Month: May 2017

by: Sasha Narain

A study conducted by the CDC, surveying high school students between the years 2011 and 2015, reported a 6.5 percent decrease in cigarette smoking. According to TobaccoFreeKids.org, this decrease reflects an overall trend in cigarette smoking amongst teens since the late 1990s. In contrast, in 2015 16 percent of high school students confirmed that they had smoked an electronic cigarette in the past thirty days, a 1.5 percent increase in use since 2011. This trend reflects not only the lack of regulation for electronic cigarettes, but also the widely held misconception that electronic cigarettes, or “ e-cigs,” are without consequence or harm to health.

While much research has demonstrated the addictive effects of nicotine, there has been little research on the long term effects of inhaling “e-liquid,” the solvent composed of propylene glycol (PG) and glycerol (GL), on respiratory health. A study conducted between UCSF, UC Berkeley, and the California Department of Public Health has found that the components of this solvent, when heated at high temperatures modeling those of e-cigarette vaping, result in the production of small carbonyl compounds, such as acetaldehyde and formaldehyde. Although e-cigarette users are not inhaling smoke, the “vapor” that they are inhaling contains neurotoxic substances that could have a negative effect on their health, and potentially the health of those around them.

Due to a lack of research, the effects of small carbonyl compounds on health are unclear in the context of smoking or vaping. However, there is a common example demonstrating the weakening effects of aldehydes. A hangover after consuming alcoholic beverages is a process in which the body is unable to break down acetaldehyde, a compound resulting from partial metabolism of alcohol. Acetaldehyde, like formaldehyde, is a part of the aldehyde family of carbonyl-containing organic compounds. Some of these compounds are considered to be more neurotoxic than alcohol and are known cancer-causing agents. By developing a study to quantify the production of these types of compounds while vaping, more research can be guided towards understanding the health risks posed by electronic cigarettes and inhalation of e-liquid.

Researchers sought to expose the danger behind the “e-liquid,” the solvent used in vaping, composed of propylene glycol and glycerol, independent of nicotine and flavoring additives. They began by isolating five e-liquid formulas and testing them at six different temperatures. Two of the formulas they selected and tested were purchased at a “vaping bar” in California. These e-liquids came in the flavors “tobacco” and “MIN TEE.” Their main ingredients were labeled as propylene glycol and glycerol, without note of the proportions of these solvents or whether they actually contained nicotine. Lastly, researchers tested propylene glycol and glycerol independently and a 1:1 mixture of propylene glycol and glycerol, in order to gauge how the chemicals themselves reacted when heated and to control for any reactions between the PG and GL. Researchers began by placing the e-liquid on glass wool and then the glass wool into a stainless steel tubular reactor. The reactor temperature was regulated by a temperature controller and the temperature of the glass wool was measured by a thermocouple. In order to mimic the duration of the average puff from an e-cigarette, compressed air constantly flowed over the tube reactor. The air was then collected by commercial 2, 4 dinitrophenylhydrazine cartridges, that were designed for air-sampling and detecting carbonyl compounds. Moreover, the researchers controlled for levels of carbonyls that were released from the steel wool by placing a piece of steel wool without the e-liquid into the reactor and measuring these “background carbonyls.” This number was subtracted from all results.

Analysis of the carbonyl compounds collected by the cartridges started with high-performance liquid chromatography (HPLC), which separates compounds by passing a liquid solvent through a column filled with a solid absorbent material. Once isolated, the compounds were identified and quantified in accordance with commercial instructions. With high levels of certainty, researchers found that through the range of temperatures the experiment was controlled for, GL produced almost ten times as much of formaldehyde and significantly greater amounts of acetaldehyde than did PG. In addition to producing formaldehyde and acetaldehyde, glycerol was also found to produce acrolein, a toxin known to be irritating to the upper respiratory tract. Moreover, glycerol began forming aldehyde products at much lower temperatures from the GL than the PG. Overall, as the temperature of the reactor increased, rates of aldehyde product formation sharply increased.

