Publisher Health

A new study led by researchers from Florida International University (FIU) reveals a mechanism linking the pesticide DDT to Alzheimer’s disease.
Published in Environmental Health Perspectives, the study shows how the persistent environmental pollutant DDT causes increased amounts of toxic amyloid beta, which form the characteristic amyloid plaques found in the brains of those with Alzheimer’s disease.
According to Jason Richardson, professor at FIU’s Robert Stempel College of Public Health & Social Work and corresponding author, the study further demonstrates that DDT is an environmental risk factor for Alzheimer’s disease. In 2014, he led a team of scientists at Rutgers University, Emory University, and UT Southwestern Medical School who presented evidence linking DDT to the disease. Now, they have data demonstrating a mechanism that may explain the association.
“The vast majority of research on the disease has been on genetics — and genetics are very important — but the genes that actually cause the disease are very rare,” Richardson says. “Environmental risk factors like exposure to DDT are modifiable. So, if we understand how DDT affects the brain, then perhaps we could target those mechanisms and help the people who have been highly exposed.”
DDT was extensively used between the 1940s and 1970s to combat insect-borne diseases like malaria and treat crop and livestock production. People highly exposed to DDT back then are now beginning or already in the range of ages with a higher risk for developing Alzheimer’s disease. Although banned in the U.S., DDT exposure is likely possible today from legacy contamination or imported foods.
The study focused on sodium channels, which the nervous system uses to communicate between brain cells (neurons), as the potential mechanism. DDT causes these channels to remain open, leading to increased firing of neurons and increased release of amyloid-beta peptides. In the study, researchers demonstrate that if neurons are treated with tetrodotoxin, a compound that blocks sodium channels in the brain, the increased production of the amyloid precursor protein and toxic amyloid-beta species is prevented.
“This finding could potentially provide a roadmap to future therapies for people highly exposed to DDT,” Richardson says.
The study was done in collaboration with Rutgers University.
Researchers used cultured cells, transgenic flies, and mice models to demonstrate DDT’s effect on the amyloid pathway, a hallmark of Alzheimer’s disease.
By exposing all the models to DDT — in the range of what people were exposed to decades ago — researchers observed an increase in the production of the amyloid precursor protein, as well as elevated levels of toxic amyloid species, such as amyloid-beta peptides, and plaques.
“We found that if we block sodium channels with the compound tetrodotoxin and then dose neurons with DDT, then they don’t increase the amyloid precursor protein and don’t secrete excess amyloid-beta,” Richardson says.
The next step for the researchers will be to test therapeutic drugs using the information they now know. Richardson shares that there already are several drugs that target sodium channels. “We are in the process of doing those studies to see if we can take an already FDA-approved drug and see if it reduces toxic amyloid accumulation,” he adds.
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Materials provided by Florida International University. Original written by Stephanie Rendon. Note: Content may be edited for style and length.

A pioneering genomic surveillance study has provided the clearest picture yet of the arms race between Streptococcus pneumoniae, the bacterium responsible for a range of illnesses such as pneumonia and meningitis, and the vaccines designed to protect against the most dominant types. A strain called GPSC10 was found to be a particular threat, due to its increased virulence, ability to transform its structure to evade vaccines and its resistance to several common antibiotics.
The study, published today (16 August) in Lancet Microbe, was led by the Wellcome Sanger Institute, National Reference Center for Pneumococci, France, and Hospital Sant Joan de Deu, Spain, as part of the Global Pneumococcal Sequencing (GPS) project. The findings demonstrate the value of genomic surveillance to inform vaccine design and highlight the challenge posed by ‘shapeshifting’ strains like GPSC10.
Streptococcus pneumoniae, also known as the pneumococcus, is a bacterial pathogen that causes diseases ranging from ear infections through to pneumonia, septicaemia and meningitis. It is responsible for around nine million global infections annually, with elderly adults and children particularly susceptible. More than 300,000 children die from pneumococcal infection each year, mainly in low- and middle-income countries (LMICs)1.
