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#apoe4
bpod-bpod · 1 year
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Flimsy Protection
APOE is a protein that carries fat in the blood. There are different genetic versions of APOE, and people who inherit one or two copies of the APOε4 (APOE4) form have a higher risk of developing Alzheimer’s disease than people with other forms of the protein, such as APOε3 (APOE3). How a fat-carrying protein contributes to brain problems has been a mystery, but scientists recently found a clue. The brain’s neurons are coated with a fatty substance called myelin, which both protects the cells and enables their high-speed firing. Studies of postmortem brains show people with APOE4 (bottom row) have less myelin (dark staining) than people with APOE3 (top row), suggesting the APOE4 neurons may be more prone to failure and degeneration. In mice, scientists have been able to fix APOE4’s shortcomings – improving neuronal myelination and the animals’ learning and memory – providing a glimmer of hope for future clinical intervention.
Written by Ruth Williams
Image from work by Joel W. Blanchard, Leyla Anne Akay, Jose Davila-Velderrain and Djuna von Maydell, and colleagues
Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, USA
Image copyright held by the original authors
Research published in Nature, November 2022
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jillypilgrim · 1 year
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11.17.22_ brilliant work by CWRU professor and researcher, irena pikuleva highlights cholesterol's role in APOE and alzheimers.
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mindblowingscience · 2 months
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Mice reach the twilight of their lives at around age two, the rough equivalent of 80 in human years. And when researchers introduce specific mutations into mice and then age them up, the mice can grow forgetful and irritable—eventually exhibiting signs of Alzheimer’s disease not unlike that of many elderly humans. “Older mice, and those with the APOE4 variant, have these exhausted, fatigued immune cells in their brains, and we discovered a similar phenomenon in human datasets,” says Sohail Tavazoie, a professor at Rockefeller University.
Continue Reading.
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thetimelordbatgirl · 1 year
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I think what doomed the MCU quality-wise was deciding to leave it open-ended and keep going. Continuity and characterizations don't stand a chance when there's no endgame in mind. Pun somewhat intended. Endgame wasn't a good movie but it took Phase 4 for a lot of people, myself included, to realize that. I think Endgame's legacy - and the MCU's for that matter - would be a lot more favorable if that movie HAD been the actual endgame.
That's an on-going point really against the current MCU: Endgame had been set up basically as the finale of Phases 1-3, meaning it feels like a perfect conclusion to everything that had been set up...but of course, cause the MCU refuses to end, even Endgame sets up stuff that we see in Phase 4, Loki being a obvious example, but instead of going back to his whole, "The sun will shine on us again." thing to Thor in Infinity War, we just...go into a Loki show in Phase 4 that in itself is just setting up Kang. And then you got the Gamora thing the movie set up that...doesn't even seem to be getting explored in the new Guardians movie as she's already with them again, as even Love And Thunder showed Thor leaving the guardians at least to do his own thing again.
And with the mention of Love And Thunder: 'Thor will return.'- again, they very confident that they'll give Thor another movie that they didn't even tell the director or Chris Hemsworth who as we know, has decided to take a break from acting due to wanting to spend time with his family after discovering he has two APOE4 Genes, making him ten times likely to develop Alzheimer's disease. Like I will point out: Disney couldn't predict this, but the fact remains that they refuse to just plan stuff out before going ahead, meaning they jumped instantly to 'Thor will return' in the same phase that already has various open endings to plots to come, with I think only WandaVision's open ending concluding....in the train wreck that was Multiverse Of Madness that in itself has ANOTHER open ending.
And yes, I know they claim to now have two plans, aka Multiverse stuff and Kang plans, but here's the thing: they entered Phase 4 by that logic with zero plans beyond doing random crap with open endings, because they couldn't just take a break to do planning so they set up random stuff we may either get or may not get. Like, if they really wanted to continue the MCU so badly after Endgame, they should have just rebooted at best or waited to do planning, as now we in a mess that's quality is showing as we see with the reactions to No Way Home, Multiverse Of Madness, Love And Thunder and now Ant Man And The Wasp: Quantumania (which is literally meant to start off the planned phase 5 too ironically).
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Sabias QUE?
