AP Biology class blog for discussing current research in Biology

Tag: Dementia

Can Concussions Lead to Higher Risks of Dementia?

According to new research, repeated concussions are linked to worsen brain function in later life, including higher risks of Alzheimers and Parkinson’s disease.

Concussion Anatomy

A concussion is a type of traumatic brain injury caused by a bump, blow, or jolt to the head or by a hit to the body that causes the head and brain to move rapidly back and forth. This sudden movement can cause the brain to bounce around or twist in the skull, creating chemical changes in the brain and sometimes stretching and damaging brain cells.

A study led by the University of Oxford and the University of Exeter, published in the Journal of Neurotrauma, included data from over 15,000 participants found that people who reported three or more concussions had significantly worse cognitive function, which got worse with each concussion after that.

The researchers found that reporting even one moderate-to-severe concussion was associated with worsened attention, completion of complex tasks and processing speed capacity. Participants who reported 3 concussions, even mild concussions, throughout their lives had significantly worse attention and ability to complete complex tasks. Those who reported 4 or more mild concussions showed worsened processing speed and working memory. Each additional reported concussion was linked to progressively worse cognitive function.

According to Dr. Vanessa Raymont, senior author of the study from the University of Oxford, head injuries are a major risk factor for dementia and “this large-scale study gives the greatest detail to date on a stark finding — the more times you injure your brain in life, the worse your brain function could be as you age.”

The research indicates that people who have experienced three or more even mild episodes of concussion should be counselled on whether to continue high-risk activities.

This article relates to AP biology because when a concussion occurs this affects the body’s ability to send signal to the brain (cell signaling). Cell signaling occurs when a cell detects a signaling molecule from the outside of the cell. A signal is detected when the chemical signal (also known as a ligand) binds to a receptor protein on the surface of the cell or inside the cell. When the signaling molecule binds the receptor it changes the receptor protein in some way. This change initiates the process of transduction. Signal transduction is usually a pathway of several steps. Each relay molecule in the signal transduction pathway changes the next molecule in the pathway. Finally, the signal triggers a specific cellular response. In cell signaling the axon sends electrical impulses from the neuron travel away to be received by other neurons. After a concussion, damage to axons is much more common than damage to other parts of the cell. The axon in the brain is a long extension of the cell which transmits impulses. The axon carries electrical impulses that help communicate within the brain and between the brain. When the axon is damaged neurons cannot properly communicate, a damaged axon has more trouble sending its signals, interfering with the brain’s ability to do its job. A concussion also makes it difficult for the cells to distribute chemicals and materials to all areas of the cell, this occurs in the synapse where impulses are transmitted from one neuron to another.

Can Your Eyes Save Your Brain?

Are Retinal Tests Able to Identify Early-Onset Alzheimer’s?

According to The Alzheimer’s Association, In 2021, 6.2 million Americans were living with Alzheimer’s Disease. 1 in every 9 people (11.3%) above the age of 65 has Alzheimer’s Disease, and these percentages only increase with age, leaving 35 percent of people above the age of 85 with Alzheimer’s or Dementia. For those who do not know, Dementia is a general term for the loss of memory and other thinking abilities, severe enough to interfere with daily life. Alzheimer’s is the most common type of Dementia, and it affects not just memory but behavior. Mainly recognized in adults above the age of 60, our current form of diagnosing Alzheimer’s is waiting until people become overly forgetful or begin to act out of character. Although early detection is occasionally possible through brain scans, this method is expensive and unsuitable for most. 

My uncle Steven was only 51 when he was diagnosed with Alzheimer’s. Although caught decently early, his changes in behavior and short-term memory loss were apparent. Often asking a question only minutes after he had previously been told the answer, my family was devastated. Before being diagnosed, my uncle was the CFO of a Fortune 500 company and was always seen as a mentally and physically strong man. Having no choice but to retire young and focus on his health was a hard truth for all of us to accept. 

Alzheimer's Disease

Sad and confused about how this had happened, I did extensive research on the causes of Alzheimer’s. Although there are multiple possible causes and factors that play into the development of Alzheimer’s disease, one way is through inheritance. Early-onset Alzheimer’s diseases, like my uncle’s, can be inherited genetically. Humans typically have 46 chromosomes in each cell of their body. Each of these chromosomes contains anywhere between 20,000 and 250,000 genes. Usually having two copies of each chromosome, one copy comes from the mother’s egg and the other from the father’s sperm. Each egg and the sperm are haploid, meaning they contain 23 chromosomes. When the sperm fertilizes the egg, two copies of each chromosome and gene are present. Although some genes are required from both parents to be passed onto their offspring, Alzheimer’s is inherited in an autosomal dominant pattern. This is one of the many ways that disorders can be passed down through families, and it means that only one parent needs to have the abnormal gene for you to get the disease. Thus people who inherit one copy of the APOE e4 allele have a significant chance of developing Alzheimer’s. However, those who inherit two copies of their allele are at even greater risk. It is important to note that not all people with the disease have the e4 allele, and not all people with the allele develop Alzheimer’s. Because in most cases, an infected person inherits the gene from an infected parent, it is not likely that my uncle developed Alzheimer’s genetically as no one else in my family tree ever had the disease.