Although researchers concede that the stainless steel tubular reactor may not exactly mimic the heating and vaporization of a real e-cigarette, this experiment demonstrates a controlled method to measure carbonyl emissions from e-liquids. The social implications of this study are broad. Having the tools to precisely measure the small carbonyl compounds that are emitted from these e-liquids enables medical researchers to more accurately define the consequences of e-cigarette use on health. Because each individual puff or inhalation from an e-cigarette yields a very small amount of e-liquid and thus a very small amount of acetaldehyde and formaldehyde, more research must be directed at the long term effects of e-cigarette use. More specifically, future studies can focus on how inhalation of these products is processed by the body, as opposed to consumption. Likewise, with this increase in medical information, legislature can make more informed decisions when regulating these products, and hopefully lower the use of e-cigarettes among teenagers. Lastly, the researchers question the effects of second and third-hand smoking. They note, “As use of e-cigarettes increases rapidly, more studies on e-cigarettes are urgently needed to ensure that consumers’ (and bystanders’) health is safeguarded.” With this model for measuring the carbonyl products from e-cigarettes, researchers are not only able to quantify the direct health effects on e-cigarette users but also have greater direction in studying indirect effects of e-cigarette usage.

by: Quinn Spencer

Did you know that there are more bacterial cells in your body than there are human cells? It has long been known that these bacterial associations play an important role on human health (probiotics anyone?), but the Eisen Lab at UC Berkeley has recently begun research that looks further into how these relationships may affect host organisms.

Carolyn Elya, a graduate student researcher in the Eisen Lab, has undertaken research to understand if bacterial associations affect gene expression in the host organism, and if so, what the molecular basis of these changes is. Her hypothesis was that different bacterial cultures in the guts of fruit flies, Drosophila melanogaster, could have an effect on the gene expression of these organisms, indicating that bacterial associations have even greater health implications than currently realized. 

Studies that involve genetic research often use fruit flies, a model organism in the scientific community. They are a particularly good organism for this study because they reach maturity and reproduce quickly, making it quick and easy to see any differential changes in adult organisms or females’ offspring. They also have a low number of chromosomes and a small genome size, making it efficient to track changes. Studies have involved fruit flies for decades, which means there are a plethora of mechanisms that researchers have to test and analyze results accurately. 

The rich understanding of fruit flies made it so that the research could focus on the molecular basis of bacterial associations.  In D. melanogaster, the typical microbe community is comprised of about 50 bacterial species in wild flies and about ten species in lab-reared flies. To strip these in lab flies, a combination of house bleach and sterile conditions was used to raise axenic flies. This allowed for the mono-association of certain bacterial colonies with D. Melanogaster. Three different bacterial strains were used to compare, chosen for their high abundance in lab stocks, and general ubiquity in gut microbe surveys. 

Following the rearing of flies on mono bacterial cultures, five-day-old female adult flies were tested for genetic expression via gut dissection and the mRNA found in these regions was sequenced. Female flies were chosen due to higher genetic content that is expressed as compared to male flies, as there is a large concentration of maternal RNAs found only in females, which affect the development of their embryos. In this original experiment, researchers were surprised to find that they did not find any significant differences in gene expression based on bacterial treatment, using ANOVA statistical testing.

Finding this result unsatisfying, the researchers expanded their research to compare axenic flies with conventionally reared flies and flies mono associated with yeast, which provides nutrition to flies without bacteria. Following the testing protocol of the first experiment, researchers once again compared results. They found two distinct groups of patterns of gene expression. One transcriptional regime was ‘conventional like,’ which included the conventionally raised flies and the flies raised on yeast with bacterial mono or poly associations. The other regime was ‘bacterial like,’ similar to the expression patterns found in the three groups of the initial experiment. The axenic groups and simple bacterial mono and poly associations fell into this group. Using ANOVA, researchers were able to understand which genes most distinguished these two groups. Genes more highly expressed in the ‘conventional like’ group were enriched for annotations for a variety of metabolic processes, most notably involving lipids and amino acids. Genes more expressed in the ‘bacterial like’ group were also enriched in metabolism annotations, although this enrichment was less pronounced and more general than for the former set. The takeaway from these results is that yeast induces metabolic changes which are not evoked by the presence of any one bacterial colony.