Since 2000, a series of pneumococcal conjugate vaccines (PCVs) have been deployed that have targeted S. pneumoniae serotypes responsible for most disease cases in infants2, resulting in a reduction in disease worldwide. Currently, PCV-13 targets 13 serotypes and PCVs targeting up to 25 serotypes are in development. However, there are more than 100 distinct serotypes, and they can affect children and adults in different ways. Knowing which serotypes to target with the PCVs, and what the likely impact will be on disease and the wider pneumococcal population, is vitally important when designing effective global vaccination strategies.
Through the work of the GPS project since 2011, a picture of the S. pneumoniae serotypes in circulation has been built up that allows trends in the bacterial population to be identified. One serotype, 24F, has been on the rise, as documented by the National Reference Center for Pneumococci, France and many other countries such as Canada, Denmark, Germany, Israel, Italy, Japan, Lebanon, Norway, Spain, and UK.
In this new study, scientists from the Wellcome Sanger Institute performed whole-genome sequencing on 419 samples of S. pneumoniae serotype 24F, collected from individuals in France between 2003 and 2018 by the National Reference Center for Pneumococci (NRCP) and Association Clinique et Therapeutique Infantile du Val-de-Marne (ACTIV), and on 91 pneumococcal serotype 24F isolates collected from individuals in Spain by the Hospital Sant Joan de Deu. To provide a global comparison, an international collection of other S. pneumoniae genomeswere added from the Global Pneumococcal Sequencing (GPS) project database.

Unless cures are found, Alzheimer’s dementia is projected to affect nearly 13 million Americans by 2050 — overwhelming families, caregivers and our healthcare system. Yet only one new therapeutic, aducanumab, has come to market in the past 20 years, and therapeutic progress remains hampered for several reasons: recruiting study participants in clinical trials for Alzheimer’s is more challenging than other disease areas, the trials take longer to complete and they are more costly. A significant increase in the number of qualified volunteers from diverse backgrounds will be needed in the coming years for clinical trials for Alzheimer’s to be successful.
To develop solutions to overcome some of the steepest barriers to recruitment, the USC Schaeffer Center for Health Policy & Economics and the Alzheimer’s Therapeutic Research Institute (ATRI) joined with Gates Ventures to convene more than 35 experts from across the private and public sectors. The advisory panel was chaired by Julie Zissimopoulos, Paul Aisen and Jessica Langbaum. A paper published in Alzheimer’s & Dementia identifies actionable and inclusive solutions to accelerate the development of novel therapies for Alzheimer’s disease that resulted from the panel.
“The steepest barriers to more efficient Alzheimer’s clinical trials are those that are keeping potential volunteers from ever participating in the first place,” says Zissimopoulos, co-director of the Aging and Cognition Program at the Schaeffer Center. “Reducing these barriers to support progress on Alzheimer’s treatments — even modest progress — would have a profound impact on the communities affected by this disease.”
Barriers Limit Access
“There is no one answer,” says Aisen, who directs ATRI and oversees many clinical trials. “These issues must be addressed from various angles. Recruitment, however, is the major bottleneck.”
Current models prevent approximately 99% of eligible volunteers from being referred to or considering trial enrollment. Black and Latino populations are especially underrepresented, even though they face higher risks of Alzheimer’s disease than white Americans.

Scientists from the Department of Traumatology and Acute Critical Medicine at the Osaka University Graduate School of Medicine developed an AI algorithm to predict the risk of mortality for patients suffering a major injury. Using the Japan Trauma Data Bank for the years 2013 to 2017, they were able to obtain records for over 70,000 patients who had experienced blunt-force trauma, which allowed the researchers to identify critical factors that could guide treatment strategies more precisely.
Trauma doctors in emergency rooms must make life-and-death decisions quickly, and often with very limited information. Part of the challenge is that the factors that would indicate the likelihood of adverse clinical outcomes are not completely understood, and sometimes the body’s own inflammatory and blood clotting changes in response to major injuries do more harm than good. A more rigorous and comprehensive approach to trauma care is clearly needed.
