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Dermatology

Effective Therapies for Atopic Dermatitis: Expert Recommendations … – HealthDay

THURSDAY, Nov. 16, 2023 (HealthDay News) -- In updated guidelines issued by the American Academy of Dermatology and published online Nov. 7 in the Journal of the American Academy of Dermatology, recommendations are presented for use of phototherapy and systemic therapies for atopic dermatitis (AD) and include strong endorsements of monoclonal antibodies and Janus kinase inhibitors.

Dawn M. R. Davis, M.D., from the Mayo Clinic in Rochester, Minnesota, and colleagues conducted a systematic review and applied the Grading of Recommendations, Assessment, Development, and Evaluation approach for assessing the certainty of evidence and formulating and grading recommendations to provide evidence-based recommendations for use of phototherapy and systemic therapies for adults with AD.

The workgroup developed 11 recommendations on management of AD in adults. These include strong recommendations for dupilumab, tralokinumab, upadacitinib, abrocitinib, and baricitinib for adults with moderate-to-severe AD. Phototherapy is conditionally recommended for adults with AD. Methotrexate is also conditionally recommended, with proper monitoring, as is mycophenolate mofetil, azathioprine, and limited-term use of cyclosporine, all with proper monitoring. There is a conditional recommendation against use of systemic corticosteroids.

"When AD is more severe or refractory to topical treatment, advanced treatment with phototherapy or systemic medications can be considered," the authors write. "In this clinical practice guideline, we make strong recommendations for the use of dupilumab, tralokinumab, abrocitinib, baricitinib, and upadacitinib."

Several authors disclosed ties to the pharmaceutical industry.

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Dermatology

Nonablative Lasers Offer a Gentle Approach to Healthy Skin – Dermatology Times

In honor of National Healthy Skin Month, it is the perfect time to encourage patients to integrate gentle laser treatments into their yearly routine to maintain healthy, radiant skin.

In recent years, laser technology has undergone significant advancements, expanding the range of available lasers for various applications. Lasers are specifically designed to target different tissue typeswith water, hemoglobin, and pigment being the most common chromophores.1

Lasers come in2 categories: ablative and nonablative. Ablative lasers vaporize tissue at the level of the epidermis in a fractionated or fully ablative manner, which is a very effective technique for skin rejuvenation; however, increased downtime, infection risk, and persistent erythema are all potential adverse effects.

Nonablative lasers deliver less thermal injury and promote dermal wound healing while protecting the stratum corneum through precise penetrating waves and cooling mechanisms.2This process, known as photothermolysis, generates heat at the dermal level, stimulating collagen and elastin production and, in some cases, scar remodeling.1,3Nonablative fractional lasers (NAFLs) achieve this by using thousands of tiny, deep columns to deliver preciseheat levels.4

Nonablative lasers can also have specific targets, such as hemoglobin and pigment. Many of these devices are used to treat redness, photoaging, and unwanted tattoos with minimal downtime due to preservation of the skin barrier.2,5See theTable1,2for a comparison of both typesof lasers.

Skin cancer is the most prevalent cancer in the United States and that more than3 million Americans are diagnosed with nonmelanoma skin cancers each year.6Repeated exposure increases the risk of developing nonmelanoma skin cancers, such as basal cell carcinoma and squamous cell carcinoma. These2 types of cancer are collectively known as keratinocytecarcinoma (KC).

In individuals with a history of prior KC, the risk of developing subsequent KC remains a significant concern. This risk is particularly pronounced in the5 years following the initial diagnosis. For instance, within3 years post diagnosis, there is a 35% probability of developing another KC, and this risk escalates to as much as 50% within a 5-year period. Factors that contribute to an increased risk of KC include being male, being older than 60 years, having a history of multiple previous skin cancers, and having substantial actinic skin damage or skin that is prone to sunburn.7