A further experiment following the unexpected results from the original analyzed the genome of the entire organism instead of just focusing on the gut. Data from whole organisms showed that the conventionally raised flies had a distinct profile compared to the other samples tested. This suggests that none of the treatments done in these experiments could recapitulate, meaning yeast alone with bacterial associations is sufficient for gut gene expression, but not so for the whole organism. There were no significant differences in whole organism transcription profiles when comparing the different mono-associated organisms.

Altogether, this research helped confirm that the presence of microbes in food and the environment has a significant effect on gene expression in the gut of D. Melanogaster. Though there were few differences seen between organisms raised on monocultures, the presence of yeast played a large role, indicating that this may be what has a more significant effect on shaping physiology. 

Carolyn Elya claims that these results were unexpected, and it is important not to jump to the conclusion that flies are insensitive to bacterial associations. Some things to take into consideration, she states, are that “bacterial species that thrive amongst lab-reared flies are not representative of natural populations” and that some of the bacteria used in this research came from non-fly species. Also, these experiments only looked at five-day-old flies, leaving for the possibility that experimenters may have “missed a critical period for interactions.” For example, these associations may have been more important in development and thus different expression patterns would be prominent in younger organisms.

These are all avenues that could lead to further experimentation. To date, the molecular mechanisms of how different bacterial associations in organisms may affect host physiology are still somewhat unknown. While these results were not what was expected, researchers now know that is is not a direct effect on gut gene expression that is responsible for changes based on microbe composition.

by: Miranda Hurtado

While rare, mitochondrial diseases can often be deadly for those who inherit them. Recent research has focused on finding ways to cure these diseases or to eliminate them altogether. One noteworthy milestone in this research is the birth of the world’s first “three parent baby” using MRT, mitochondrial replacement therapy.

This “three parent baby” contains DNA from three individuals. The father’s sperm remains intact during this process while the nucleus from the mother’s egg cell is extracted and inserted into a donor egg cell. This technique effectively replaces the mother’s mitochondrial DNA with the donor’s mitochondrial DNA. While the baby technically has DNA from three people, the baby’s physical features and traits are determined by nucleic DNA. The donor’s mitochondrial DNA contributes very little to the baby’s appearance or characteristics, other than the absence of a potential mitochondrial disease. Hence, there would be virtually no changes in the appearance of the baby due to this procedure. For women with a history of mitochondrial disease and a desire to become a mother, this procedure could prevent the development of the deadly illnesses in their children.

Although the birth of this child is certainly groundbreaking, MRT has not been studied extensively enough to be adopted and practiced regularly. It remains illegal to perform this procedure in many countries, including the United States, and only has recently become legal in the United Kingdom. Research on the mitochondrial genome is required to understand the potential risks involved in conducting MRT. Some of that research has taken place at UC San Francisco by Patrick O’Farrell, PhD.

Dr. O’Farrell is a professor at the department of Biochemistry and Biophysics at the University of California, San Francisco whose research lab focuses on the cell cycle and mitochondrial genome. In his lab’s latest publication in the June 2016 issue of Nature Genetics, titled “Selfish drive can trump function when animal mitochondrial genomes compete”, they found that closely related mitochondrial genomes have a better chance of being transmitted from mother to child. When mitochondrial genomes were not closely related, the introduced genome was not favored for transmission regardless if the other genome had a harmful mutation. O’Farrell refers to this mechanism as “selfish selection”.