Chris Hemsworth revela que tiene alta probabilidad genética de padecer Alzhéimer
Chris Hemsworth está descubriendo muchas cosas de sí mismo durante el rodaje de “Limitless”, el documental que protagoniza para National Geographic y que tiene como objetivo explorar el verdadero potencial del ser humano.
Hace unos días confesaba sus sensaciones tras llevar a cabo un ayuno de cuatro días, un período sin comer que le llevó a pensar que se estaba “volviendo loco”.
Pero ahora las noticias son aún peores, y es que el popular actor que da vida a “Thor” en las películas de Marvel ha descubierto que tiene un mayor riesgo de sufrir la enfermedad de Alzhéimer.
El esposo de la actriz española Elsa Pataky se sometió a un exhaustivo examen genético para ver qué podía esperar en el futuro y las pruebas descubrieron en su ADN dos copias del gen APOE4, uno de su madre y otro de su padre. Éste está relacionado con un mayor riesgo de sufrir la enfermedad, e impactado por la noticia, ha anunciado el asunto públicamente y ha mostrado su temor por el deterioro que el Alzhéimer podría causar en su cuerpo, asegurando incluso que su “memoria está empeorando”, aunque no tiene del todo claro que no sea “un efecto placebo”.
“Creo que mi próxima aventura podría ser el final, pero no se basa en nada que nadie me haya dicho en Marvel ni en ningún tipo de plan. Creo que todo es cuestión del nacimiento de un héroe, de su viaje y de su eventual partida. ¿Estoy ya en esa etapa? No sé, ¿quién sabe?”.
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Limitless with Chris Hemsworth en Disney+
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meret118 · 1 year
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“His makeup includes two copies of the gene APOE4, one from his mother, the other from his father, which studies have linked to an increased risk of Alzheimer’s disease.”
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desertsanpedro · 6 days
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Medical News Today: "When they did this, there was a “strong increase” in lipid droplet accumulation, which was particularly pronounced in the presence of APOE4."…is this condition caused by SAD (Standard American Diet) of sugar / carbs resulting in a high level of blood insulin all day long?? We know the SAD has resulted in an epidemic of metabolic disease and diabetes!!
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rnomics · 1 month
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IJMS, Vol. 25, Pages 2409: A Cross-Sectional Study of Protein Changes Associated with Dementia in Non-Obese Weight Matched Women with and without Polycystic Ovary Syndrome
Dysregulated Alzheimer’s disease (AD)-associated protein expression is reported in polycystic ovary syndrome (PCOS), paralleling the expression reported in type 2 diabetes (T2D). We hypothesized, however, that these proteins would not differ between women with non-obese and non-insulin resistant PCOS compared to matched control subjects. We measured plasma amyloid-related proteins levels (Amyloid-precursor protein (APP), alpha-synuclein (SNCA), amyloid P-component (APCS), Pappalysin (PAPPA), Microtubule-associated protein tau (MAPT), apolipoprotein E (apoE), apoE2, apoE3, apoE4, Serum amyloid A (SAA), Noggin (NOG) and apoA1) in weight and aged-matched non-obese PCOS (n = 24) and control (n = 24) women. Dementia-related proteins fibronectin (FN), FN1.3, FN1.4, Von Willebrand factor (VWF) and extracellular matrix protein 1 (ECM1) were also measured. Protein levels were determined by Slow Off-rate Modified #aptamer (SOMA)-scan plasma protein measurement. Only APCS differed between groups, being elevated in non-obese PCOS women (p = 0.03) relative to the non-obese control women. This differed markedly from the elevated APP, APCS, ApoE, FN, FN1.3, FN1.4 and VWF reported in obese women with PCOS. Non-obese, non-insulin resistant PCOS subjects have a lower AD-associated protein pattern risk profile versus obese insulin resistant PCOS women, and are not dissimilar to non-obese controls, indicating that lifestyle management to maintain optimal body weight could be beneficial to reduce the long-term AD-risk in women with PCOS. https://www.mdpi.com/1422-0067/25/4/2409?utm_source=dlvr.it&utm_medium=tumblr
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syscyber · 2 months
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Promising discovery for Alzheimer's treatment
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The findings were published on 8 Jan 2024 in Communications Biology and include discoveries of a druggable target and a drug candidate, made by Meenakshisundaram Balasubramaniam, Ph.D., the paper’s first author.