Autosomal dominant inheritance

Moving forward with my research, I looked into possible treatments; unfortunately, most drugs are still in trial or only applicable to individuals diagnosed before any level of severe memory loss occurs. While this is a sign of good progress, I can’t help but feel there must be some better solution to diagnose Alzheimer’s before it becomes too late. Thankfully, Dr. Ashleigh Barrett-Young and her team agreed.

Working at Otago’s Dunedin Multidisciplinary Health and Development Research Unit, Barrett-Young and her team of researchers have investigated the retina’s potential to indicate Alzheimer’s earlier in life. As stated by Barrett-Young, “In the near future, it’s hoped that artificial intelligence will be able to take an image of a person’s retina and determine whether that person is at risk for Alzheimer’s long before they begin showing symptoms, and when there is a possibility of treatment to mitigate the symptoms.” The Dunedin study analyzed the retinal nerve fiber layer (RNFL) and Ganglion cell layer (GCL) of 865 people at the age of 45. Dr. Barret-Young and her team reported that thicker RNFL and GCL were associated with better cognitive performance, while a thinner RNFL was linked to a more significant decline in processing speed. Adding to their report, “These findings suggest that RNFL could be an indicator of overall brain health. This highlights the potential for optical scans to aid in the diagnosis of cognitive decline.” Since treatment for Alzheimer’s is yet to be discovered, the ability to identify the disease in preclinical stages could allow the possibility of aid before it’s too late. Although further studies are required to determine if retinal scans can predict precisely Alzheimer’s, or just the expected cognitive decline of the brain, researchers have hope. 

So, while this solution sadly offers no benefit to my uncle, I feel hopeful that this new diagnosis technique will be beneficial for the millions of people who would have had family members or friends combating Alzheimer’s disease but caught it early enough to intervene and do something about it. 

Can you get a disease from being outside?

The Alzheimer’s diseases and several genetic defects have been identified to connect with early onset family genetics. In this study chemists, toxicologists, and biologists have researched the environmental effects connected with health issues. The researchers examined the point that the human race would have all gone extinct if our bodies didn’t have the ability to metabolize, absorb, or excrete trace substances. In 2005, there was a lot of talk about the “exposome” causing many diseases. This research topic is very  interesting because it explains that everything you are exposed to can cause cancer. The fact that our exposome is everything we contact in our lives is concerning. Average light, invisible car exhaust and ambient street noise are all linked to birth defects. And now Alzheimer’s has been statistically linked to the environment.

Although Alzheimer’s is generally linked with age, researchers also believe it is linked to living in cities and poorer neighborhoods. According to new research unveiled at a recent global gathering of Alzheimer’s experts in London, stressful life events, poverty and racial inequities contribute to dementia risk in late life. A Study at the University of Wisconsin looked at levels of socioeconomic disadvantages such as poverty, education, housing, and employment to determine whether there was a stronger link to developing Alzheimer’s than by chance alone. They found that people in poor neighborhoods had worse cognitive performances in all aspects, which is linked to the fact that they had disproportionately higher levels of the Alzheimers disease biomarker in their spinal fluid. This could be considered an example of the effects that their exposome pose on their health. For example, in poorer neighborhoods, they have less access to healthy foods, safe exercisee options and healthy environments. This unhealthy environment leads to increased risk of diabetes,  cancer, and early death.

New Developments in the Biology of Alzheimer’s Disease

Recent work by Boston University School of Medicine researchers shows developments in a new model for the biology of Alzheimer’s disease, which could lead to entirely new approaches in treating the disease. Alzheimer’s disease disrupts one’s cognitive abilities, including memory, thinking, and behavior. It accounts for 60-80% of all dementia cases. The neurodegenerative disease is caused by clumps and accumulations of 2 proteins –beta-amyloid and tau– which cause nerve cell injury and in turn, dementia.

Comparison of a normal brain (left) and the brain of a person diagnosed with Alzheimer’s (right).

Recent work by the BUSM researchers has shown that the clumping and accumulation of the tau protein are largely due to stress. The accumulation of tau produces “stress granules” (RNA/protein complexes). The brain responds to these stress granules by producing important protective proteins. However, with excessive stress, there is a greater accumulation of stress granules, which in turn leads to greater accumulation of clumped tau, which causes nerve cell injury. In this study, researchers are using this model to show that reducing the level of stress granules could lead to improved nerve cell health. It may be possible to reduce the level of stress granules by genetically decreasing TIA1, a protein required for stress granule formation.