Now, a team of researchers from the Osaka University Graduate School of Medicine have analyzed a database of all trauma cases recorded in Japan using machine learning algorithms. This included patient information, such as age and type of injury. In addition, mass spectrometry and proteome analysis were performed on serum from trauma patients at the hospital in Osaka. This provided more specific information on blood markers that could indicate an increase or decrease of specific proteins. “Our study has important clinical implications. It can help identify the patients at highest risk who may benefit most from early intervention,” says first author Jotaro Tachino.
The team used a hierarchical clustering analysis on the data and found that 11 variables were most correlated with an increased mortality rate, which included the type and severity of the injury. In addition, they saw that patients at highest risk often exhibited excessive inflammation or even an acute inflammatory response. They also found protein markers that signaled downregulated coagulation strongly associated with negative outcomes.
“The method that we used for this project can also be extended to the development of new treatment strategies and therapeutic agents for other medical conditions for which large datasets are available,” says senior author Hiroshi Ogura. This work may greatly optimize the allocation of scarce ER healthcare resources to save more people. The team also hopes that this research might help shed light on ways to help calm the inflammation pathways that can run out of control in the wake of traumatic injuries.
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Materials provided by Osaka University. Note: Content may be edited for style and length.

Contact hypersensitivity (CHS), commonly known as contact dermatitis, is an itchy rash that develops when certain substances come in direct contact with the skin. Usually, it is the result of an allergic reaction and can make patients feel uncomfortable. Common substances such as perfumes, household chemicals, and accessories can trigger itchy rashes from contact dermatitis. Although common, the underlying physiological mechanisms that trigger CHS remain elusive.
Recently, a research team from Fujita Health University School of Medicine, Japan, has been able to shed light on the precise molecular mechanisms that trigger CHS. The group had previously shown that genetic mutations in the interleukin (IL)36RN gene, which is responsible for the synthesis of the protein interleukin-36 receptor antagonist (or IL-36Ra), may result in enhanced CHS. They also observed that the mutations led to the increased formation of neutrophil extracellular traps (NETs), which are mesh-like structures of DNA and proteins released by neutrophils to capture pathogens.However, the immunological pathophysiology of NETs in CHS remained unclear.
On two previous occasions, the research team successfully established links between IL-36Ra and psoriatic lesions as well as between IL-36Ra and wound healing. The same team has now been able to dive in deep to further explore the underlying mechanisms. Their study was recently published in Scientific Reports (published on Aug 4, 2022) and shows that NETs could be a potential therapeutic target for CHS. The lead author, Dr. Yurie Hasegawa, a graduate student at the Fujita Health University School of Medicine, along with co-authors Dr. Yohei Iwata and Prof. Kazumitsu Sugiura, together demonstrated that NETs play a prominent role in the CHS response in the presence of a high number of inflammatory cells like CD4+ and CD8+ T-cells. “NETs may also exacerbate immune reactions in CHS. Therefore, the inhibition of NET formation may be a new therapeutic strategy in contact dermatitis,” explains Dr. Hasegawa about the rationale of their study.
To test their hypothesis, the team evaluated NET formation in Il36rn-/- mutant mice as well as wild-type mice under the influence of CHS-responsive CD4+ and CD8+ T cells. They first tested the effects of Cl-amidine on the CHS response in the mutant and wild-type mice and found that the number of infiltrating inflammatory cells and area of NETs decreased in both mice types.
Histopathology and cell assays confirmed that the mutant mice had considerably more macrophages and CD4+ and CD8+ T cells than the wild-type mice. Moreover, they demonstrated elevated levels of inflammatory cytokines like IL-1, CXCL1, CXCL2, IL-17A, tumor necrosis factor-α, and IL-36. Interestingly, there were striking differences in IFN-γ and CXCL1 levels between Cl-amidine-treated mutant mice and untreated wild-type mice, but not in the levels of inflammatory cytokines.
