Disease/Health

Use Your Head Wisely: Sports and Concussions

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With the news of Aaron Hernandez’s post-mortem brain autopsy being recently released, the sports community and general public are starting to wonder if the hard-hits of football and other sports are causing longer-term damage than we once believed. Researchers at Boston University found evidence of serious chronic traumatic encephalopathy (CTE), the worst that they had ever seen in a 27-year-old brain. What is CTE? How is it caused? And most importantly, is there anything we can do to prevent it?
CTE is a progressively degenerative disease that can only be diagnosed post-mortem by the atrophy and deterioration of certain areas of the brain.  It occurs in people who are constantly receiving concussions or other forms of traumatic brain injuries. A biological understanding of how a concussion occurs is important to understanding why such severe CTE damage can happen with repeated blows to the head.

Picture: CTE Damage compared to a normal brain. Significant atrophy can be observed.
A high impact blow to the head causes the cell membranes of your brain cells to stretch and allow ions to pass which are not normally allowed to pass. This causes the cells to try and pump the ions out to regenerate their previous equilibrium. While doing this, cells are using high levels of energy to run the pumps which results in an energy crisis in the brain.

Ions entering into the cell after head trauma is experienced.

If a second concussion is experienced within the time span where the brain is still in an energy crisis, there can be very grim results. In rats, research has found that if a second concussion happens within 3 days of the first concussion, memory impairment is significantly greater than if a second concussion is experienced after 5 days. If more than 5 days separates the two concussions, then they act as 2 separate concussions, rather than one large one. This research supports the current return to play rules that have athletes sit out for 10-12 days after a concussion before returning to their sport.
What can we do to help prevent or lessen the severity of a concussion?

  • For people participating in sports, it is important that they wear protective headgear. Whether the sport is soccer, football, cycling, or other high impact sports, there are many options out there that can lessen the impact on the head and decrease the risk of concussion.
  • After receiving a concussion, it is important to take yourself out of situations were another concussion could occur. As demonstrated in rats, there is a period of recovery in your brain where your brain needs to rest and heal itself. Receiving a concussion during this time will significantly worsen the outcome and healing process.
  • Research has indicated that consuming omega-3 fatty acids either before or after concussion can help in recovery time. Omega-3 fatty acids can be found in fish.

There is no cure for concussions. There is no magic powder that can restore the brain to the way that it was before brain injury. For those participating in high-contact sports, caution needs to be exercised in preventing head injury so that one concussion doesn’t lead to the life-long problems of CTE.
 
For more information about Aaron Hernandez
Image can be found here
Featured image is a photograph taken by the author of her brother heading the ball during a soccer game.

Disease/Health

The Invisible Injury

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Every sport has common injuries. Gymnastics has wrist and back problems , football had ACL  tears, basketballs has sprained ankles. Of course those injuries overlap into other sports, but another injury that they all have in common, along with many other sports, are concussions. Concussions are tricky because unlike a broken arm, you can’t see when a someone is concussed.
 
Since you can’t see what is going on, it’s hard to know what exactly is happening in the brain. Concussions happened when someone is hit or hits their head. The initial place of contact is where the coup (French for “blow”) injury takes place. However, the brain also receives a second injury called the contrecoup, which is the result of the brain smacking the other side of the head.

 
People sometimes refer to concussions as a brain bruise, however the brain responds to this “bruise” quite differently than any other bruise in the body. After the initial hit, the lipid membrane in the brain get stretched allowing ion (positive and negative charged molecules) to be released when they shouldn’t be. The rapid shift in ion placement is correlated with migraines that people may experience after a blow to the head. This efflux of ions leads to an energy crisis because now the brain has to work overtime to pump the ions back into the places they should be. This process can take days, which is why it is important not to sustain another concussion during the healing process.
 
This stretch also damages the axons. Axons are like tunnels that carry signals from one end to the next. When they are damaged it’s like there is a rock in the middle of the tunnel, now no more signals can pass through. In severe cases this can lead to the death of that cell and unlike other cells in the body, neurons rarely under go cell division.
 
The brain also experiences impaired neurotransmission and also protease activation. Impaired neurotransmission is associated with impaired cognition and slowed processing and reaction time. While protease activation is associated with persistent impairments.
 
Although the damage done by a concussion is not visible, it is important to realize what is actually going on in the brain after a traumatic brain injury.

