AP Biology class blog for discussing current research in Biology

Author: sesaad

Progress in Treating Huntington’s Disease Thanks to CRISPR Technology

Scientists have discovered a new way to treat Huntington’s disease, thanks to CRISPR technology. Their research has reduced symptoms of the disease in the mice that they tested on. 

Huntington’s Disease, which is a neurological disorder, is caused by a genetic mutation in the HTT gene. More specifically, repetitive and damaging sequences in the HTT gene cause Huntington’s disease. It causes progressive loss of movement, coordination, and cognitive functions. 

Researchers have discovered a possible solution to these symptoms: CRISPR technology. 

According to the article, “CRISPR is a genome-editing tool that allows scientists to add, remove or alter genetic material at specific locations in the genome.” One of the risks of CRISPR use is that it can affect off-target genes and molecules, causing unwanted alterations in chromosomes and genes. 


Study author Gene Yeo, PhD, explains how our cells struggle to copy repetitive DNA, which can lead to errors that cause repetitive sequences to increase with each generation. As we learned in class, the process to copy DNA is a complex one where there are many factors at play. DNA is replicated in a semi conservative manner, meaning that the old DNA strands are conserved and combined with the new, complementary strands. There is a replication fork, with a leading and lagging strand, on which DNA is replicated in the 5’-3’ direction. For replication on the leading strand, RNA primase adds RNA, DNA polymerase III adds nucleotides to the open end of the RNA, then a sliding clamp attaches to the DNA polymerase III and slides it along the strand, resulting in the leading strand being synthesized. 

The scientists directly targeted the RNA involved in the DNA replication process to remove toxic protein buildup that is responsible for the mutation in the HTT genes. They were able to complete this process using CRISPR, and without disrupting other important genes. 

After testing on mice, they reported that their research has resulted in improved motor coordination, less striatal degradation and reduced toxic protein levels. These improvements on the mice’s condition lasted for up to 8 months, and had no on other RNA molecules, making scientists optimistic that this treatment could be effective for humans. 

Detecting Cancer Early in Dogs

Scientists have discovered different factors that may be able to predict a dog’s cancer diagnosis. Previous studies done on this have mostly focused on European breeds, but the doctors in this study wanted to focus on breeds that are most commonly found in the United States. Dr Andi Flory, a veterinary oncologist, led this research by collecting data from 3,452 dogs. They found that the median age at which the dogs were diagnosed was 8.8 years. 

We have learned in AP Bio about what causes cells to become cancerous in humans, and sadly, it’s similar in dogs. If cells become damaged, this can affect their ability to know when to stop reproducing, causing them to reproduce uncontrollably. Other factors, such as mutations in onco genes, can cause similar uncontrollable cell reproduction. Cells that become cancerous are different from normal cells in that they will divide even if they haven’t received a signal to do so or if the area they belong in is filled with cells already.

Canis lupus familiaris.002 - MonferoMale dogs were generally diagnosed at a younger age than females. Furthermore, fixed dogs had earlier detection as well, compared to dogs that had not been fixed. Purebred dogs had cancer detected at a younger age compared to mixed-breed dogs. There are many things that could cause cancer in dogs. It’s possible that a cell was damaged or altered, or that an outside factored changed their DNA, which therefore could affect their genes that influence the behavior of cells. 

The scientists have concluded that, based on the findings, pet owners start cancer screenings for the dogs at age seven. 

PetDx, the pet diagnostics company that conducted the study, has created a blood-based canine cancer test. This liquid supposedly detects cancer in dogs by looking for “genomic alterations” in blood. However, doctors question the validity of this test. In general, there are few tools that are successful in early cancer detection in jobs-even ultrasounds and x-rays, and including these liquid biopsies previously mentioned. That being said, the test’s ability to identify true cases is 54.7% accurate. Additionally, they can identify metastasized cancers (cancers that have spread) at a rate of 87.5 %, but only at 19.6% for small cancers. However, these tests do not officially detect cancer. Veterinary oncologist Cheryl London acknowledges that this study is especially useful for recognizing patterns in dogs’ diagnosis, and for encouraging pet owners of certain types of dogs to get screened sooner for early detection. The earlier the diagnosis, the earlier the treatments can begin. As we learned in class, treatments can be either chemotherapy, which is killing the rapidly dividing cancer cells, or the treatment can be a physical removal of the cancerous tumor. 

There’s A Fungus Among Us

Recent discoveries suggest that certain types of fungi that are responsible for severe lung infections have become more widespread in the United States. 

The first type of fungi, Histoplasma, responsible for histoplasmosis infections, was previously only found in the Midwest, and sporadically (no pun intended) found in parts of the East and South. 