According to the American Society for Dermatologic Surgery, even precancerous skin lesions such as actinic keratosis and actinic cheilitis have the ability to transform into squamous cell carcinoma.8There is, however, good news for those who already have sun-damaged skin and are looking to improve the overall health of their skin. A recent retrospective study conducted at the Massachusetts General Hospital Dermatology Laser and Cosmetic Center in Boston found that in patients treated with NAFLs for facial KCs, only 20.9% subsequently developed a KC, whereas the control group had a 40.4% rate of subsequent KC development. After accounting for age, gender, and skin type, individuals in the control group had a higher likelihood of developing new facial KC compared with patients who underwent laser treatment.9

In 2014, a study in theJournal of Cosmetic and Laser Therapyexamined a group of 10 female participants. These individuals, ranging in age from 35 to 53 years and with skin types I to IV, exhibited mild to moderate facial photodamage. This photodamage was characterized by various features, including hyperpigmentation, telangiectasia, skin laxity, skin roughness, and actinic keratosis. These individuals underwent a series of treatments using a nonablative fractional Q-switched 1064-nm Nd:YAG laser. The therapeutic regimen included4 sessions spaced at 2- to 4-week intervals, with follow-up assessments at1 and3 months after the final treatment session.

Baseline assessments using the Glogau scale revealed that6 participants were classified as type II (indicating wrinkles in motion), and4 participants were designated as type III (indicating wrinkles at rest). Impressively, at the 3-month follow-up after the final session, 60% of participants exhibited a notable 1-point or greater enhancement in their overall Glogau scale score. Moreover, it was observed during the study that the laser treatments resulted in substantial improvements in various skin irregularities: Hyperpigmentation decreased by 70%, telangiectasias by 80%, laxity by 80%, tactile roughness by 60%, and actinic keratoses by 60%. The investigators concluded that the nonablative fractional Q-switched 1064-nm Nd:YAG laser demonstrated both safety and efficacy in ameliorating mild to moderate photodamage with minimal downtime and discomfort and without any discernibleadverse effects.10

In a 2021 study published in the same journal, researchers investigated the safety and effectiveness of a 1565-nm NAFL for addressing facial photoaging. Patients underwent3 NAFL treatment sessions (1 month apart) on1 side of their face, and then the treated side was compared with the untreated side between sessions. The results showed significant improvements in facial skin laxity, wrinkles, and pores as well as reduced sagging of the nasolabial groove on the NAFL-treated side compared with the untreated side (baseline). Additionally, the study compared NAFL with microneedle fractional radiofrequency (MFR) and found similar outcomes for MFR-treated skin but that NAFL offered a more convenient treatment option due to itsshorter downtime.11

Nonablative lasers have emerged as a gentle yet highly effective approach to achieving healthier skin. They utilize precise photothermolysis to stimulate collagen and elastin production and promote dermal wound healing with minimal downtime. These lasers can reduce the development of KC and improve the overall health of sun-damaged skin. NAFLs have also demonstrated remarkable success in ameliorating photodamage and improving hyperpigmentation, telangiectasias, skin laxity, and tactile roughness.

In conclusion, nonablative lasers represent a promising solution for individuals seeking healthier and more youthful-looking skin with fewer associated risksand downtime.

Nina Venturaisa doctor of osteopathic medicine candidate and a master of health services administration candidate at Lake Erie College of Osteopathic Medicine in Elmira, New York.

Mara C. WeinsteinVelez, MD, FAAD, is a board-certified dermatologist and the director of cosmetic and laser dermatology at University of Rochester Medical School in New York.

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Nonablative Lasers Offer a Gentle Approach to Healthy Skin - Dermatology Times

Dermatology

Aging, Acne, and the Armamentarium: Hot Topics From the Science … – Dermatology Times

Im not a cosmetic dermatologist, but patients ask me all the time what they should be using. They come in with little pieces of paper, things that theyve ripped out of magazines. Is this good? Is that good? and I dont always know what to say. This conference allows me to learn more about these individual active ingredients, said Hilary E. Baldwin, MD, about the Science of Skincare Summit 2023 held in Austin, Texas. The scientific rigor of the meeting in discussing over the counter treatment options was especially helpful, noted Baldwin, who added, I think its very important for us all to be on the same page and be making soundscientific recommendations.