For more reading on what happens in the brain after a concussion, check out: https://www.ncbi.nlm.nih.gov/pubmed/25232881
Photo: http://www.braininjury.com/injured.shtml
Featured Image: https://breakthruptfitness.com/concussion-now-what/
 

Community/Disease/Health/Hot topics/Uncategorized

I Have Concussion. I Need to Recover.

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Nowadays, concussion occurs so often in many sports, such as football, cycling, baseball, basketball, and water sports, etc. It would be great if its negative impact to the brain is reduced by increasing its occurrence. Unfortunately, we can’t “adapt” to concussion and recover faster by increasing its occurrence.
 
It’s actually the opposite!
 
Therefore, the coaches need to understand about the concussion and its impact to the brain in order to help the players realize the importance of concussion and to provide the safe and healthy environment.
 
Concussion is not just something that will go away in one week, or “I will be fine”. The level of brain damage depends on the severity of one concussion and the frequency of having concussion.
 
One study involving the concussion center at NYU discovered the brain atrophy (shrink) after one concussion, meaning that many neurons are damaged and died. Abnormally ion flux is present, leading to inappropriate releasing of excitatory neurotransmitter and initiating the depolarization. This can affect negatively to our emotion. Problems such as anxiety and depression are at risk of developing.
 
In addition, the concussion can cause hyperglycosis and lactate accumulation as well as impaired oxidative metabolism. This condition is very bad for our cells, because the cells become acidic from lactase, leading to brain damage, and cell apoptosis (death).
 

 
Repeating experience concussion can also develop high risk of Alzheimer’s disease and other neurodegenerative disease. Some cases can lead to death when the individual have second impact syndrome. This syndrome generally is a second concussion that occurs when the first concussion hasn’t resolved (recovered) yet. Although this syndrome is rare, football players are eight-time higher of having it.
 
Then, the recovering is absolutely important after the concussion. It can reduce or prevent the risk of developing the neurodegenerative diseases, or even death. During the recovering process, the individual need to rest and recover their brain without rushing through the process. Their brain is required some time to heal. Therefore, avoid studying, learning, thinking hard, and anything that can trigger the concussion’s symptoms (such as bright light). In addition, they should take more short naps when the brain is tired. Finally, omega 3 fatty acid is suggested as the treatment for concussion. It aids the recovering process and limits the damage done to axons as well as preventing the apoptosis of neurons.
 

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Alzheimer’s Disease: I Don’t Want to Get Aging

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Alzheimer is a common disease, related to aging. A progressive disease that destroys memory and other important mental functions. It’s scary to think of Alzheimer’s disease (AD) as the 6th leading cause of death in the United States.
 
How can we prevent developing AD, when we get older?
 
Cause of Alzheimer’s disease
Many studies showed that the inappropriately turning on/off of PI3K/ Akt/ mTOR signaling pathway is a causative node in Alzheimer’s disease (AD).
 
Products from constant activation of PI3K/ Akt/ mTOR signaling pathway
Generally, after the pathway is activated, it phosphorylates Akt in downstream, leading to variety of phosphorylation in different substrates. For example, both FOXO and GSK3β are inactivated, result in reducing stress resistance, DNA repair and induction of glycogen synthesis and lipid synthesis, respectively. Akt also activates mTOR, increasing inactive IRS-1 and decreasing IRS -1/2. Later on, the insulin receptor substrate (IRS) is dysfunction, developing insulin and IGF-1 resistance.
 
In addition, PI3K/ Akt/ mTOR signaling pathway also produces tau and Aβ. The hyperphosphorylated tau protein leads to neurofibrillary tangles (NFT), known as a primary marker of Alzheimer’s disease. It is linked to cognitive decline and synaptic loss, particularly in glutamatergic neurotransmission. In addition, the overload Aβ oligomers leads to inappropriately increased activation of PI3K/ Akt / mTOR signaling pathway through increasing levels of IRS-1 phosphorylation and thereby contribute to insulin resistance.

 
Risk factors
There are many risk factors distributing to Alzheimer’s disease, besides aging and diabetes:

  1. Genetic factor: those, who have family history with Alzheimer’s disease (AD), they will have a higher chance to develop it at young age. The risk genes are apolipoprotein E-e4 or APOE-e4/ -e2/ -e3. There is a genetic test available for APOE-e4 and the other rare genes. In addition, deterministic genes directly cause the autosomal dominant AD or familial AD, such as amyloid precursor protein (APP), presenilin-1 (PS-1) and presenilin-2 (PS-2).
  2. Head injury: especially the trauma occurs repeatedly, or involves loss of consciousness; for example, head injury during collision in sport
  3. The risks for cardiac disease is strongly linked with the developing of AD later on. Many condition can deteriorate the heart health, such as heart disease, diabetes, stroke, high blood pressure, and high cholesterol.
  4. Regularly consuming tobacco and alcohol: these substances impact on the brain health.
  5. Mutation in non steroidal antiinflammatories (NSAIDs): impairing to encounter inflammatory pathway, producing by the intracellular oxidative stress.
  6. Diet: poor diet can provide enough antioxidants to our bodies, result in high inflammatory level in brain and later brain cell damaged.