These findings were discovered through a series of experiments involving mainly Drosophila melanogaster, otherwise known as the common fruit fly. In order to study the effects of competing mitochondrial genomes, flies containing a genome with a “temperature sensitive lethal mutation” were paired with related genomes and unrelated genomes. The related genomes share more DNA in common with the original genome than unrelated genomes do. Due to the mutation’s unique reaction to differing temperatures, fruit flies were observed while the temperature was varied and the mutation alternated between active and inactive. For the fruit flies that had a closely related genome inserted alongside the genome with the mutation, the genome with no mutation was successfully transmitted to future generations. Although the fruit flies with the unrelated genome were able to reproduce, it was observed that this particular lineage did not last beyond a few generations due to the lethal mutation being passed down. Interestingly enough, it was also noted that the changes in the temperature, particularly when the temperature was optimal for the mutation, did not affect the fruit fly’s ability to reproduce – it only affected the number of generations the flies were able to produce. Due to these observations, O’Farrell and his lab were able to conclude that selfish selection indeed occurs when mitochondrial genomes compete.

The paper is drawn to a close with the following quote:

 “To conclude, our findings show that competition between distantly related mitochondrial genomes can be dominated by the selfish drive of a genome rather than its contribution to the fitness of an organism. As a caution, the incompatibilities observed suggest that the success of planned efforts to treat mitochondrial diseases using mitochondrial donors may well depend on the competitive strength of the donor’s mitochondrial genome.”

Dr. O’Farrell directly acknowledges the importance of his research in terms of treating mitochondrial diseases and briefly mentions its implications and highlights another important aspect of the mitochondrial genome being transmitted. Genomes that are distantly related may successfully be passed onto progeny as long as they are “competitively strong” genomes. “There’s constant battles [among genomes] and the mitochondrial transmission represents a rather intense battle” says Dr. O’Farrell. He further explains that the strong genomes or “bully genomes” are usually the ones with mutations that allows the genome to transmit at a faster speed. These “bully genomes” then have the ability to wipe out the weaker genomes or “wimpy genomes.” Therefore, two things must be taken into consideration: the compatibility between genomes and their competitive strengths. Both these aspects are important to consider when analyzing and researching mitochondrial replacement therapy. 
While mitochondrial replacement therapy has both supporters and opponents, research in the scientific community continues to move forward. Although not of immediate application to the “three parent child” treatment , Dr. O’Farrell’s research contributes to the knowledge needed to further advance this technique. If MRT gains momentum and is backed by data that reaffirms its safety and sustainability, the number of people who are born with fatal mitochondrial diseases may drastically decrease over the next several years.

by: Jianne Jung

19,500,000 animals die every year from animal experiments for various purposes, including effectiveness test for medicines, safety tests for cosmetics, and toxicity testing of commercial chemicals. One of the most significant purposes of animal testing is preclinical drug analysis. All over-the-counter pills, like Advil and Tylenol, were proven to be safe based on a number of preclinical trials on animals. Although animals share some common physiological characteristics with humans, they are not 100% identical to the human body. So, how can the preclinical drug assessment be done more effectively? The Clark Lab at UC Berkeley has done research on modeling a chip-based microarray platform to perform a better toxicity screening of different chemical compounds on neural progenitor cells (NPC). As this platform can screen for over 500 different sets of living conditions for cells, it is a powerfully high-content, high-output screening method that demonstrates the potential of the chip-based cell screening as a promising preclinical drug characterization method.

Because of the inefficiency of in vivo preclinical drug testing using animals, there have been approaches to develop a progenitor/stem cell screening model. One of the commonly used cell screening models includes culturing matrigel-encapsulated stem cells on a culture plate called “six-well plate.” As the name suggests, it is a plate with six wells in which cells or tissues can be cultured. A disadvantage of using this plate for cell culture is that it only provides 2D environment for cells; when stem cells encapsulated by gel are put into the well, they stick to the bottom of the plate. A past study on stem cell culture by Barcelos-Hoff et al. concluded that 3D culturing is more similar to in vivo environment than 2D culture models, which may create significant differences from in vivo studies when used. The 3D microarray chip platform developed by the Clark Lab includes two chips: a pillar chip and a well chip. A well chip has microwells where different media can be loaded. A pillar chip has matrigel-encapsulated stem/progenitor cells, NPC in this particular study, on each pillar. The pillar chip is then “stamped” to the well chip so that cell colonies are immersed into cell media. This platform allows 3D screening of stem cells which is a promising alternative to 2D cell culture plate and animal experiments.