They next used the immunofluorescence staining to show that the mutant mice had more NETs in their ear tissues than the wild-type mice. However, treating mice with Cl-amidine — an inhibitor that suppresses the formation of NETs — resulted in a decreased CHS response, suggesting that NETs could be a potential therapeutic target for CHS.
Thrilled by their findings, the team is looking forward to further exploring the connections between NET formation and CHS treatment. Dr. Hasegawa explains, “Our study is the first to suggest the involvement of NETs in the immune responses in CHS. All our findings collectively indicate that the blockade of NET formation by Cl-amidine may be a potential treatment approach for allergic contact dermatitis.”
Let’s hope that their discovery facilitates the development of novel therapeutics for the safe and effective treatment of contact dermatitis.
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Materials provided by Fujita Health University. Note: Content may be edited for style and length.

Over three million people are infected with the hepatitis E virus every year. So far, no effective treatment is available. An international team has investigated which factors are important for the virus in the course of its replication cycle and how it manages to maintain the infection. The researchers analysed various mutations of the virus and found changes that may allow the virus to trick the immune system. The team from the Department for Molecular and Medical Virology at Ruhr-Universität Bochum led by Dr. Toni Luise Meister, Dr. Daniel Todt and Professor Eike Steinmann reports in the journal PNAS of 15 August 2022.
Advantages and disadvantages of mutations
Antibodies are an important defence mechanism against viral infections in our body. They specifically bind mostly to surface proteins of viruses to render it harmless. But, viruses have developed strategies to evade this neutralisation. During an infection with the hepatitis E virus, random mutations often give rise to virus variants that can coexist within an infected person. The antiviral agent Ribavirin, which many chronically infected patients receive, can even increase the formation of such variants.
The research team took a closer look at eight capsid protein variants from samples of chronically infected patients treated with ribavirin in the laboratory. The team wanted to know: Do the genetic changes bring advantages or disadvantaged for the virus? Do they influence the virus’ ability to replicate or its infectivity?
“While seven of the investigated mutations behaved exactly like the wild type virus, we found differences in one mutant,” reports Toni Luise Meister. This mutation affects the capsid protein, which is essential for packaging the viral particles. “The viruses with this mutation are assembled incorrectly, are probably smaller than the wild type virus, and the capsid protein does not accumulate in the cell,” describes Daniel Todt. These particles are not infectious, but are correctly recognised and bound by antibodies of the immune system. “This could be an advantage for the virus. These defective particles could potentially catch antibodies, so that there are no longer enough to neutralise correctly assembled, infectious virus particles,” speculates Eike Steinmann.
Hepatitis E
The hepatitis E virus (HEV) is the main cause of acute viral hepatitis. Around 70,000 people die from the disease every year. After the first documented epidemic outbreak in 1955 to 1956, more than 50 years passed before researchers took a closer look at the issue. Acute infections usually heal on their own in individuals with an intact immune system. In patients with reduced or suppressed immune systems, such as organ transplant recipients or HIV-infected patients, HEV can become chronic. HEV is also particularly threatening for pregnant women.
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Materials provided by Ruhr-University Bochum. Original written by Meike Drießen. Note: Content may be edited for style and length.

Motion analysis of video recorded on a smartphone accurately detected narrowed arteries in the neck, which are a risk factor for stroke, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
Fatty deposits (plaque) can accumulate in arteries causing them to narrow (stenosis). Narrowed arteries in the carotid artery (in the neck) can cause an ischemic stroke, which occurs when a vessel that supplies blood to the brain is obstructed by a clot. Nearly 87% of all strokes are ischemic strokes.
“Between 2% and 5% of strokes each year occur in people with no symptoms, so better and earlier detection of stroke risk is needed,” said lead study author Hsien-Li Kao, M.D., an interventional cardiologist at National Taiwan University Hospital in Taipei, Taiwan.