In addition to Baldwins insights,Dermatology TimesExpert Perspectivescustom video seriesalso features insights from Cheri N. Frey, MD; Adelaide A. Hebert, MD, FAAD; Kavita Mariwalla, MD, FAAD; Darrell S. Rigel, MD, MS; and Saranya P. Wyles,MD, PhD.

I think the future of skin care and care in general for our acne patients is very bright, Baldwin said. On the pharmaceutical side, we have new combination therapies. We have our first new triple combination therapy. We have even better formulations coming down the pipe, where we recognize that many of our acne medications can be quite irritating and that irritating medications dont get used.

Baldwin is optimistic about the future of acne care: probiotics, prebiotics, and postbiotics and their potential to manage acne using more natural means. Some companies, she said, are attempting to manufacture a subtype ofCutibacteriumacnes(formerly known asPropionibacterium acnes).

It would be a very natural approach, which would not be using antibiotics, Baldwin said. We wouldnt have to worry about antibiotic resistance, and I think its a possibility that we might be going there or in the future, or even [using] bacteriophages to kill theC acnes,as opposed to using an antibiotic todo that.

Hebert echoed interest in recent acne research and innovations.

We know in our skin of color patients, they tend to have postinflammatory hyperpigmentation as their acne lesions resolve, and weve learned that they have more inflammation within their acne lesions, and that results in the increased pigmentation, which persists considerably longer than their acne lesions, Hebert said.

Herbert also commented onC acnes. She is excited to learn more about its role in the driving inflammatory componentsof acne.

Acne appears to be developing in patients at a younger age, added Hebert, who is also a pediatric dermatologist. This may be due to estrogens in the food chain, among other causations, she said.

Fortunately, some of the new medications have been studied down to age 9, Hebert said. We are having an expanded understanding of acne in the younger age group, but were also developing therapies in that part of the age spectrum that can be beneficial to our patients.

Wyles was intrigued to see new hallmarks of aging emerge. DNA damage, oxidative stress, reactive oxygen species, and mitochondrial dysfunction contribute to skin aging.

If we look at an active retinaldehyde, they can affect that skin turnover and break apart those factors that are contributing to senescence and modify those, Wyles said. Were still early in trying to understand how those are affecting it, but its a new way of looking at skin care from anovel mechanism.

Both Wyles and Frey mentioned retinoids as cornerstones of the antiaging therapeutic armamentarium.

Weve been looking at new molecules, Frey said. How do we deliver efficacy in the way that retinoic acid or tretinoin can?... I think the science behind the new molecules that are coming out is really,really impressive.

Frey thinks everyone could benefit from retinoids, especially folks who live in sunny climates or have a history of skin cancers. We do have some evidence that retinoids help to prevent skin cancers and specifically those cellular changes that lead to pre-cancers and skin cancers, Frey said. It is probably a crime if a dermatologist doesnt recommend a retinoid for those patients because the benefits go beyond just anti-aging. They go beyond the surface. Were really talking about making an impact and preventing skin cancer in those patients.

Mariwalla described pre-aging as a new hot topic in dermatology. You cant prevent [aging] from occurring, but what you can do is modulate it, Mariwalla said. You can modulate your experience of it. You can modulate how your skin responds to it, and what were learning now is that aging isnt just somethingthats chronologic.

Rigel discussed the direct relationship between ultraviolet exposure and aging, noting that a lack of sun protection contributes significantly to the risk of skin cancer and accelerates the skin aging process. Fortunately, he noted that advances have been made in the field, especially for skin of color.

Previously patients complained about the sheen and how sun protection, Rigel said. The good news is that there are new products out there that really get rid of that problem... you can use it in a way to really make your skin protected and still look great, he explained. Thats basically what I say to them , and the fact is that they do adopt them. Most of my darker skinned patients really enjoyed having the tinted sunscreens to have the protection and stilllook great.

All6 experts were excited by the science and the advancement in the field, and appreciated the opportunity to come together to share and discuss research and practical implications. As Mariwalla said, One of the things thats great about the Science of Skin Care Summit is that you get to see whats on thehorizon.

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Aging, Acne, and the Armamentarium: Hot Topics From the Science ... - Dermatology Times

Dermatology

Prior Treatment Options and Outcomes for SD – MD Magazine

Transcript

Linda Stein Gold, MD: Now, Neal, Im going to come back to you for a minute because this is something that we havent talked about that much. When we look at our treatment armamentarium, where have we been?