To prove that this platform can be implemented to toxicity screening, two steps were taken. The first step was a viability assay to prove that cells can actually be cultured using the platform inside the matrigel. The second step was to screen the NPCs cultured in various toxins to check the effects of each toxin on proliferation and differentiation rates of the NPCs. For on-chip viability assay, fluorescent live-cell dye was used to stain calcein, which gave a visual representation of live cells after being submerged in diverse media. Calcein fluorescence intensity increased over the time period from the day of culture. From this observation, it became clear that the NPCs proliferated as time passed from the moment they were cultured. Moreover, the fact that the NPCs were proliferating was a good indicator that the 3D microarray platform is, in fact, suitable for stem cell culture.

The next step was to utilize the 3D microarray platform for the purpose of toxicity screening. Upon confirmation that the platform works well for stem cell culture, on-chip cytotoxicity assay was performed to test the 3D model’s ability to screen for toxicity and its potential as a future system of drug characterization. In the experiment, the Clark lab cultured a chip-based microarray to screen human NPC. Initially, NPCs were cultured, and they were either differentiated or left as multipotent state, the state of cells where they can differentiate into their directed types. Then, on-chip cytotoxicity assay using different cell culture environments was done to those two groups of NPCs to compare each medium’s differing effects on cell viability on differentiated and undifferentiated cells.

While the animal models are not completely compatible with human physiology and are often expensive, this chip-based microarray model requires a minimum amount of reagent for screening. Using less reagent and compact design of the microarray platform makes it much more efficient to carry out stem cell screening experiments in terms of cost, time, and effort. Also, the platform allows experiments specific to human cells. The human-specificity of the platform could help people to get preclinically assessed more effectively with drug candidates. Furthermore, as the platform makes the preclinical trials of medicines highly cost-efficient, consumers can ultimately hope for lower prices for expensive medicines. Samuel Lim, a PhD candidate researcher at the Clark Lab, remarked that “the research team was inspired by thalidomide, which is a drug that treated nausea during pregnancy in the past and caused lots of birth defects because of the toxic effect it has for undifferentiated cells. It’s amazing how the development of such a high-throughput and highly efficient platform was motivated by the tragic past of thalidomide.” Lim also stated that “this research can partially replace the problem of a large number of animal deaths from animal testing.” Due to the highly human-specific platform mimicking in vivo environment of human cells, the medical researchers can expect fewer errors in their preclinical trials of certain medicines when using the microarray stem cell platform than testing the medicines in vivo with animals. According to Lim, the next step for the research is to reach out for funding from stakeholders, such as corporations that can benefit using the stem cell microarray platform, to apply this platform in real medical research.

by: Chelsey Rodriguez

In 1953, cognitive scientist Colin Cherry puzzled the world with what is known as the “Cocktail Party Effect.” This phenomenon questions how it is that we are able to focus on a particular sound in any given setting- such as a single conversation in a loud party. For at least a decade, scientists have speculated that specific neurons tune themselves so that we can focus on specific aspects of sound and ultimately detect speech. However, the mechanism used to extract meaning from noise is still unknown. A group of researchers at UC Berkeley’s Helen Wills Neuroscience Institute published their findings addressing this issue in Nature Communications in December 2016. Previous research theorizes that the brain makes assumptions of auditory information so that it does not have to perform more processing tasks than it needs. While this may be true, the Theunissen and Knight labs provided evidence in their publication that the human brain allows new auditory information to influence the way sounds are represented in the brain. In other words, not only does the brain use previous experiences with speech in order to make sense of sound, but it also becomes hypersensitive to new information so that it can easily mold prior auditory information stored in the brain.

Previous research has determined that in a specific region within the brain called the auditory cortex, neurons filter out noise from the environment in order to discriminate speech against non-speech. Moreover, there are different levels of “filters” that happen in the brain, and neuroscientists have posed the question, “do these different filters interact with one another?” This is important for understanding how auditory information is processed because it could help explain whether or not a person’s prior knowledge and experiences influence the information that is being passed throughout the brain. In particular, scientists are interested in figuring out whether or not a person’s internal state affects their perception of sounds present in reality. 