“This was an exciting ‘eureka’ moment for us,” Kao said. “Existing diagnostic methods — ultrasound, CT and MRI — require screening with specialized medical imaging equipment and personnel. Analysis of video recorded on a smartphone is non-invasive and easy to perform, so it may provide an opportunity to increase screening. Though more research and development are needed, the recordings and motion analysis may be able to be implemented remotely, or a downloadable app may even be feasible.”
Arteries in the neck are just beneath the skin’s surface and changes in the velocity and pattern of blood flow through them are reflected in the motion of the overlying skin, Kao explained. However, these differences are too subtle to be detected by the naked eye.
This study, conducted between 2016 and 2019, used motion magnification and pixel analysis to detect the minute changes in pulse characteristics on the skin’s surface captured in a smartphone video recording.
A group of 202 Taiwanese adults (average age of 68 years; roughly 79% men) who received care at a single Taiwanese hospital participated in the study. Among the participants, 54% had significant carotid artery stenosis, meaning they had at least 50% blockage that was previously diagnosed by ultrasound, while 46% did not have significant stenosis. Recordings were captured with participants laying on their back, with their head tilted back in a custom-made box that minimized outside movement. An Apple iPhone 6, 64GB, was mounted to the box to capture a 30-second video recording of the person’s neck. The older generation phone was used as researchers believed it would be more common to the average user, Kao explained.
Researchers found that the video motion analysis algorithm had an 87% accuracy rate of detecting stenosis in the group known to have carotid artery stenosis. All study participants also had standard Doppler ultrasound testing to confirm narrowing in their arteries and to gauge and validate the estimates from the video motion analysis.
“More research is needed to determine whether video recorded on smartphones is a promising approach to help expedite and increase stroke screening,” Kao said. “Carotid artery stenosis is silent until a stroke happens. With this method, clinicians may be able to record a video of the patient’s neck with a smartphone, upload the videos for analysis and receive a report within five minutes. The early detection of carotid artery stenosis may improve patient outcomes.”
There were several limitations to the study including the small number of study participants, all of whom were considered at high risk for a cardiovascular event. In addition, neck length and neck angle were not analyzed, which may affect the results of the video analysis. Skin color is not likely to hinder applications to a broader population since a standard lighting method was used for this assessment, according to Kao.
The study was funded by the Ministry of Science and Technology in Taiwan.
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Materials provided by American Heart Association. Note: Content may be edited for style and length.

Completely unexpectedly, the enzyme ceramidase emerges as a new target structure for the therapy of SARS-CoV-2 infections. This is reported by Würzburg researchers in the journal Cells.
Fluoxetine, a common antidepressant, inhibits the SARS-CoV-2 coronavirus in cell cultures and in preparations from human lung tissue. This was demonstrated by researchers at Julius-Maximilians-Universität (JMU) Würzburg in the summer of 2020. However, the mechanism of this inhibition was utterly unclear, so the teams continued their research.
To this end, they developed the molecule AKS466, which is very similar to fluoxetine and also suppresses coronavirus. After extensive comparative studies published in the scientific journal Cells, it is now clear how the antidepressant inhibits the replication of the coronaviruses.
Excess of ceramides inhibits the SARS-CoV-2
Fluoxetine, as well as AKS466, trap the viruses in the lysosomes of the cell. Put simply; these are small vesicles in which digestive processes take place. In the lysosomes, both active substances also suppress the activity of an enzyme group, the acid ceramidases. This increases the concentration of ceramides, a group of the body’s lipids. The excess of ceramides is ultimately responsible for preventing the SARS-CoV-2 coronavirus from reproducing.
“The enzyme ceramidase is a new, completely unexpected target structure for antiviral therapy,” says Professor Jochen Bodem from the JMU Institute of Virology and Immunobiology. His group collaborated on this project with the teams of JMU professors Jürgen Seibel (Organic Chemistry) and Markus Sauer (Biotechnology and Biophysics) intensively. The work was funded by the pharmaceutical company Novartis and the Free State of Bavaria.
Consequences for therapy research
The new findings are significant for the fight against SARS-CoV-2.