Neal Bhatia, MD: Well, you mentioned how we all do trials. We all have to bring something to the market for some indication. Psoriasis and atopic dermatitis have been the popular flavors over the years, but to bring something truly to the market for seborrheic dermatitis has not been a goal not only of any project or product, but even [by] a lack of interest by the dermatology world. That being said, we can apply the mechanisms of action of the therapies we know work for those anti-inflammatory approaches and apply them to seborrheic dermatitis in a very similar way. But the more we have good trial data, the more we have good before and after pictures, the more patient-related outcomes, like weve seen with a couple of the trials that were going to talk about, the more we can impact that. Yes, weve been using ketoconazole shampoo, antifungals over the counter, hydrocortisone lotion, but again, its like throwing things at the mirror to see if they stick. But at the same time, we havent had really some dedicated treatments until a few years ago. We had a 510(k) device that had a really interesting approach. It had shea butter,vitis vinifera, gluconic acid, and lanolin; all of that, which was in a nice green base that really did work well. But unfortunately, that product isnt as commonly found as it was. The other part of it, again, and you touched on this, Linda, is about the patient perception. If they feel like theyre looking in the mirror and seeing dryness, they think theyre dirty, or someone looks at them as not really taking care of their hygiene, which is not fair. So we have to really get back to good counseling on fundamentals of cleansing and moisturizing, maybe going back to sulfacetamide cleansers like we used to, thinking about how long do we leave cleanser on, and how long do we leave shampoo on? These are things that patients really need some handholding to say, "Look, you need to let these shampoos sit for 5 minutes and then rinse." Youre not just treating your hair, but youre treating your whole head. Same with cleansing. They have to think about what they are using in the shower versus what are they using in the evening. So, all these little nuances, aside from the prescription products we use, the fundamentals of skin care have to be just as important.

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Prior Treatment Options and Outcomes for SD - MD Magazine

Neuropathology

Senolytics show promise in combating brain aging and COVID-19 … – News-Medical.Net

In a recent study published in the journal Nature Aging, an international team of researchers observed that senolytics can alleviate physiologic brain aging and coronavirus disease 2019 (COVID-19) neuropathology.Senolytics are a class of drugs that selectively target and eliminate senescent cells, which are cells that have stopped dividing and contribute to aging and age-related diseases.

Most COVID-19 patients often experience diverse neurologic complications. Further, autopsied brain tissue transcriptomic data suggest associations between severe COVID patients' cognitive decline and brain aging signatures. While recent reports implicate senescent cells in neurodegeneration and cognitive decline in aged mice and in vivo neuropathology models, their contribution to human brain tissue aging and COVID-19 pathology in the central nervous system remains unknown.

Study: Senolytic therapy alleviates physiological human brain aging and COVID-19 neuropathology. Image Credit:Jose Luis Calvo/ Shutterstock

In the present study, researchers tested the effects of senolytics on physiological brain aging and COVID-19 neuropathology. First, they generated human brain organoids (BOs) from embryonic stem cells and physiologically aged them for eight months. Subsequently, the BOs were treated with two doses of senolytics, such as the dasatinib-quercetin (D+Q) combination, ABT-737, and navitoclax, for one month at a two-week interval.

Senolytic interventions significantly reduced senescence-associated -galactosidase (SA--gal) activity, indicating the elimination of senescent cells. This was further confirmed by significantly higher levels of lamin B1 (a nuclear marker downregulated in senescence) in treated BOs. Next, the team investigated the cell types involved in senescence phenotypes by co-immunolabeling with a senescence marker (p16).

Over three-fourths of p16-positive cells coimmunostained with astrocytes (positive for glial fibrillary acidic protein), while approximately 15% co-localized with mature neurons (positive for neuronal nuclei antigen). These two brain cell populations represented a majority (> 90%) of p16-positive cells. The team found a significant reduction in senescent astrocyte populations following treatment, with the D+Q combination being the most potent. However, the effect of senolytics in reducing senescent neurons was less apparent.