Histoplasma pas-d

Medicare records from 2007 through 2016 reflect a serious cause for concern: 47 states and Washington D.C. have now reported a significant amount of cases of histoplasmosis. The second type of fungi, Blastomyces, which is responsible for the lung infection blastomycosis, has followed a similar pattern to Histoplasma

How do these infections occur? People inhale the spores from these harmful fungi, and they attack our immune systems. They do this by attacking B and T cells. The T and B memory cells ultimately remember the pathogen to prevent a repeated infection, and in the meantime, the cytotoxic T cells attempt to destroy the cells that the pathogen has already infected. The infection occurs if the immune system is unable to fight off the pathogens. 

Coccidioidomycosis is the third type of lung infection that has become more widespread. Coccidioides fungi used to only exist in the southwest, but have spread throughout the entire Western region of the United States. 

Letting these lung infections go undiagnosed can be fatal, so scientists hope that these recent discoveries will push doctors to test for fungi more frequently when confronted with patients that have lung infections.

When You Want to Wake Up and Smell the Roses but You Can’t Smell

Does it smell?! (8937541843)

It is March, 2020. Friends of friends of friends are beginning to contract COVID-19. What is one of the most common symptoms you hear about? The loss of smell. This  research article explains how COVID-19 has affected people’s sense of smell, why it’s important to restore this integral sense, and how researchers are working to do so. 

Icaro de A.T. Pires recalls when he realized that he had lost his sense of smell: his grape juice tasted flat. Two months after contracting COVID-19, he was unable to smell the beach on his vacation. Distraught by his inability to smell the salt of the sea, he realized how much he valued his sense of smell and its ability to bring up positive memories. Pires, an ear, nose, and throat doctor, recalled a deaf patient who had also lost her sense of smell, but instead of being unable to smell her vacation location, she was unable to smell at work, which was essential for her job at a perfumery. 

According to the British Medical Journal, about 5.6 percent of people, six months after having COVID-19, have not fully regained their ability to smell and taste. This is concerning if one considers that about 550 million people have had COVID-19. 

SARS-CoV-2 is not the first virus to eradicate people’s sense of smell, but the amount of people who have been affected by it has intensified the need for a solution to smell loss. 

The olfactory sensory neurons work similar to the taste bud cells in terms of cell signaling. There are olfactory receptors in the olfactory epithelium (on the roof of the nasal cavity) that detect smells. There are dendrites within these receptors that are covered in cilia. When these cilia are stimulated by odorants that have entered the nose (in a G-protein-coupled receptor process), this depolarizes the olfactory receptor cells and sends electrical signals to the olfactory bulb, which are tied to the olfactory epithelium by axons, making the olfactory bulb the postsynaptic cell. These then send the signal to the brain that a scent has been received.  

Location of olfactory ensheathing cells (OECs) within the olfactory system

The olfactory sensory neurons are vulnerable to mucus, bacteria, and viruses that might inhibit their ability to work. Recent studies show that SARS-CoV-2 indirectly affects the olfactory system by killing sustentacular cells that support olfactory neurons. This attack harms the olfactory epithelium, causing the neurons to receive less odor molecules. Over time, the inflammation that effects the olfactory sensory neurons decreases, but for some people recovering from COVID-19, it can take up to months for them to regain their sense of smell. 

Researchers are exploring smell training, a process by which a participant smells four different smells 30 seconds each, twice a day for about three months. Generally, smell training seems to work, with about 30-60% of people having improved senses of smell after completing the training. 

The process requires discipline and endurance: taking even one day off can undo your weeks or months of progress. However, this is counteracted by the fact that there are no negative side effects, with the exceptions of frustration for those it does not work for. Doctors want to warn their patients about the possibility that, despite one’s dedication to smell training, it still might be unsuccessful in restoring your sense of smell. 

Researchers are not completely sure how smell training helps, but they have ideas of some possibilities. It is possible that the training stimulates growth of replacement olfactory cells, or it possibly strengthens pathways in the brain. There is also data that shows that smell training boosts the amount of olfactory sensory neurons; however, is unclear exactly how smell training works.  

There are other possible solutions to help restore one’s sense of smell, such as steroids, supplements, or more advanced solutions such as epithelial transplants. 

The article explains how that people do not recognize the importance of their sense of smell until it is gone. In fact, in a survey done on 400 people, 19% percent said that they would rather give up their sense of smell than their cell phone. Would you rather give up your sense of smell or your cell phone? What about giving up your sense of smell or your little left toe? 15% percent of people said that they would rather give up their sense of smell over their little left toe. 

Researchers are continuously researching solutions to restoring people’s sense of smell. People who have lost their sense of smell for an extended period of time from COVID-19 are struggling with their ability to live their lives to the fullest-they want to wake up and smell the roses, but they cannot. 

