Figure 1

What does it look like?

Many people in today’s world don’t know or haven’t seen someone they know have been diagnosed with schizophrenia, but it is one of the most discussed psychological disorders to date. So, many are left with the ruminating thought: what does it look like? According the to DSM-5 (the standard classification of mental disorders by mental health professionals in the United States), a diagnosis of schizophrenia consists of two or more core symptoms, one of which must be hallucinations, delusions, or disorganized speech for at least one month. Other symptoms include but aren’t limited to:

• Level of work, interpersonal relations, or self-care is significantly below what it was before the start of symptoms
• Signs of disturbance that have lasted at least 6 months
• Schizoaffective disorder and depressive or bipolar disorders with having psychotic symptoms ruled out
• The disturbance is not caused by substance abuse or or other medical condition.

Figure 2: Commonly prescribed lithium capsules.

What happens after diagnosis?

A large part of understanding what schizophrenia looks like is also understanding what medical professionals are prescribing to try and treat schizophrenia. While there is no single treatment that has proved to be effective at treating schizophrenia, lithium (seen in Figure 2) has been one of the most commonly prescribed. This is because it has been shown to be an effective mood stabilizer, a treatment for aggression and excitement, and treatment of affective symptoms. But, like mentioned earlier, lithium isn’t effective for treating schizophrenia and therefore it often is not prescribed as a standalone treatment.

Figure 3: A simplistic overview of how antipsychotics work into the brain.

Lithium is not the only prescription for treating schizophrenia however! There are also what are known as first and second generation antipsychotics that have been used as a treatment. These medications have been indicated for the treatment of both acute episodes of psychoses and maintence therapy of schizophrenia. First-generation antipsychotics are better used for treating positive symptoms of schizophrenia, such as delusions and hallucinations. They have also been shown to decrease the risk of repeated episodes of psychosis. Second-generation antipsychotics on the other hand have been used to treat both negative and positive symptoms of schizophrenia, such as withdrawal. The benefit of second-generation antipsychotics is that they also reduce relapse rates in patients.

The difference between the two generations comes from their mechanisms of action. First-generation antipsychotics inhibit dopaminergic neurotransmission as well as noradrenergic, cholinergic, and histaminergic blocking areas. Second-generation antipsychotics work by blocking D2 dopamine receptors and serotonin receptor agonist action.

What we’ve learned

Through many years of study, professionals have determined the signs and symptoms of schizophrenia and have gotten really good at noticing these signs early in development. They haven’t yet found a “fix all” solution to schizophrenia, but they have developed some treatments to the symptoms such as lithium and first and second generation antipsychotics, the latter of which act on dopamine neurotransmission. Perhaps the future holds a solution to schizophrenia and not just they symptoms.

There are many interesting scientific topics that can be very informative to the public. There are many that are worth learning about and one that the public should make an effort in learning more on are diseases that result in inhibition and blockage of receptors in the brain. One of these diseases is called Alzheimer’s Disease. According to the CDC, Alzheimer’s disease is one of the most common types of dementia that affects the parts of the brain that control thoughts, language, and memory [1]. The risk of Alzheimer’s increases with age with almost six million people living with Alzheimer’s as of 2020 [1]. So far, research on Alzheimer’s is currently ongoing with more information learned each day. 

A recent study on Alzheimer’s was done by looking at how Insulin signaling pathways and other molecules affect the progression of Alzheimer’s in people. It was learned that Insulin pathways in the brain, normally controlling the clearance of amyloid Beta and tau metabolism, can be blocked by the presence of a repressor protein [2]. This blockage’s outcome is the development of resistance against Insulin, which would then lead to Alzheimer’s Disease.  

However, there are ways that the body can prevent Alzheimer’s from occurring. There is more than one pathway that contains inhibition and activation enzymes occurring within the brain that influences the progression of Alzheimer’s disease. One pathway through Insulin signaling is with Phosphatidylinositol 3-kinase (PI3K) presence. PI3K is a serine/threonine protein kinase that is responsible for the activation of Akt, an oncogene responsible for maintaining cellular functions like metabolism, transcription, protein synthesis, proliferation, growth and survival of neurons [2]. The activation of Akt would then lead to the phosphorylation inactivation of GSK-3 Beta, a serine/threonine-specific protein kinase with multiple signaling processes, such as insulin signaling pathways [2]. Since GSK-3 Beta is an important factor in Alzheimer’s development, it’s inhibition caused by PI3K is important. If GSK-3 Beta was not inhibited, this would lead to tau phosphorylation and increased assembly of amyloid plaques causing symptoms of dementia and cognitive impairment [2]. With all these steps in mind, this shows that PI3K is an important factor to stop the development of Alzheimer’s disease. 