An estimated 50-65% of people with Alzheimer’s disease have inherited the Alzheimer’s gene, Apolipoprotein E4 (APOEε4), from one or both parents. About 25% of people have one copy of APOEε4 and are three times as likely to develop the disease. Those with two copies (one from each parent) make up 2-3% of the population and are 12-15 times as likely to develop Alzheimer’s.
Balasubramaniam, co-principal investigator on the NIH grant with Griffin, said UAMS built the first known full-length structure of APOEε4 protein in 2017, which he created using bioinformatics and computational modeling techniques. This foundational work led to the discovery of the druggable site on the APOEε4 protein, ApoE4. (APOEε4 refers to the gene, and ApoE4, without the epsilon symbol and no italics, is the protein.)
Balasubramaniam’s unique skills and curiosity, Griffin said, were the catalyst for the discoveries. “I don’t know of anyone else in the world but Dr. Balasubramaniam who can do the work that’s in this paper,” Griffin said of the assistant professor and Inglewood Scholar in the Department of Geriatrics.
Other research team members listed in the USMS article.
UAMS
Related story: The Despair of Persons Living With Alzheimer’s Disease by Jason Karlawish at The History Reader
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jhavelikes · 2 months
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Microglia, the immune cells of the brain, wither away as Alzheimer’s disease takes hold in both mice and humans, and APOE4, a key gene variant implicated in Alzheimer’s, may mediate these changes, according to new research. Mice reach the twilight of their lives at around age two, the rough equivalent of 80 in human years. And when researchers introduce specific mutations into mice and then age them up, the mice can grow forgetful and irritable—eventually exhibiting signs of Alzheimer’s disease not unlike that of many elderly humans. “Older mice, and those with the APOE4 variant, have these exhausted, fatigued immune cells in their brains, and we discovered a similar phenomenon in human datasets,” says Sohail Tavazoie, a professor at Rockefeller University. The team dubbed this new class of exhausted cells TIM, for terminally inflammatory microglia. TIM have lost the ability to efficiently remove plaque from the brain and thus may contribute to Alzheimer’s.
Burnt out immune cells may drive Alzheimer's disease - Futurity
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bpod-bpod · 1 year
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Risk Regions
In the brains of Alzheimer’s disease patients, protein clumps accumulate – in the form of amyloid plaques and tau tangles – leading to neurodegeneration. Certain regions of the brain are more susceptible to this pathology than others, but why? Recent research based on brain scans of hundreds of middle-aged and older volunteers, suggests it’s something to do with regional differences in the activation of a protein called APOE. Indeed, these heat maps show areas of the brain where APOE is especially active (top row, orange and red areas), and where tau tangles are especially abundant (bottom row, orange and red areas) – note the striking overlap. APOE is a fat-handling protein, and a specific version of it – APOE ε4 – is associated with increased risk for Alzheimer’s. While questions about the disease mechanism remain, the finding of this APOE-pathology link provides a piece of the puzzle that will likely inform future research and interventions.
Written by Ruth Williams
Image by Diana Hobbs, Washington University
Research by Aylin Dincer and colleagues, Mallinckrodt Institute of Radiology, Washington University School of Medicine, Saint Louis, MO, USA
Image copyright held by Diana Hobbs
Research published in Science Translational Medicine, November 2022
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pc7ooo-ru · 2 months
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Испанские ученые нашли связь между болезнью Альцгеймера и атеросклерозом
Мутация гена APOE4, связанная с болезнью Альцгеймера, также ускоряет развитие атеросклероза, утверждают ученые из испанского Национального центра исследований сердца и сосудов. Открытие обнаружено в ходе анализа данных мониторингового проекта PESA, в рамках которого более 4 тыс. испанцев были подвергнуты всестороннему наблюдению за состоянием их кровеносной системы.
