to neural plasticity at synapses.

These two main environmental factors affect each other, but they are in interplay with other environmental and genetic factors as well. Things such as prenatal and perinatal stress, parental age, exposure to toxins, prenatal infections, and melatonin deficiency can all contribute to immune system abnormalities. Malnutrition, copper overload, and melatonin deficiency contribute to zinc deficiency.

Mutations in genes can affect zinc homeostasis as well, and increased age of the parents gives a higher chance for mutations. Exposure to toxins and zinc deficiency also may cause genetic mutations, and when they are in those genes that encode for scaffolding proteins, receptor proteins, or signaling cascade proteins, it does not allow for proper synapse function, contributing to the expression of ASD.

Thus, it is hard to pin-point the exact cause of ASD, but it is obvious that there is important environmental contributors along with the genetic components of the disease. It will be important to educate parents about proper nutrition so they get the nutrients they need, such as zinc, to help the baby develop properly and protect against maternal and fetal infections. It will also be important to be aware of the possible effects that exposure to toxins or other environmental agents may have on the body as well. As more is learned about zinc, the immune system, environmental contributors, and their interactions with autism-implicated genes, maybe someday we will be able to prevent or even cure people with ASD.

Disease/Health/Hot topics

What Does Concussion Do to Our Neurons?

Posted on April 25, 2017 by / 0 Comment

Concussions are difficult to spot and treat without an obvious injury to the brain. A brain scan will not show bleeding or large-scale damage. But concussions can cause serious injury to the brain at the cellular level.
Ion leaking is one dramatic example of the effects of concussion on the brain. The impact of a concussion tears tiny holes in the membranes of neurons. Ions, because they are only single atoms, are able to uncontrollably flow in and out of the cell through these tears. Neurons use sodium ions to carry electrical signals. They take in sodium at exactly the right time to create an action potential. When sodium rushes in all at once, neurons become stuck in an inactive state. Ion flux may explain the migraine symptoms that can come with concussion. Similar movement of ions occurs in migraines, and people with a history of migraines are more likely to have worse concussion symptoms.
A concussion can send the brain into an energy crisis. Moving ions in and out of cells costs a lot of energy, even for a healthy brain, because it takes energy to run the tiny pumps that transport the ions. After a concussion, the brain needs even more energy. The brain works extremely hard to restore the balance of ions. Since blood flow to the brain is reduced after a concussion, the low supply of energy makes the high demand worse. Energy crisis probably explains why getting a concussion makes the brain more sensitive to a second concussion. Research has shown that if a second concussion happens after glucose metabolism rises back to normal, the two concussions act as separate small injuries instead of one massive injury.
The stretching forces of a traumatic brain injury are known to damage axons in the brain. Axons are the long, thin parts of neurons that carry signals, kind of like wires. It makes sense that these delicate structures are especially vulnerable to concussion. When the brain bounces against the skull, axons can partially tear or completely disconnect from neurons. Myelin, the fatty insulating layer on axons, gives some protection against concussions. That might explain why young children are more vulnerable, since the process of making myelin happens early in life. Axon injury is probably an important factor in the slowed thinking that comes with concussion.
Some of the more subtle signs of concussion, such as migraine or mental fogginess, might be too slight for someone to know that their brain is seriously injured. As we learn more about the causes of concussion symptoms, hopefully we will be able to develop accurate tests for concussions.

Disease/Health

Parkinson’s – a Disease Divulged

Posted on April 25, 2017 by / 0 Comment

Parkinson’s – A Disease Divulged
You never expect it will happen to you. When it does, your whole world seems to start spinning in a different direction. One morning, as I was getting ready for school, my mom came downstairs in a mess of tears, and through sobs told me that her brother had been diagnosed with Parkinson’s disease. Even though I wasn’t really sure what Parkinson’s disease was at the time, I was still devastated by the news. A very close family member of mine had been diagnosed with a disease.
As devastating as this new was in the beginning, I needed to find a way to cope. I couldn’t spend every time with my uncle feeling bad about his diagnosis. Five years later, I put his diagnosis behind me and treat my uncle the same as I had before. We still joke around just as often and dance around the kitchen at my grandparents’ house. Every now and then his hand will shake with a tremor and I am reminded of the disease, but he is luckily still functioning at full capacity.
For my generation (young adults), Michael J. Fox’s Parkinson’s actions are before our time. Therefore, we are not as aware of the disease or what it entails. So for those who aren’t aware, this is what researchers and doctors believe is at the root of Parkinson’s.
Alpha-synuclein and Lewy Bodies
In the brain region called the substantia nigra, neurons get a buildup of misfolded proteins. The substantia nigra is a location in the brain that holds a considerable amount of the brain’s dopamine.

When a specific protein called alpha-synuclein gets phosphorylated, it isn’t able to get broken down. In Parkinson’s disease, alpha-synuclein is hyperphosphorylated causing them to aggregate. These aggregations are then called Lewy bodies. A bunch of Lewy bodies in a neuron cause the neuron to die and a loss of dopamine. Interestingly, it seems that most of these problems affect the communication between intent of movement and the actual movement. This causes the patient to have slowed and rigid movements and tremors.

Although this disease spreads throughout the body over time and can even lead to death, depending on the degree of severity and treatment, it can take several years for it to become a negative impact on daily routines. The current treatment for Parkinson’s is the use of a drug called L-dopa. This drug helps to reintroduce dopamine in the substantia nigra, helping the signal for movement to be improved, which in turn reduces symptoms. Doctors actually will prescribe a patient a high dose of L-dopa to diagnose Parkinson’s. If the patients symptoms decrease, the diagnoses is considered confirmed.
You never expect it will happen to you. A diagnosis of someone that is close to you will have a tremendous effect on your life, but learning about a disease and how to cope with it will not allow the disease to hinder your relationship. So for now, I will keep on dancing with my uncle in the middle of my grandparents’ kitchen as long as I can. Parkinson’s will not take that away from us.

Brain image: https://s-media-cache-ak0.pinimg.com/736x/30/4e/ba/304eba7a5b82d65d8b1b43242343e44b.jpg