 
Prevention?
It is suggested that keeping the brain healthy is the way to slow down the process of AD or not having AD by eating health diets, staying socially active, avoiding tobacco and excess alcohol, and exercising both the body and mind.
 
 
 

Disease/Health

Death Before Death: Alzheimer’s Disease

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The ability to think is quite remarkable, and one that we often take for granted. It enables us to make decisions, to express our concerns, to giggle at our favorite jokes, to share memories, to express our love for one another…
 
And yet, here we are: every 66 seconds, this is taken away from someone in the United States. They develop Alzheimer’s Disease (AD), one of the most common forms of dementia that largely affects those of advanced age through memory loss and eventually mental functioning. With no cure, medications can only be administered to slow the progression of the disease.

As the brain itself wither’s away, so do the memories. When the memories are gone, so are the people attached to them. When your loved ones are gone, you are alone… isolated in your own mind.
 
“Death before death,” coined by Joey Comeau, was the feeling shared by caregivers of AD individuals, in which they mourn the loss of their loved one twice; once when their memory dissipates and again when they have physically passed.
 

Amyloid-beta plaques and neurofibrillary tangles are the primary roots of the mind trap that is AD. Because of the plaques and tangles, neurons are unable to properly communicate with each other, which can lead to neuron death and brain atrophy.
 
A recent study linked the development of AD (through measuring plaques and tangles) to overnutrition. Overnutrition has many connections to other co-morbid complications such as diabetes, cardiovascular disease, obesity, hypertension, and hyperlipidemia. AD shares a couple traits with these disease states, including its processing of insulin and its response to stress on the body.
 
In AD, overnutrition leads to insulin resistance. The insulin degrading enzyme is not able to function properly, which leads to the buildup of Amyloid beta-plaques. Overnutrition also induces neuronal stress, particularly within the endoplasmic reticulum (ER). This stress activates the RTK pathway, leading to an increase in tau levels, thus more neurofibrillary tangles. ER stress also induces pro-inflammatory cytokines, perpetuating malfunctioning pathways and the cycle of stress on the brain.
 
While efforts continue in search of a cure, proper diet and exercise are a great way to reduce your risk for developing Alzheimer’s Disease.
 
[featured image is original art by author]
 

Disease/Health/Hot topics

Overnutrition and Alzheimer’s Disease?

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Here we go again, another blogger harping on the importance of proper nutrition and the consequences that accompany bad food choices. Nowadays, it seems like every health issue boils down to what we eat and how much we eat. Everyone has an opinion on what you should and shouldn’t eat, often contradicting one another. The amount of information out there is quite overwhelming, and can steer people away from implementing better habits. The problems that are often brought up, with regards to poor nutrition, are obesity, diabetes, heart disease, and so on. The list is somewhat endless, and so, what on Earth could I add to such a list?
 
 
I did know that eating healthy can improve cognitive functioning, but I never thought about the reverse effect. It has been shown that overnutrition (too many calories) can put someone at a higher risk for developing Alzheimer’s Disease. As someone who is already at a higher risk, due to a family history of Alzheimer’s, the idea that something as basic as nutrition could increase my risk is rather important.
 

How is Overnutrition Associated with Alzheimer’s?

When we eat, we activate one of the many pathways in our brains, one of which involves insulin. Overeating can lead to an overactivation of the pathway, which seems to be the case in Alzheimer’s. Insulin levels increase throughout the body when we eat and can activate the PI3K pathway located in our brains. Insulin does this by binding to a receptor on the neuron, which turns on the enzyme known as PI3k. PI3k can ultimately lead to the turning on of many other enzymes such as AKT and mTOR. Our body naturally produces other enzymes that can turn off this particular pathway (i.e. PTEN, FOXO, GSK).
 