Подробнее на https://7ooo.ru/group/2024/01/24/893-ispanskie-uchenye-nashli-svyaz-mezhdu-boleznyu-alcgeymera-i-aterosklerozom-grss-276150864.html
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omagazineparis · 2 months
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Chris Hemsworth et Elsa Pataky : histoire d'amour en montagnes russes
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Vous connaissez le célèbre acteur Chris Hemsworth et la ravissante Elsa Pataky, mais connaissez-vous l'histoire tumultueuse de leur relation ? Découvrez leur parcours amoureux, leurs hauts et leurs bas, dans cet article captivant. L'inoubliable première rencontre Chris Hemsworth et Elsa Pataky se sont rencontrés pour la première fois en 2010, grâce à l'agent de talent de Chris. Leur première apparition sur tapis rouge a eu lieu en septembre 2010, lors du Gala d'ouverture du Pavillon Resnick au Los Angeles Museum of Art. " Il n'y a pas eu de moment de révélation ", a déclaré Chris lors d'une interview en 2020. " Dès la première fois où nous nous sommes rencontrés, nous nous sommes simplement compris. Elle est amusante, extravertie, a de l'humour et une attitude passionnée envers la vie, ce qui est agréable à suivre." Les cloches du mariage Quelques mois seulement après avoir officialisé leur relation, Chris et Elsa se sont mariés lors d'une cérémonie discrète le 26 décembre 2010, dans le pays natal de Chris, l'Australie. " Tout s'est passé rapidement et cela semblait juste. Cela avait du sens ", a avoué Chris en 2016. " Il n'y avait pas de grand plan derrière tout ça, pour être honnête. Nous étions en vacances et nous nous sommes dit, 'Pourquoi ne nous marions-nous pas aussi ?' Il aurait peut-être dû y avoir plus de préparation, mais tout s'est bien passé." Bébé numéro 1 En janvier 2012, le couple a confirmé qu'ils attendaient leur premier enfant. Elsa a donné naissance à leur fille, India Rose, le 11 mai 2012. Le temps des jumeaux En janvier 2014, une autre annonce de grossesse excitante est venue, avec la confirmation que Elsa attendait des jumeaux. Elle a accouché de leurs jumeaux, Tristan et Sasha, le 18 mars 2014. Un déménagement en Australie Chris et Elsa ont vécu à Los Angeles pendant les premières années de leur mariage. En 2015, ils ont déménagé dans le pays natal de Chris, en Australie, s'installant sur la côte à Byron Bay. Ce déménagement a permis un mode de vie plus paisible et privé. "Il n'y a pas une seule personne avec qui j'interagis, ni d'amis proches à moi, qui soit vraiment dans l'industrie , et c'est donc extrêmement rafraîchissant", a partagé Chris en 2020. "C'est génial pour mes enfants et ma femme." Des moments d'incertitude En octobre 2016, un tabloïd australien a rapporté que le mariage de Chris et Elsa était en danger. Cependant, la star de Thor a mis fin aux spéculations avec un message plein d'humour sur Instagram. "À la recherche d'une nouvelle femme selon les médias trompeurs", a-t-il écrit. "Chérie, tu m'aimes toujours, n'est-ce pas ?!" Elsa a confirmé en écrivant, "Ahora y siempre ! Toujours et pour toujours !" Cependant, lors d'une interview en 2017, Chris a admis que tout n'était pas toujours parfait. "Ma femme et moi sommes tombés amoureux, avons eu des enfants, ne nous sommes pas vraiment vus pendant quelques années, puis nous sommes retombés amoureux", a-t-il partagé. Un anniversaire marquant Le couple a célébré 10 ans de mariage en 2020. "10 ans ensemble !", a jubilé Chris sur Instagram. "J'attends avec impatience les avancées de la médecine moderne et de la science, et de profiter encore de quelques centaines d'années !" A lire également : Taylor Swift : personnalité de l’année 2023 – une icône transcendante Un diagnostic qui change la vie En 2022, Chris a joué dans le documentaire de National Geographic, Limitless, et a découvert qu'il avait un risque plus élevé de développer la maladie d'Alzheimer car il avait hérité de deux copies du gène APOE4. Face aux craintes de Chris de ne pas pouvoir un jour reconnaître sa femme et ses enfants, Elsa a décidé de se transformer en une version plus âgée d'elle-même en utilisant des effets spéciaux de maquillage. La star australienne a déclaré que sa femme était "toujours belle". Des vies séparées Bien que Chris et Elsa aient commencé l'année 2023 avec des voyages au Kenya et