RNA sequencing revealed the upregulation of lamin B1 messenger RNA (mRNA) levels across all senolytic treatments. Additionally, 81 senescence-related mRNAs were consistently suppressed with senolytic treatments. Further, aging clock predictions were performed based on whole-transcriptome sequencing. D+Q treatment of nine-month-old organoids returned their gene expression age to levels of eight-month-old organoids.

This phenotype was not observed with other tested senolytic interventions. D+Q treatment-induced changes in gene expression correlated with mammalian signatures of pro-longevity interventions, such as rapamycin administration and caloric restriction. Next, the team estimated the prevalence of senescent cells in the autopsied frontal cortex from the brains of age-matched patients who died due to severe COVID-19 or non-neurologic and non-infectious causes.

Brains of COVID-19 decedents showed over seven-fold increase in p16-positive cells than those from non-COVID-19 controls. Next, human BOs were exposed to different viral pathogens to examine how (neurotropic) viruses contribute to aging-induced neuropathology. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection was mainly detected in neurons, microglia, and neural progenitors.

Seven SARS-CoV-2 variants were also tested, and their senescence phenotypes were ranked by SA--gal activity. Most variants significantly increased SA--gal, but the Delta variant exhibited the most potent induction. Moreover, there was a distinctive colocalization of viral spike and SA--gal in Delta-infected BOs. Besides, a statistically higher induction of senescence was evident between organoids infected for five and 10 days.

Increased senescence observed at 10 days post-infection (dpi) relative to 5 dpi suggested that SARS-CoV-2 infection may have triggered secondary senescence. Interestingly, non-infected senescent cells were enriched within 150 m of infected senescent cells, supporting the putative bystander effect of infected cells in triggering secondary senescence. Senescence was also triggered by infection of BOs with Japanese encephalitis virus (JEV), Zika virus (ZIKV), or Rocio virus (ROCV).

The researchers examined the associations of transcriptomic changes between COVID-19 patients and SARS-CoV-2-infected BOs. Among nearly 1,600 genes with differential expression between infected and non-infected BOs, there were 485 differentially expressed genes in COVID-19 patients' brain samples. Notably, known senescence and aging pathways were enriched in this common gene set.

Long-term senolytic treatment prevents selective accumulation of senescent cells in physiologically aged human BOs.af, BOs were generated and grown in vitro for 8months and subsequently exposed to two doses (one every 2weeks) of either navitoclax (2.5M), ABT-737 (10M) or D+Q (D, 10M; Q, 25M) within the following month, after which organoids (n=814) were collected for in situ analysis.a, SA--gal assay was performed on organoid sections. Each data point in the bar graph represents a single organoid analyzed. Data presented as means.d.; at least eight individual organoids were analyzed per condition; one-way analysis of variance (ANOVA) with Tukeys multiple-comparison post hoc corrections.b, Lamin B1 staining was performed on organoid sections. Each data point in the scatter plot represents the integrated intensity of each cell within organoid sections. At least eight individual organoids were analyzed per condition; one-way ANOVA with Tukeys multiple-comparison post hoc corrections.c,d, Representative images from quantifications shown ina,b, respectively. Scale bar, 0.3mm.e, Representative immunofluorescent images of regions from organoids treated with the indicated senolytics and vehicle control. Samples were individually immunolabeled with antibodies against GFAP, Sox2 and NeuN and co-stained for p16. Arrows indicate coimmunoreactivity of NeuN and p16. Scale bar, 50m.f, Bar graphs showing colocalization quantification performed on organoid sections. Data presented as means.d.; three individual organoids were analyzed per condition; one-way ANOVA with Tukeys multiple-comparison post hoc corrections. a.u., arbitrary units.

Next, the team evaluated the impact of the selective elimination of senescent cells with senolytic interventions. Senolytics significantly reduced the number of BO cells with SA--gal activity five days after SARS-CoV-2 infection. Of note, the impact of senolytics was more prominent in BOs infected with the Delta variant, and senolytics reverted Delta variant-induced lamin B1 loss and p21 upregulation.