In this experiment, the researchers performed electrocorticography (ECoG) in epilepsy patients who already had pieces of their skulls removed and electrodes implanted. ECoG utilizes these electrodes to record electrical activity in the brain. During the actual experiment, the patients were directed to listen to a garbled sentence. Afterwards, they were asked if they could understand what was said in the soundtrack, which none of the patients were able to do. The second sound they heard was a clear version of the garbled sentence- after hearing this sentence, the patients affirmed they understood the noise. Finally, the participants were exposed to the exact same garbled sentence as before. After hearing the clear version, they were able to understand the nonsensical sentence. It was almost as if they could not avoid hearing the clear version. This auditory experiment is very similar to the face and vase illusion. When people first look at the picture, the viewer either sees a face or a vase- let’s assume a face in this example. When the opposite image, the vase, is pointed out to the viewer then the person will continue to see the vase no matter what; that is exactly what happened in this experiment. After the listener was introduced to the meaning of the garbled sentence, the listener continued to extract meaning from the sentence even when it didn’t make sense.

While the behavioral experiments were happening, the researchers were running ECoG recordings. During these recordings, Theunissen’s team was able to record from approximately 500,000 neurons in the auditory cortical area of the brain. After hearing the garbled sentence for the first time, there was not much neural activity in brain regions related to speech. However, after hearing the garbled sentence for a second time (following the clear version of the sentence), a different neural pattern emerged. More specifically, this new neural pattern closely resembled the neural activity recorded when the clear sentence was played. 

On the neural level, how can this be? Using a special mapping technique, the group was able to analyze the data and reveal that the brain was responding to traits of the clear sentence which were present in the garbled version. As well, they found that in order to decode speech effectively, the auditory cortex splits complex traits of sound into different levels of neurons. This split leads to various filters of spectro-temporal modulation, or pitch and frequency. This “Spectrotemporal Receptive Field is always there, and it’s plastic at the level of the auditory cortex” said co-author Frédéric Theunissen, a professor at UC Berkeley and member of Helen Wills Neuroscience Institute. This ever-occurring auditory modulation is what allows our brains to change the way it focuses on sound, and ultimately understand something as challenging as the garbled sentence for the second time. Thus, the researchers were able to conclude that neurons in the auditory cortex tune themselves in order to understand speech-like sounds after being introduced to new information related to language. By doing this, the brain can induce enhancement in the understanding of degraded speech signals. The tuning also allows the brain to focus on relevant information and ignore the rest that’s present in a person’s environment.

By understanding how the brain decodes auditory information, researchers and product developers can create speech devices that carry out the same processes. “If we understand not only at the periphery level but also centrally, we can provide information to the brain so that it can reconstruct the signal,” said Theunissen. These kinds of devices can then help improve speech impediments in populations of patients who may need help with constructing those sound signals. Professor Theunissen believes that “this kind of research could help alleviate issues with deafness by leading to improved designs of hearing aids.” In addition, tools used for speech recognition, such as Siri, can greatly improve with the knowledge gained in experiments such as those done in the Theunissen lab.

by: Brenda Martinez

There comes a time when some people start forgetting their meaning in life. Not only are they affected by this problem, but the families are as well. In a study done in the American Journal of Geriatric Psychiatry, published in January 10, 2017, stated that “patients with dementia with Lewy bodies often experience visual hallucinations”. This creates problems for both the patient and caregiver. Many caregivers forget to take care of themselves because they spend most of their time invested in their loved ones – developing bad sleeping habits, depression, or other illnesses. Family members such as grandchildren struggle to understand what exactly is happening. Additionally, many established daily routines are easily manipulated when someone in the family suffers from Lewy bodies because they require significant time investment. John-Paul Taylor and his team conducted several experiments at Harvard University on a small group of individuals to discover why people who suffer from Dementia with Lewy bodies (DLB) struggle with visual hallucinations. 