en Espagne, les fans ont remarqué qu'ils semblaient passer moins de temps ensemble plus tard dans l'année. En octobre, le couple a pris des vacances séparées, Elsa emmenant les jumeaux au Japon et Chris passant du temps en Islande avec India. Puis, en novembre, Chris est allé à Abu Dhabi avec ses frères, tandis qu'Elsa volait en solo pour un événement sur le tapis rouge en Espagne. "L'état du mariage de Chris et Elsa est une énigme", a déclaré une source exclusivement à In Touch. "Les vacances séparées sont un gros signal d'alarme, mais ce n'est pas que ça. Ils restent très unis en tant que famille, mais ils se sont éloignés en tant que couple." Réunion de Noël Cependant, Chris et Elsa ont affiché un front uni pour les fêtes, passant Noël 2023 ensemble avec leurs proches en Australie. - Chris Hemsworth et Elsa Pataky sont-ils toujours ensemble ? - L'état actuel de leur relation reste incertain, mais ils ont passé Noël 2023 ensemble en Australie. - Combien d'enfants ont-ils ensemble ? - Chris et Elsa ont trois enfants : India Rose et des jumeaux, Tristan et Sasha. - Pourquoi Chris Hemsworth et Elsa Pataky ont-ils déménagé en Australie ? - Ils ont déménagé pour vivre une vie plus paisible et privée, loin de l'industrie du divertissement. - Chris Hemsworth a-t-il des préoccupations concernant la maladie d'Alzheimer ? - Oui, il a découvert qu'il était à risque élevé de développer la maladie d'Alzheimer en 2022. - Comment Chris et Elsa se sont-ils rencontrés pour la première fois ? - Ils ont été présentés l'un à l'autre par l'agent de talent de Chris en 2010. Dans cette histoire d'amour en montagnes russes, Chris Hemsworth et Elsa Pataky nous montrent que même les couples célèbres ont leurs hauts et leurs bas. Leur voyage continue, et nous les suivons avec attention. Read the full article
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superturtleenemy · 4 months
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APOE4 gene trigger🤢
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sbgridconsortium · 4 months
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Structure of Equity - Jamaine Davis - Meharry Medical College
Sharing some of our #SBGrid member tales from the last year. This one from September 2022.
Numbers speak clearly to Jamaine Davis. As a boy growing up on Long Island, math came so easy to him that one of his family nicknames was "the professor."
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Other numbers have shaped his ambitions at Meharry Medical College in Nashville, Tennessee, where Davis runs one of the few labs in the world that uses structural biology to help explain biological health disparities.
For example, U.S. Black adults are twice as likely to have Alzheimer's disease compared to non-Hispanic Whites. And despite a somewhat lower overall lifetime risk of breast cancer, Black women experience a 40% higher death rate from breast cancer than White women at every age and are more likely to be diagnosed with fast growing and late-stage breast cancer.
"My research program is basically at the intersection of structural biology, genetics and disease, and health disparities," says Davis of the big-picture questions that guide his lab's work. "What are the molecular mechanisms that dictate who develops diseases like cancer or Alzheimer's? And then how do we design effective therapies? How do we target the right pathways for the right treatment for that patient?"
One project in the early stages focuses on a gene (ABACA7) that has a stronger effect on risk of Alzheimer's disease in Blacks than the better known ApoE4 gene risk variant. "It's actually the strongest risk factor for developing Alzheimer's in African Americans known so far," Davis says.
As he explains it, ABACA7 transports lipids out of cells, handing off the lipids directly to ApoE, and also interacts with Tau, another protein that goes awry in Alzheimer's. Two missense variants in ABACA7 confer the risk.
"So we've been studying these mutations to see what impact they have on lipid transport," Davis says. "Once we're done, we can look at the people who particularly carry this mutation or variant, see what downstream processes are altered, and design therapies to rescue that. And these variants so far have only been identified in African Americans."