On the one hand, ceramides could be directly suitable as active agents against the virus.
On the other hand, the fluoxetine-like molecule AKS466 might be superior to the original. This is because fluoxetine inhibits the enzyme group of acid sphingomyelinases, leading to side effects when used. AKS466 does not inhibit these enzymes — it should have fewer adverse side effects.
Thus, the Würzburg researchers are showing two new ways that could lead to an improved therapy of SARS-CoV-2 infections. Next, they would like to clarify the question of how the two active substances manage to trap coronaviruses in the lysosomes.
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Materials provided by University of Würzburg. Original written by Robert Emmerich. Note: Content may be edited for style and length.

Researchers at Tel Aviv University have developed a method that employs musical tests and a portable instrument for measuring brain activity to detect cognitive decline in old age. According to the researchers, the method, which is based on the measurement of 15 minutes of electrical activity in the brain while performing simple musical tasks, can be easily implemented by any staff member in any clinic, without requiring special training.
The researchers: “Our method enables routine monitoring and early detection of cognitive decline in order to provide treatment and prevent rapid, severe deterioration. Prophylactic tests of this kind are commonly accepted for a variety of physiological problems such as diabetes, high blood pressure or breast cancer; however, to date no method has yet been developed to enable routine, accessible monitoring of the brain for cognitive issues.” The researchers further note that tests of this kind are particularly important in light of increasing longevity and associated growth of the elderly population.
The study was led at Tel Aviv University by PhD student Neta Maimon from the School of Psychological Sciences and the Buchmann-Mehta School of Music, and Lior Molcho from Neurosteer Ltd, headed by Prof. Nathan Intrator from the Blavatnik School of Computer Science and the Sagol School of Neuroscience. Other participants included: Adi Sasson, Sarit Rabinowitz, and Noa Regev-Plotnick from the Dorot-Netanya Geriatric Medical Center. The article was published in the journal Frontiers in Aging Neuroscience.
As part of the study, the researchers developed a groundbreaking method combining a portable device for the measurement and innovative analysis of electroencephalography (EEG), developed by Neurosteer, and a short musical test of about 12-15 minutes, developed by Neta Maimon. During the test, the subject is connected to the portable EEG device by means of a adhesive band with only three electrodes attached to the forehead. The subject performs a series of musical-cognitive tasks according to audible instructions given automatically through earphones. The tasks include short melodies played by different instruments, with the subjects instructed to perform various tasks on them at varying levels of difficulty. For example, pressing a button each time any melody is played or pressing it only when the violin plays. In addition, the test includes several minutes of musically guided meditation designed to bring the brain to a resting state, as this state is known to indicate cerebral functioning in various situations.
Neta Maimon, who specializes in musical cognition, explains that music has great influence on different centers in the brain. On the one hand, music is known to be a quick mood stimulant, particularly of positive emotion. On the other hand, in different situations, music can be cognitively challenging, activating the frontal parts of the brain, especially if we try to concentrate on different aspects of the music, and at the same time perform a particular task.
According to Maimon, if we combine these two capabilities, we can create cognitive tests that are quite complex, yet also pleasant and easy to perform. Furthermore, music that is positive and reasonably rhythmic will enhance concentration and performance of the task. Thus, for example, the famous “Mozart effect,” showing improved performance on intelligence tests after listening to Mozart’s music, actually has nothing to do with Mozart’s music, but rather the fact that music creates a positive mood and stimulates us to a state that is optimal for performing intelligence and creativity tests.
Accordingly, the researchers hypothesized that with musical tools, it would also be possible to challenge the subjects to an extent that would enable testing of the brain’s frontal activity as well as raising their spirits, thus enhancing their performance on the test while the overall experience is pleasant.
The study included an experiment at the Dorot-Netanya Geriatric Medical Center. Neta Maimon: “Anyone hospitalized at Dorot, or any other geriatric rehabilitation institution, undergoes a standard test called “mini-mental,” designed to evaluate their cognitive condition as a routine part of the intake process. The test is conducted by an occupational therapist specially trained for it, and includes a variety of tasks. For example, enumerating the days of the week or months of the year backwards. In this test, up to 30 points can be accrued. A high score indicates normal cognition.