 
As mentioned previously, Alzheimer’s contains an overactivation of this pathway, as well as, shuts down the “off switches”, which leads to the production of neuro-fiber tangles (NFTs) within the neuron and A-beta plaques outside of the neuron. Together, the tangles and plaques create a bad environment for our neurons, thus killing the neurons. The killing of the neurons contribute to the memory loss that is attributed to Alzheimer’s.
 
 
Featured Image Created by the Author

Disease

The Fear of Forgetting

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Alzheimer’s Disease is currently the 6th leading cause of death in the United States, and it is increasing in prevalence across the world. Why are the numbers are on the rise? Scientific research leads us to believe that nutrition and genetics are two of the principle factors involved in the manifestation of Alzheimer’s disease.
Cause of Alzheimer’s disease
Aging is the primary cause of Alzheimer’s disease. A pathway in the brain called the PI3- Kinase/Akt pathway, through its on and off switching is responsible for the physiological responses necessary for successful aging. As people age, this pathway is not regulated as well. If this pathway is not controlled accordingly, damage to the neurons is not adequately repaired, and new synapses are not formed correctly within the brain.
The PI3-K/Akt pathway is activated by insulin and insulin growth factor, and once initiated, a series of proteins are activated. If there is excessive insulin, and the pathway is active too much, this leads to several different problems, which ultimately lead to Alzheimers disease.
 
About the PI3-K/Akt pathway
The PI3-K/ Akt pathway has three major proteins involved, which are PI3-K, Akt, and mTOR. When these proteins are activated, the production of A-Beta oligomers is increased. As these A-Beta oligomers are produced, they will build up and bind to the dendrites of neurons, causing synaptic loss, and reduced signaling between neurons. The activation of PI3-K, Akt, and mTOR protiens also causes increased production of tau proteins. The tau protein composes the cytoskeleton, and is needed to maintain the structure of neurons. If it is overproduced, it can cause neurofibrillary tangles, which inhibit proper neuron functioning.
 
Recognizing Alzheimer’s disease in the brain
Alzheimer’s is easily identified in the post- mortem brain because the A-Beta plaques and tau protein neurofibrillary tangles are visible. These accumulations of proteins impair memory and cognitive functioning, which is recognizable in people with Alzheimer’s disease.
 
Prevention?
There are currently a few medications available that can temporarily slow the progression of the disease; however, there are no medications that can actually stop the development of Alzheimer’s. There is evidence in the scientific literature that reducing food intake could prevent Alzheimer’s disease. By decreasing caloric intake, insulin levels will be lower. Insulin is the activator of the PI3-K, Akt/mTOR pathway, so with less insulin, the pathway will not be overstimulated, leading to trouble. If this pathway is able to properly regulate its on and off switching, then repair and growth can occur appropriately within the brain. Given this information, the best way to prevent against Alzheimer’s disease is by eating a healthy diet.

An illustration of the A- Beta plaques and neurofibrillary tangles in a brain, leading to Alzheimer’s disease.
 
 
For more information on Alzheimer’s disease and the PI3-Kinase/ Akt/mTOR signaling pathway, please visit:
https://moodle.cord.edu/pluginfile.php/625272/mod_resource/content/0/AD%20and%20insulin%20signaling.pdf
 
 
 
 
 

Community/Disease/Health/Hot topics/Uncategorized

Another Year, Another Misplaced Memory: Aging and Alzheimer’s Disease

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Where are my keys?

“Oh no, I misplaced my keys yet AGAIN this week. My memory must be going. But wait. Does this mean..Could I possibly have..It couldn’t be..Alzheimer’s Disease?” Alzheimer’s disease (AD) is the sixth leading cause of death in the United States with an alarming and increasing mortality rate. With the vast number of improvements in healthcare within the past decade, mortality rates of various leading causes of death in the United States, including heart disease, various cancers, and diabetes have decreased; but the mortality rate of AD continues to climb due to the lack of a cure and effective medication to prolong the lives and cognitive functioning of AD victims. Many people today are haunted by the questions “Am I at risk for developing AD?” and “Why is this disease so fatal and difficult to cure?”
 

Celebrating another year of life and an increased risk for AD

AD is often attributed to genetic factors when genetically inherited forms of AD are actually extremely rare. Scientists have realized that the true cause of AD is still unknown today.  There are many factors that play into AD development, including diet, exercise, diabetes, cardiovascular disease, and other environmental and genetic factors. But recently, aging has been highlighted as the major risk factor in the development of AD. But why?
It is due to abnormal control of a specific pathway in the brain called the P13-K/Akt signaling pathway. This pathway is associated with cell growth, proliferation, and consequently healthy aging and longevity when its activity is carefully regulated. Lack of normal control of this pathway is also involved in many other major diseases, including cancer, type 2 diabetes mellitus, heart disease, and neurodegeneration. So, what is going wrong in this pathway to cause AD and its characteristic symptoms of cognitive decline and memory loss?
 