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In individuals with African ancestry, the phospholipid-transporting ATPase ABCA7 (ABCA7) gene has stronger associations with Alzheimer’s disease risk than in individuals with European ancestry and than the apolipoprotein E (APOE) ɛ4 allele. The Davis lab is exploring the structure and function of key ABACA7 mutations and how they contribute to alterations in transporting lipids, which may influence Alzheimer’s in African Americans. Credit: Courtesy of J.Davis.
Davis began his academic training on a different career path. With his early affinity for math and science, he reasoned that chemical engineering made sense as a college major. But near graduation at Drexel University, he realized that the typical next step for someone with a chemical engineering degree was a job at an oil company. He hadn't taken one biology course in college, but he found himself drawn to biomedical research instead.
He seized an opportunity to work in a biophysics lab at a neighboring school, University of Pennsylvania, where his mentor Jacqueline Tanaka gave him a peek at the scientific career he could have in biophysics and opened his eyes to the kind of academic role model he could be. Her excitement for X-ray crystallography and for increasing the proportion of women and minorities in science inspired him to go to graduate school.
"She built her career in structural biology and mentoring, hand in hand," Davis says. "She saw some potential in me, and I was at a crossroads." Davis had also been unaware of the extent of health inequities across the country and of the low representation of minorities in academia.
For his thesis, Davis chose the lab of Harvey Rubin, a dynamic speaker who fostered an immediate interest in infectious disease. In Rubin's lab, Davis characterized an enzyme that enables Mycobacterium tuberculosis to enter (and possibly exit) the dormancy stage in the lungs of people.
When Davis finished his PhD in 2007, he was the first Black to earn a doctorate in biochemistry and molecular biophysics at UPenn. "I had a great time," he says. "They were very supportive. But it is pretty shocking. If you look at Twitter, there are other people posting the same kind of statistic. They're the first Black to graduate from a certain program at a certain institution. It does show there is still some under-representation across different departments."
He followed up with two postdoctoral fellowships at the National Cancer Institute. He first showed that a novel protein in Shigella (bacteria that cause food poisoning) was not a protease, as some suspected. A second project elucidated the binding modes of a protein with multiple domain repeats implicated in the development of cancer.
Then he thought about how best to combine his interests in a distinctive research program. He chose Meharry, one of the oldest and largest historically black U.S. academic health centers. (Davis is also a member of the Vanderbilt University Center for Structural Biology.)
Historically black colleges and universities are powerhouses in educating African Americans who go on to earn doctoral degrees in science, technology, engineering, math, and medicine, as Davis and his co-authors reviewed in a commentary (Cell, 2022). Blacks make up 12% of the U.S. workforce, but only 5% of working physicians and 3.6% of full-time faculty conducting research at medical schools.
When the COVID-19 pandemic hit, Davis found new opportunities for mentorship and community outreach. Soon after the pandemic took hold, a student-driven community formed on Twitter with the handle @BlackInBiophys and a logo designed by Taneisha Gillyard, a former postdoc in the Davis lab. Davis spoke at a virtual meeting held by the group.
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A former postdoc in the Davis lab, Taneisha Gillyard, designed the logo for @BlackInBiophys, a student-driven community that formed on Twitter during the pandemic. Credit: Taneisha Gillyard.
In a short time, a strong sense of community developed among people who may have never met in person, but know a lot more about each other through social media, Davis says. People share grant writing tips, training and job opportunities, and generally celebrate the scientists, their contributions, and career options for the next generation.
The visibility may help change other statistics about Black researchers receiving less NIH funding and being cited less often than their white colleagues, Davis says.
Davis also teamed up with Meharry colleague Jennifer Cunningham-Erves to develop a funded community outreach project to address community concerns about vaccines. He has spoken about the basic science of mRNA at townhall-style community meetings, in person and virtual. The online recordings have reached people from Chicago to New York to Haiti.
The project collaborates with a consortium of more than 90 churches in middle Tennessee and Better Options TN, a community nonprofit organization. To understand concerns, the Meharry team interviewed people in the Southern United States. They developed and organized content on a frequently updated web site, https://yourcovidvaxfacts.com/en.
"We asked about their thoughts about the vaccine and the virus," Davis says. "The biggest one, particularly for Black Americans, was the distrust with government and healthcare. But I was very impressed with some of the questions that the public had. They weren't getting answers, and they wanted answers. If you remember, one of the major issues with people not getting a vaccine was that they thought it would affect their DNA. They just weren't familiar with mRNA."