The experiment included the testing of 50 elderly people hospitalized at Dorot who scored 18-30 on the mini-mental test, indicating various levels of cognitive functioning. The participants performed the musical-cognitive tasks, administered automatically. The EEG device registered the electrical activity in the brain during the activity, with the results analyzed using machine learning technology. This allowed mathematical indices to be identified that were precisely correlated with the mini-mental test scores; in other words, we obtained new neuro-markers (brain markers) that may stand alone as indices of the subject’s cognitive status.
Maimon adds: “We have actually succeeded in illustrating that music is indeed an effective tool for measuring brain activity. The brain activity and response times to tasks correlated to the subjects’ cerebral conditions (correlating to the mini-mental score assigned to them). More importantly, all those who underwent the experiment reported that, on the one hand, it challenged the brain, but on the other it was very pleasant to perform.”
The researchers conclude: “Our method enables the monitoring of cognitive capability and detection of cognitive decline already in the early stages. all by simple and accessible means, with a quick and easy test that can be conducted in any clinic. This method is of special importance today due to the increase in longevity and accelerated population growth, particularly among the elderly. Today, millions of people around the world already suffer or are liable to suffer soon from cognitive decline and its dire consequences, and their number will only increase in the coming decades. Our method could pave the way towards efficient cognitive monitoring of the general population, and thus detect cognitive decline in its early stages, when treatment and prevention of severe decline are possible. It is therefore expected to improve the quality of life of millions around the world.”
Keren Primor Cohen, CEO, Ramot at TAU: “We are pleased that a company based on a technology developed at TAU continues its collaboration on creative and multidisciplinary research. Ramot will continue to promote and invest in novel technologies, as well as help TAU researchers to maximize their research’s potential.”

Researchers at Lund University in Sweden have developed a new method for studying age-related brain disorders. The researchers have focused on the neurodegenerative disorder Huntington’s disease and the results have now been published in the journal Brain.
Basic medical research often faces the challenge of developing disease models that correspond to specific disease mechanisms or the disease to be studied. This is a challenge that needs to be solved in order to produce new effective treatments. One example of a disease that is difficult to model for an understanding of the underlying mechanisms is Huntington’s disease. In part, this is due to the difficulty in recreating adequate animal or cellular models.
By reprogramming skin cells into neurons, Johan Jakobsson and his research group have been able to study Huntington’s disease in an innovative way that he believes could be significant for successful studies of several age-related brain disorders.
“We took skin biopsies from patients living with Huntington’s disease and reprogrammed the skin biopsies into neurons. We then compared these neurons with reprogrammed neurons from healthy people. The results are very interesting. We have found several defects that explain some of the disease mechanisms in neurons from patients with Huntington’s disease. Among other things, we observed that neurons from patients with Huntington’s disease show problems in breaking down and recycling a particular kind of protein — which can lead to a lack of energy in these cells,” says Johan Jakobsson, professor of neuroscience at Lund University.
The researchers have also measured the biological age of the cells and observed that the reprogrammed neurons retain their biological age, which is significant if they are to be used for research in the new model system.
“One very important component in our new model system is the age of the neurons. It is possible to measure a cell’s ‘biological age’, which we have done, and these cells retain their true biological age. In other words, the reprogrammed neurons are old, making the model system relevant in the study of other age-related neurodegenerative disorders such as Parkinson’s and Alzheimer’s,” says Johan Jakobsson.
Huntington’s disease is fatal, and scientists are yet to find any treatment or cure.
“We believe our model will provide answers and clues that are significantly more relevant for the disease than the clues obtained from animal studies, and that in the long term it will lead to breakthroughs for some form of treatment,” says Johan Jakobsson.
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Materials provided by Lund University. Note: Content may be edited for style and length.