People with Lewy bodies are difficult to care for because they go through a wide array of emotions, and it is uncertain when they will act out. Every case of Lewy bodies is different and though people can research how to help their loved ones, the solutions they find may not work for their specific case. In addition, DLB is a disease that many doctors have trouble diagnosing.  Lewy bodies are proteins that are found in the brainstem, affecting the dopamine neurotransmitter, which leads to Parkinson-like symptoms. Though this disease is hard to diagnose, as it may take more than a year or two for symptoms of DLB disease to appear in a patient, it is very common. DLB is an umbrella term that refers to Parkinson’s disease dementia, as well as dementia with Lewy bodies. Parkinson’s disease is caused by a lack of dopamine which in turns affect various brain functions. This disease takes a long time to diagnose and people suffering it may live for a very long time thereafter. Though Parkinson’s dementia and dementia with Lewy bodies are two different diseases, they both affect the brain in a similar manner. For instance, one of the brain chemicals, acetylcholine, weakens and begins to inactivate, which can affect perception and behavior. 

Though the actual causes for these DLB hallucinations are still unknown, researchers have realized that, because the superior colliculus, a region in the midbrain that can be affected by Lewy bodies, is important for the visual system, it may responsible for the visual hallucinations brought on by Lewy bodies. There are two forms of Lewy bodies: a pure form and a mixed form which incorporates changes throughout the brain tissue. Those with pure form DLB only have symptoms associated with DLB and no other disease. The mixed form, which is most common, is where DLB symptoms become associated with Alzheimer’s or Parkinson’s Disease.  Along with the Lewy body proteins, patients with DLB have an unknown protein called alpha-synuclein. Alpha-synuclein causes a misfolding of a layer of the brain, resulting in aggregation. 60-80% of people with DLB will experience visual hallucinations that are caused by alpha-synuclein and its associated brain tissue misfolding. Many have complex visual hallucinations, changing the way they perceive the world – including how they perceive animals, people, and faces. Afflicted individuals often cannot recognize familiar faces or even perceive a person because all they see is a pixelated face. Subsequently, many patients with DLB become very aggravated and lose their sense of self. 

John-Paul Taylor and his team compared people with Alzheimer’s to people with DLB in an attempt to solve the mystery of the different neuropathological conditions the brain forms in different patients. Both Alzheimer’s and DLB consist of memory problems. The key difference between the two is that Alzheimer’s deals with memory loss, whereas DLB deals more with movement impairments and visual hallucinations, along with memory loss, as well. They chose to study Alzheimer’s and DLB because DLB and Parkinson’s are too similar. The focus of the study was to identify neurodegenerative changes that may be the cause of hallucinations in DLB patients. 

They tested 13 elderly postmortem patients and compared them to 10 postmortem Alzheimer’s patients, and 10 postmortem DLB patients. According to the methods outlined in the paper, they compared the different brain tissues through quantitative neuropathological methods. At the autopsy, the midbrain was dissected from the cerebrum. They also tested for brain density and whether or not age affected any lesions of the brain. Neuronal and glial cells were counted from every layer in the brain.

Their findings suggested that there were no differences in the different layers of the brain. They did find some, but not enough, evidence differentiating the two pathologies, since the sample size was small. When comparing neuronal densities, they found that only Alzheimer’s showed a density reduction, when compared to the control. Though the cause is not clear as to what exactly is happening in the brain when visual hallucinations occur, these scientists are one step closer to solving the problem. As a result of this experiment, it is now known that alpha-synuclein plays an important role in visual hallucinations. These new findings may make it easier for future research to be done on both the brain overall, as well as those specifically with dementia with Lewy bodies, which could ultimately lead to harnessing enough understanding to create a treatment for DLB.

Erskine, Daniel, Alan J. Thomas, John-Paul Taylor, Michael A. Savage, Johannes Attems, Ian G. Mckeith, Christopher M. Morris, and Ahmad A. Khundakar. “Neuronal Loss and Α-Synuclein Pathology in the Superior Colliculus and Its Relationship to Visual Hallucinations in Dementia with Lewy Bodies.” The American Journal of Geriatric Psychiatry (2017): n. pag. Web.