Racial Discrepancies in Kidney Disease: Why They Exist and How Researchers Are Addressing Them

Racial Discrepancies in Kidney Disease

“While Black people make up about 12% of the U.S. population, they comprise 35% of Americans with kidney failure.” (The New York Times) “They are 3 times as likely to have kidney failure compared to White Americans.” (

What causes these statistics? According to the New York Times, it’s a mix of social, economic, and genetic factors. 

One gene variant, APOL1, is responsible for the genetic predisposition to kidney disease. Having two copies of this variant is prevalent in people of sub-Saharan descent, and it’s the main contributor to kidney disease. The variants make bodies resistant to efforts taken to moderate one’s blood pressure, a significant risk factor of kidney disease. 

Dr. Olabisi, a kidney specialist at Duke University, advises against attributing all racial disparities of kidney disease to genetics. To do so would be to ignore the drastic effects of social and economic inequalities that lead to these jarring statistics. 

Identifying the Gene Variant 

About a decade ago, Harvard researchers began looking for the cause of kidney disease. They found that the APOL1 gene, which normally destroys harmful protozoa, had variants that intensified the function of the gene, making it detrimental to the body. 

These variants evolved in people of Sub-Saharan descent because they originally protected against African sleeping sickness. There is another type of variant that averts malaria but can cause sickle cell disease. Similarly, the APOL1 variant protects against one disease, but possibly causes another. 

As we learned in class, sickle cell anemia is rooted in a difference of amino acids in the primary structure of the hemoglobin of red blood cells. In position 6 of the structure, there should be glutamic acid. However, there is valine, causing the protein to fold oddly in its tertiary structures. In its quaternary structure the cells don’t react with each other as they should. As a result, he cell creates a “sickle” shape, which cannot transfer oxygen through it as successfully as the round shape. 

Sickle Cell Disease (27249799083)

Researchers have delved into numerous hypotheses over the year. They considered using medications to block the gene’s variants from harming the body. To find out if APOL1 was required for the kidneys to function, they consulted an Indian farmer whose kidneys functioned properly even though he didn’t have the APOL1 gene. They created a drug, and while the the dose still has to be adjusted, it’s on its way to being successful. 

Semantics of Genetic Predispositions  

The topic of genetic predispositions raises concerns among academics about the rhetoric that we use to describe people who are affected by the APOL1 gene variants. 

Many people of different ethnicities and races have certain genetic predispositions to diseases. For example, Ashkenazi Jews have genetic predispositions to diseases such as Gaucher disease, which affects the spleen and liver, and African Americans people are more likely to have sickle cell disease.  

Professor of biological sciences at North Carolina Agricultural and Technical State University warns against harmful rhetoric when he says, “We don’t want to fall into the myth of the genetically sick African.” I agree with his statement

It is scientifically accurate that different ethnicities have genetic predispositions to certain diseases. However, acknowledging that can be a slippery slope, especially when you consider that the most commonly known genetic predispositions effects marginalized members of society. This rhetoric partially absolves societal leaders (scientists, public servants) of effecting change in implementing preventative measures, such as improving healthcare.  This rhetoric can easily slip into having Social Darwinist undertones that portray marginalized groups as genetically inferior. Do you think awareness of the language we use is important in academic spaces? Please answer in the comments if you have an opinion on this. 

Ongoing Research

On another note, two twin brothers’ experiences helped further researchers’ understanding of the variants. They were asked to be part of a study that tested an arthritic drug on Black Americans to see if it could cure kidney disease. They tested positive for the APOL1 variants, which came to explain one of their kidney failures. 

Researchers believe that the APOL1 variants are harmful when there are secondary factors involved, such as an antiviral response to lupus like interferon. 

Dr. Olabisi’s study is pending, but in the meantime, Vertex, a drug company, wants to conduct its own research. There’s only one problem: scientists haven’t agreed on how the variants cause kidney disease, so it is unclear what a new drug should obstruct. Vertex, though, has still had some success. 

They predicted that “the variants spurred APOL1 proteins to punch holes… in kidney cells” (The New York Times) 

After testing on animals that were given the APOL1 variants, they found a drug that worked by identifying that it eliminated 47.6% of protein in urine, which points to improved kidney function. This is a significant step the ongoing research of trying to determine how to treat kidney disease. 

In Dr. In Olabisi’s study, he plans to test 5,000 members of his community for kidney disease and the APOL1 variants, and then prescribe them with the drug used for arthritis. 

These scientists and doctors are optimistic about the future of their research, and therefore, the future of kidney disease treatment and prevention, especially as it pertains to those disproportionately affected.

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