While these factors play a significant role in Alzheimer’s disease, Alzheimer’s can also be caused by factors in a person’s life that are not just medical. For example, traumatic or stressful events happening in a person’s life could increase their chances of getting Alzheimer’s [3]. Such events could include being fired from a job, divorce from a significant other, witnessing combat, declaring bankruptcy, and the death of a family member [3]. These factors show that an increase in anxiety levels or stress can lead to Alzheimer’s progressing at a faster rate. This is more evident in further studies on Alzheimer’s disease.  

As depicted in the study, inhibition of insulin signaling pathways causing neurodegenerative processes linked to the progression of Alzheimer’s, and other diseases such as Huntington’s and Parkinson’s [3]. It would be very beneficial to learn more about how Alzheimer’s affects a person from both external factors that are in the form of stressful scenarios for the person and internal factors that are within the person’s body.

1. https://www.cdc.gov/aging/aginginfo/alzheimers.htm
2. https://www.sciencedirect.com/science/article/pii/S019701862030098X?via%3Dihub 
3. https://www.alzheimers.net/the-stressful-life-events-that-can-lead-to-alzheimers

Dancing Against Alzheimer’s Disease

My favorite video on the internet is of an elderly woman, who once was a ballerina, doing the upper body movements for one of the pieces she performed in the Swan Lake ballet. As a former ballet dancer myself, I enjoy hearing the music and watching others dance to it. Now, I don’t just love this video because it is ballet, but I love this video because the woman dancing has Alzheimer’s Disease. If you want to watch the video, which I totally recommend you do, the video is linked here.

Basics of Alzheimer’s Disease

In case you are unfamiliar with Alzheimer’s Disease, I will provide a brief crash course. There will be a quiz at the end of it, so make sure you’re paying attention. Just kidding. Alzheimer’s Disease is progressive disorder that leads to severe memory loss. Alzheimer’s Disease is biologically characterized by the death of neurons (brain cells) and abnormally decreased brain mass. The death of neurons tends to be linked to two things: amyloid plaques and neurofibrillary tangles. These words sound a little scary, but I will try to help them make sense.

Amyloid Plaques

Amyloid plaques are formed from beta-amyloid proteins, which are naturally occurring in the brain. These proteins, in an Alzheimer’s Disease brain, clump together and form a large mass between neurons multiple neurons.[1] With the beta-amyloid mass impeding on cell function and communication, the neurons begin to die.[2]

Neurofibrillary Tangles

Neurofibrillary tangles are similar to amyloid plaques in that they both are an abnormal accumulation of protein. Where amyloid plaques are caused by the accumulation of beta-amyloid proteins, the neurofibrillary tangles are caused by an accumulation of proteins called “tau.” It helps to think of neurofibrillary tangles like nets made out of tau, as pictured below. The tau proteins, which are found inside of the neuron, stick to each other to block the transport of nutrients from the neuron cell body to the other side of the cell.[3] So, I know that was a lot of information thrown at you but, to sum it up, amyloid plaques and neurofibrillary tangles are both present in Alzheimer’s brain and are both a build-up of proteins outside of the cell (plaques) and inside of the cell (tangles).

What Causes Alzheimer’s Disease?

Now, you may be asking yourself, “What causes Alzheimer’s Disease?” You pose an excellent question, and this is something I wondered as well. Researchers don’t know for sure what causes the buildup of these proteins, but many of them speculate it is a result of improper intracellular communication in the insulin signaling pathway. Again, I know this may not be a familiar topic, but I will try to explain it the best I can. To do this, I think it helps to have an image. The image below gives a brief rundown of the insulin signaling pathway and what changes are seen in brains with Alzheimer’s Disease, and I will talk you through what is going on in the image.