Davis felt their concerns and trust issues as well. He initially was cautious about being vaccinated himself, waiting to see more data about its safety in people. "Even being a scientist, I was hesitant," he says. "I didn't want to be one of the first," he says. But as he explained the science and helped alleviate concerns of others, he also convinced himself to get the vaccine too.
Meanwhile, back in the lab after the pandemic disruptions, Davis and his team are working to improve health outcomes for populations most at risk, one variant protein and pathway at a time.
- Carol Cruzon Morton
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jcmarchi · 4 months
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Center Maps New Path for Alzheimer’s Prevention and Treatment - Technology Org
New Post has been published on https://thedigitalinsider.com/center-maps-new-path-for-alzheimers-prevention-and-treatment-technology-org/
Center Maps New Path for Alzheimer’s Prevention and Treatment - Technology Org
The new brain center will focus on research translating genetic, metabolic and molecular insights into interventions that protect those at risk before brain changes set in.
The medical community can foresee a looming increase in Alzheimer’s disease, the most common form of dementia, as the population ages. The number of Americans affected is projected to nearly triple by 2050, from 6 million to 16 million.
Although the Food and Drug Administration has approved a couple of treatments for early disease designed to slow progression, the injury to brain tissue that strikes at memory — and at patients’ very identity — seems irreversible.
Brain, neural networks – artistic interpretation. Image credit: Growtika via Unsplash, free license
Researchers at the Keck School of Medicine of USC are determined to gain a deeper understanding of factors underlying Alzheimer’s and use what they find to intercede, decades before damage sets in. Driving this work is a new interdisciplinary program, the USC Center for Personalized Brain Health.
The starting place for the center’s work is a relatively common genetic variant, called APOE4. The one in four people who carry one copy of the gene are at higher risk for Alzheimer’s. Compared to the general population, the 2 or 3% of people who have two copies face eight to 12 times the risk for the disease. More than half of Alzheimer’s patients have the APOE4 gene.
“USC has a really rich ecosystem … The new center will bring together diverse investigators and providers with a unified vision — a future in which Alzheimer’s disease is no longer a serious threat.”
“Most people with APOE4 don’t get neurological attention until they have dementia,” said endocrinologist Hussein Yassine, MD, director of the Center for Personalized Brain Health and associate professor of neurology, medicine and physiology and neuroscience at the Keck School of Medicine. “Our center is going to provide resources to these individuals well before they get the disease, in hope that this may be the right time to intervene.”
The center’s central projects comprise building a registry of APOE4 carriers, imaging the brain for early detection and intervention, developing interventions (such as diet and exercise) that can be deployed for prevention, profiling Alzheimer’s-related changes that precede clinical symptoms, and developing drugs focused on neuroinflammation once clinical dementia ensues.
“Alzheimer’s disease is one of the biggest challenges we face in human health,” said Carolyn Meltzer, MD, dean of the Keck School, May S. and John H. Hooval, M.D., Dean’s Chair and professor of radiology. “Taking it on calls for research that is both creative and rigorous, backed by enabling resources. That combination makes the Center for Personalized Brain Health an exciting vehicle for the Keck School to ignite lasting change in dementia research and care while advancing precision medicine.”
A connection between basic science and clinical impact for Alzheimer’s disease
Yassine and his colleagues have already uncovered details about the mechanisms behind Alzheimer’s disease and its progression. The Center for Personalized Brain Health will channel these insights into a larger-scale endeavor linking lab findings to clinical care, and vice versa.
According to Yassine, that translational focus fulfills a complementary role alongside existing infrastructure at the Keck School and the university overall: The USC Zilkha Neurogenetic Institute pursues basic discovery, and the USC Mark and Mary Stevens Neuroimaging and Informatics Institute identifies the changes dementia causes in the brain. Meanwhile, there are outstanding resources for clinical research at the USC Alzheimer’s Therapeutic Research Institute and the USC Alzheimer Disease Research Center.
“USC has a really rich ecosystem,” Yassine said. “The new center will unite diverse investigators and providers with a unified vision — a future in which Alzheimer’s disease is no longer a serious threat.”