Figure 1. The interconnectedness of genetic and environmental factors that play into cognitive decline present in AD.
 

Leaving the light on in the AD Brain 

The P13-K/Akt signaling pathway is carefully regulated in a healthy brain, meaning that it is turned on and off in response to various molecular signals or processes to promote healthy cell proliferation, growth, and functioning. This can be compared to turning on and off the lights in the living room of a home. In order to conserve energy and money (via the payment of a monthly electric bill), many people will turn the living room lights on when they are in the room and will turn the lights off when they are no longer in that room. The P13-K/Akt pathway is overactive in the AD brain and it is not being shut off; this is similar to leaving the lights on in the living room, even when no one is in the room.
The P13-K/Akt pathway is initially activated by insulin. When insulin binds to and activates its receptor in the membrane of a cell, it leads to a phosphorylation cascade within the cell, or the activation of a number of enzymes in a specific order via the addition of phosphates onto those enzymes. The activation of the insulin receptor eventually leads to the activation of P13-K and ultimately the activation of Akt. The activation of Akt leads to a variety of molecular processes. When activated, Akt acts as both an activator and deactivator of a variety of enzymes. The actions of Akt consequently result in a lack of anti-stress response (which is needed for our body and brain to respond to stress in a healthy way) and prevention of its own (Akt) inactivation. Both of these results contribute to the lack of regulation of the P13-K/Akt pathway seen in AD brain. When this P13-K/Akt pathway is overactivated, it ultimately leads to insulin resistance, similar to that seen in type 2 diabetes mellitus due to unhealthy diet habits. When this pathway is constantly ON (which is not normal in a healthy brain), the body attempts to compensate for this over-activation by reducing the number of insulin receptors in the membrane of cells. With less receptors to respond to insulin, there is less activation of the pathway. However, this often leads to complete insulin resistance in the brain, which is fatal due to the high energy needs of brain cells.
Figure 2. Depiction of unhealthy eating habits leading to insulin resistance and the formation of Alzheimer’s disease.
 
P13-K/Akt overactivation also leads to the hyperphosphorylation (too much phosphorylation) of a protein called tau in the brain. These phosphorylated tau proteins end up aggregating within brain cells and start to stick to each other, creating what is known as neurofibrillary tangles (NFTs). NFTs are characteristic of AD brain and they inhibit the functionality of neurons and neuronal communication within the brain. The presence of high numbers of phosphorylated tau proteins within brain cells also mediates the formation of extracellular amyloid-beta plaques, which is also characteristic of AD brain. These amyloid-beta plaques accumulate outside of the cell and bind to the insulin receptors of the P13-K/Akt pathway that are in the membrane of brain cells and activate the pathway (positive feedback). The impairment of neuronal communication and transmission of signals in the brain leads to memory impairment and cognitive decline, both of which are symptoms of AD.
 

Figure 3. Comparison of a healthy, regulated P13-K/Akt pathway and a nonfunctional, non-regulated P13-K/Akt pathway seen in AD.
 
Healthy Body, Healthy Brain: The future of AD
AD is a major topic of current research and scientists are consistently learning more about the AD brain in order to develop a better understanding of the physiological processes occurring that lead to AD development in the brain. AD is a particularly difficult disease to study due to the complexities of studying a live human brain. Although there are current medications used to slow the progression of AD symptoms, such as memory loss and cognitive decline, there is still no proven prevention or cure. The only scientifically supported prevention for AD today is exercise and healthy eating. So maybe all of these new fitness programs aren’t so bad after all? Healthy body, healthy brain, who could complain? With the advancement of healthcare and scientific research, we hope to continue to develop a better understanding of the pathophysiology of AD that will aid in the creation of future AD preventions and cures. Although there is always hope in the future, there is no solid promise today.
 