Insulin Signaling Pathway and Why it Relates to Alzheimer’s Disease

Usually, a hormone called insulin binds to a receptor in the brain, which is portrayed by the field goal post at the top of the image. The hormone binding to its receptor then triggers an intracellular communication pathway that starts with a protein called the insulin receptor substrate (IRS). Activation of this protein leads to activation of an enzyme with the acronym PI3K, which then signals activation of two different molecules: an enzyme referred to as Akt and a protein called mTOR. When Akt is activated, it inhibits glycogen synthase kinase (GSK-3B—another enzyme). In Alzheimer’s Disease, however, this entire pathway is abnormal. Firstly, there is less insulin binding to the receptor in brains with Alzheimer’s Disease due to something called insulin resistance. Because less insulin is binding to the receptor, there is less activation of IRS, which creates a snowball effect that leads to less activation of PI3K, then decreased activation of mTOR and Akt. Because there is less activation of Akt, GSK-3B is not inhibited as much as it should be. It is at this point where the two protein build-ups that I discussed previously can be explained. Therefore, because GSK-3B is not inhibited, activity is increased and leads to the formation of neurofibrillary tangles and amyloid plaques as a result of neuroinflammation. This is a very simplistic explanation but following along with Fig. 2 is helpful in wrapping your mind around what is happening.

[1] https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease

[2] https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease

[3] https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease

Artstract by: Alex Braun

Protein basics

To understand how to help prevent yourself from developing Alzheimer’s disease, it helps to have some background information about the disease. Alzheimer’s disease is thought to be caused by the abnormal buildup of proteins in and around the brain cells. One of these proteins is amyloid, deposits of which form plaques around brain cells. The other protein, tau, deposits of which form tangles in the brain cells (NHS et al., 2021).

Amyloid Plaques

Amyloid is a protein fragment that the body produces naturally.  Amyloid plaques are hard, insoluble accumulations of beta amyloid proteins that clump together between the neurons. The reason these plaques are hard to dissolve in the fluid between cells is because the enzyme that cuts the amyloid precursor protein (APP), cuts strands that are too large. Since these strands are too large, they are “sticky” and start clumping into deposits which are referred to as plaques (BrightFocus et al., 2020).

Neurofibrillary tangles

Neurofibrillary tangles are insoluble twist fibers primarily consisting of the protein, tau. These tangles form when tau is misfolded in a peculiar way. Specifically, in Alzheimer’s disease, tau forms a C-shape in the core in the core of the tangle with a loose end sticking out randomly. Once a tangle has been started, more tau proteins are recruited to make it longer (BrightFocus et al., 2020).

This all sounds scary, so how can one help prevent developing Alzheimer’s disease

Well, it’s not exactly as simple as just “do this and you won’t get Alzheimer’s” because life would be too easy if that was the case. You can however, live a healthy lifestyle and keep an active brain to help reduce your chances of developing Alzheimer’s disease

Cardiovascular and Alzheimer’s

Cardiovascular disease has been linked with an increased risk of Alzheimer’s disease. You can reduce your risk of developing both cardiovascular disease and Alzheimer’s disease by not smoking, drinking alcohol in moderation, eating a balanced diet, and exercising (NHS et al., 2021). I know this sounds redundant to say, but seriously, just live healthy and you’ll be better off.

Staying mentally active

There’s some evidence to suggest that rates of dementia are lower in people who remain mentally and socially active throughout their lives. One may be able to reduce their risk of Alzheimer’s disease by reading a book, learning a new language, playing an instrument, group sports, being social (NHS et al., 2021) One could also play “brain training” computer games which haven’t been fully proven to prevent Alzheimer’s, but who knows, you might even have some fun.

Other factors

Factors that are not directly responsible for Alzheimer’s disease but play a role in development include hearing loss, untreated depression, and loneliness (NHS et al., 2021) So, if you know someone who is lonely or depressed, go be their friend so you can help them reduce their risk of developing Alzheimer’s.

Works cited

Amyloid plaques and neurofibrillary tangles. BrightFocus Foundation. (2020, March 13). Retrieved from https://www.brightfocus.org/alzheimers-disease/infographic/amyloid-plaques-and-neurofibrillary-tangles.

NHS. (2021, July 5). Causes of Alzheimer’s Disease. NHS choices. Retrieved from https://www.nhs.uk/conditions/alzheimers-disease/causes/.