Indeed, the Center for Personalized Brain Health’s interdisciplinary efforts will integrate expertise in genetics, neuroscience, neuropsychology, computer science, radiology, pharmacy and nutrition in order to break ground, and provide help, on numerous fronts.
Following the clues from gene to potential Alzheimer’s prevention
APOE4 is a version of a gene that encodes a protein that helps the body transport and use certain fats and oils. Exploring the connection between metabolism and brain health drew Yassine to zero in on omega-3 fatty acids and their role in the brain’s self-maintenance system among those with APOE4 decades before the onset of clinical disease.
A 2017 imaging study of APOE4 carriers aged 35 showed that their brains were hungry for omega-3s. That change appears years before damage begins accumulating and decades before the typical onset of Alzheimer’s disease symptoms. In this difference, Yassine saw the potential for prevention and launched the PreventE4 trial to test whether starting omega-3s early in people with APOE4 can slow down disease progression.
Identifying APOE4 carriers showing subtle, early changes in their brain could yield new information about Alzheimer’s progression and — more importantly — inform interventions that lower risk.
So Yassine has teamed up with Kai Chen, PhD, associate professor of research radiology at the Keck School, to invent a new imaging technique that traces omega-3s in the brain. Bringing this probe forward from lab studies to human observation will be one major focus of the Center for Personalized Brain Health.
“We’ll be giving personalized advice, and we think that if we can start at 40 — instead of 60 or 65 — we’ll have a better chance at defeating Alzheimer’s disease.”
The center will also maintain a drug development program, with one promising lead currently under investigation. This search started with findings that the APOE4 dementia brain accelerates the breakdown of omega-3s in the brain, such that simply ingesting more doesn’t help.
Aiming to halt the breakdown process itself, Yassine teamed up with Vsevolod Katritch, PhD, associate professor of quantitative and computational biology and chemistry at USC Dornsife College and a member of the USC Michelson Center for Convergent Bioscience, to identify a new compound, called BRI-50054, that reversed omega-3 breakdown in lab studies.
Together with Stan Louie, PharmD, professor of clinical pharmacy at the USC Mann School of Pharmacy and Pharmaceutical Sciences, the team is planning to develop BRI-50054 into a drug for Alzheimer’s disease.
The Center for Personalized Brain Health brings together complementary expertise across USC schools to advance this compound and others in a pipeline of candidates for early medical intervention.
“It looks like we have to fix the wiring that’s destroying the omega-3s,” Yassine said, “and take action before it’s too late.”
In a third main element of activities at the Center for Personalized Brain Health, researchers will examine another possible early warning sign for Alzheimer’s disease in those with APOE4.
The same part of the brain that helps people navigate through the world, like internal GPS, is also the primary location stressed by being starved of omega-3 fatty acids. That detail suggests that detecting the deterioration of an APOE4 carrier’s ability to find their way around during middle-age might play into earlier diagnosis of Alzheimer’s.
Colleagues at the USC Viterbi School of Engineering and USC Schaeffer Center for Health Policy & Economics are contributing to a forthcoming Center for Personalized Brain Health project using sensors and wearable devices to spot a rise in navigation errors among people with APOE4 around the age of 50.
“There may be digital footprints that can tell us something is off,” Yassine said. “We want to see if we can capture those changes early and get information that will allow us to intervene.”
Feeding into all the above focus areas, the Center for Personalized Brain Health aims to build up a cohort of APOE4 carriers age 40 and above in the Los Angeles area.
This effort, dubbed USC GeneScreen, requires the completion of a short questionnaire and the return of a swab for testing to identify those with the gene. Ultimately, the Center for Personalized Brain Health aims to enlist 1,000 people with APOE4 to participate in research and, if they desire, receive personalized care from a dedicated clinic launching in 2024.
Depending on factors such as whether a person has one or two copies of the gene, recommendations could include a modified diet, regular exercise and avoiding activities that risk head trauma.
“People should know, if you’ve discovered you are an APOE4 carrier, you will have a place to go,” Yassine said. “We’ll be giving personalized advice, and we think that if we can start at 40 — instead of 60 or 65 — we’ll have a better chance at defeating Alzheimer’s disease.”
Source: USC
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