In an experimental model of Alzheimer’s disease, the research team found that reducing the TIA1 protein led to striking improvements in memory and life expectancy. However, although stress granule levels decreased (leading to better protection), the team observed that the clumps of tau became larger. The researchers further looked at the tau pathology and found that the while small clumps of tau (known as tau oligomers) are toxic, larger tau clumps are generally less toxic. According to pharmacology and experimental therapeutics professor Benjamin Wolozin, this discovery would explain why the experimental models experienced better memory and longer life expectancy. The implications and ability of TIA1 protein reduction in order to provide protection may lead to further novel developments in the biology and treatment of Alzheimer’s disease.


Petri Dish Brain Models…Endless Possibilities.

Side View of the Brain

Who would have thought that modern science could develope a brain stimulation with actual brain cells in a petri dish? Well researchers led by Doctor Rudolph E. Tanzi have done just that.  They have made substantial steps in the field of medical brain research specifically in the Alzheimer’s research field. Rudolph E. Tanzi is a prominent neuroscientist at Massachusetts General Hospital in Boston. One of Tanzi’s colleagues and also a neuroscientist, Doo Yeon Kim, suggested that they grow brain cells in gel. From this suggestion researchers under Tanzi’s lead created a brain scenario in a petri dish and then gave this model Alzheimer’s disease. Tanzi and his group took embryonic stem cells, which have the potential to become any type of cell in the body, and grew them with a mixture of chemicals. Said chemicals cause the stems cells to become neurons, which they then gave those neurons Alzheimer’s genes and were all growing in a commercially available gel in a petri dish. Those genes then caused plaques and later tangles which are indicative characteristics of Alzheimers. Dr Tanzi was quoted, “Sure enough, we saw plaques, real plaques…We waited, and then we saw tangles, actual tangles. It looks like you are looking at an Alzheimer brain.” This manufactured real Alzheimer’s brain stimulation opens new doors for research that was hindered because previously on mice with imperfect formsof the human Alzheimer’s genes. Doctor P. Murali Doraiswamy of Duke University states, “It could dramatically accelerate testing of new drug candidates.” Although the Petri Dish Model lacks some real life qualities it can still be utilized as a start for quick, cheap, and easy drug testing. Doctor Sam Gandy of the Icahn School of Medicine at Mount Sinai in New York states that the new discovery is, “a real game changer.” Tanzi is now starting to test 1,200 drugs on the market and 5,000 experimental drugs, a project that was impossible to perform on mice. Tanzi also wishes to test a protein, amyloid, that clumps into the plaques. He found an enzyme, that when blocked prevents tangles from forming. Dr. Gandy wishes to use the the system to study the influence of genes, such as ApoE4, which contributes to about 50% of Alzheimer’s cases. Dr. Doraiswamy of Duke stated, “The lack of a viable model for Alzheimer’s has been the Achilles’ heel of the field.” Tanzi’s model is the first step towards defeating this “Achilles’ heel” which opens infinite new doors in the research of finding new medications to cope with the devastation of Alzheimer’s disease.

For more Information: 

Official Alzheimer’s Research Page

Neuroscience Research 

Actual Article




Don’t forget your sleep

Photo Credit: Me

Let’s face it there are many nights when we don’t get the sleep we need for some reason or other.  Not getting the recommended eight hours of sleep is pretty much the norm for students, but according to a new study this lack of sleep could really be hurting us later on.  This new study found that disrupted sleep appears to be associated with the build-up of amyloid plaques, which are a known to be a hallmarks of Alzheimer’s disease, in the brains of people who did not yet have any memory problems.

The author of the study Yo-El Ju, who works with Washington University School of Medicine conducted the study by testing the sleep patterns of one hundred people, ages 45 to 80, who were free of dementia.  Half of this group had a family history of Alzheimer’s.  Sleep diaries and questionnaires were used to learn about the patients sleeping habits as well as a device placed on the participants for two weeks to measure sleep.

The study found that 25% of the participants had evidence of amyloid plaques, which are known to be able to show up years before symptoms of Alzheimer’s appear.  Most of these people spend an average of eight hours in bed, but only 6.5 hours asleep due to waking up at night.  The study found that people who were waking up more than five times an hour were more likely to have the amyloid plaque build-up than the people who didn’t wake up much at all.  The study also said that people who slept less efficiently were more likely to have markers of early stage Alzheimer’s disease.  Dr.Ju says it will take more time and data to fully understand the link, but I think for now it is safe to say that sometimes we should put our homework down and get to sleep.

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