 
If you would like to learn more information about the neurophysiological development of Alzheimer’s disease with aging, please visit: 
http://www.sciencedirect.com/science/article/pii/S053155651300065X?via%3Dihub
Featured Image from:
http://www.pureherbalayurved.com.au/alzheimer-disease-ayurvedic-treatment-melbourne.htm
Images from: 
http://www.biochemsoctrans.org/content/33/5/1041
http://www.sciencedirect.com/science/article/pii/S155252601302918X

Community/Disease/Health

Overeating as a Cause for Alzheimer’s Disease

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We all know that eating too much can cause obesity, stroke, heart failure, cancer and a load of other problems for our body, but does overeating have adverse consequences for our brain?
When we consume food it is broken down into smaller molecules, namely glucose, that can be used by individual cells for energy. When there are high levels of glucose in the body, a hormone called insulin is released. Insulin helps to break down glucose to a form that is actually usable by the body. It acts as a “key” for glucose to get to cells that need energy.

Like the rest of our body, the brain uses energy in the form of glucose to survive and function. Unfortunately, the “key” insulin, that is helpful in other places in the body, binds to cells that it is not supposed to when it is in the brain. Insulin turns on a cascade of signals called the PI3K/ AKT pathway. Recent research has shown that the PI3K/AKT pathway is expressed in high amounts in the brains of people with Alzheimer’s disease.
The PI3K/ AKT pathway, when active, can tell the brain cells to produce plaques and tangles in the brain. These plaques and tangles, made up of sticky proteins and malformed proteins, are hallmark signs of Alzheimer’s Disease. The plaques and tangles can lead to death of parts of the brain because they get in the way of the normal brain function.
Now, let’s go back to the overeating.
When you overeat, there is too much glucose in your brain, which leads to insulin release. Insulin promotes the PI3K/AKT pathway that can eventually lead to the accumulation of plaques and tangles and death of parts of the brain. People with Alzheimer’s disease have been shown to have a loss of brain matter and parts of their brain missing that are necessary for normal functioning. While working on only part of a brain, it’s no surprise that people with Alzheimer’s cannot form memories, are disoriented, or have problems with language.
So what? We need to skip Thanksgiving meal to save our brains? I don’t know that this is necessarily the solution to saving our brains. Instead, being conscientious of food choices and choosing healthy exercise patterns can help to regulate how insulin interacts with the PI3K/AKT pathway in our brain. If you start practicing these habits at a young age, your brain will thank you as it gets older. So go, overindulge on your turkey and stuffing, but when November 23rd is over, be sure to keep your health and brain health in check.
Information for this post was found here
For further information about plaques and tangles
For information on how to eat a balanced diet
Image link

Community/Disease/Health/Uncategorized

Where Did My Car Keys Go? Alzheimers in a Nutshell

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http://www.cbsnews.com/news/new-clues-to-memory-loss/

Everybody has a family member with alzheimers or knows somebody that does. It seems like that rates of this neurodegenerative disorder are going up, but is this really the case? Are the rates of alzheimers going up because of the environments or because of our diets, or simply because the life expectancy is going up as well and this disorder is sprouting up because people are living longer now. This is a disorder that effects many people close to home, and there are a lot of people out there that grow up knowing they are at a high risk for alzheimers because it runs in there family. So what is this disorder? What is going on in the brain?

One of the most common things we know about this disorder is that people begin to lose their memories. Both long term and short term memory are affected in the early stages and slowly progress to get worse as the disorder takes its course. The first form of memory that is truly affected is episodic memory. This is what helps you remember little things like where you put your school backpack, or that you have your oven on and are cooking food in there. In alzheimers, this is seen early on as people forgetting where they put their car keys, or why they walked into a room. This is so commonly overlooked in those beginning stages because people will believe that they are just getting older and have normal memory lapses. Because of this, alzheimers can go unnoticed for quite some time, which can be dangerous for the individual, especially if they live alone.

In the alzheimers brain, there are things called amyloid plaques and neurofibrillary tangles. These are very prominent, and when you look at the brain of an alzheimers person, they are one of the reasons why you see so many spaces and gaps. Those gaps are also there because neurons are dying and disappearing essentially. The neurofibrillary tangles are created through a process. The PI3k pathway in the brain becomes overactive, which causes the tau protein to become hyperphosphorylated. This hyperphosphorylation leads to the development of the NFT’s (neurofibrillary tangles). These tangles are connected to cognitive decline and behavioral changes. There is still much to be studied with alzheimers, and treatments are being tested. It will be interesting to see where the science is at 20 years from now, and if we have found a cure or not. Even if we haven’t found a cure, have we found a way to treat or slow down the effects of the disorder.
 
Sources:
https://moodle.cord.edu/pluginfile.php/625272/mod_resource/content/0/AD%20and%20insulin%20signaling.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2655107/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898682/

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