Pretreating BOs with senolytics before infection resulted in a significant reduction of virus-induced senescence. Layer 6 corticothalamic neurons and gamma-aminobutyric acid (GABA)ergic ganglionic eminence neurons were the two populations with significantly higher incidence of senescence following infection, and senolytic interventions prevented cellular senescence in these populations.

Finally, the researchers infected K18-hACE2 mice (that express the human angiotensin-converting enzyme 2 [hACE2] under the regulation of keratin 18 [K18] promoter) with SARS-CoV-2 Delta. Senolytics with blood-brain barrier permeability, such as D+Q, navitoclax, and fisetin, were administered 24 hours post-infection, with subsequent treatments every two days. Infected mice had shortened life spans, with a median survival of five days.

However, fisetin or D+Q treatment significantly improved survival. All control animals died by 10 dpi, whereas 13% of navitoclax-, 38% of D+Q-, and 22% of fisetin-treated mice were alive at 12 dpi (experimental endpoint). Senolytics, especially D+Q, caused a profound decrease in COVID-19-related features and significantly reduced viral gene expression in mice brains.

The brains of infected mice exhibited an increase in inflammatory senescence-associated secretory phenotype (SASP) and p16 senescence markers, and (all) senolytic treatments normalized senescence and SASP gene expression of infected animals to the levels observed in non-infected brains. Delta infection also caused a loss of dopaminergic neurons in the brainstem, with a concomitant increase in astrogliosis. However, recurrent administration of senolytics partially prevented the loss of dopaminergic neurons and abrogated the onset of astrogliosis.

Taken together, the study demonstrated that senescent cells accumulate in physiologically aged human BOs, with long-term senolytic intervention(s) substantially reducing cellular senescence and inflammation. Further, D+Q treatment uniquely induced anti-aging and pro-longevity gene expression changes in BOs.

Besides, COVID-19 patients' brains exhibit rapid accumulation of cellular senescence relative to age-matched controls. Neurotropic viruses (ROCV, JEV, and ZIKV) and SARS-CoV-2 can infect BOs and induce cellular senescence, and the SARS-CoV-2 Delta variant triggers the most potent induction of senescence. Short-term senolytic interventions could reduce SARS-CoV-2 gene expression in infected BOs and prevent senescence of GABAergic and corticothalamic neurons.

Notably, senolytics ameliorated COVID-19 neuropathology in infected K18-hACE2 mice, improved their survival and clinical score, and reduced SASP, senescence, and viral gene expression. Overall, the findings highlight the vital role of cellular senescence in brain aging, COVID-19, neuropathology, and the therapeutic impact of senolytics.

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Senolytics show promise in combating brain aging and COVID-19 ... - News-Medical.Net

Neuropathology

Startling discovery at Great Salt Lake could lead to damaging health … – FOX 13 News Utah

SALT LAKE CITY Scientists have revealed a startling discovery made at a lake bed of the Great Salt Lake that could potentially impact the health of many Utahns.

Samples of neurotoxins gathered from a dried up lake bed were so large they shocked scientists who have been studying them for years.

The air sample had a very large signal, one of the biggest I have seen and I was very worried, said Dr. Sandra Banack, senior scientist at Brain Chemistry Labs.

Banack said the toxins in a nonhuman primate can trigger the neuropathology of Alzheimer's disease and ALS. She and her colleagues are concerned about what an exposed lake bed means when wind picks up the toxins and people breathe them in.

What we don't want to see is the increased risk of ALS among citizens here in the Wasatch Front," explained Dr. Paul Alan Cox, Executive Director of Brain Chemistry Labs.

While the study shows an increase is possible, its hard to prove.

We're talking, you know, a disease that can take 10-20 years to manifest. It's not like you can just go out and say, 'yes, that is the cause,' said Dr. James Metcalf, a senior research fellow at Brain Chemistry Labs.

The study simply tells scientists they need to do more research.

And that may then give us links as to which people are vulnerable to the action of this toxin," said Metcalf, "whether it's contributing to an increased rate of disease and ultimately protect people.

In the meantime, its the unknown risks while Wasatch Front residents keep inhaling the air that worries scientists.

As scientists, we feel very strongly that all efforts should be made to refuel the Great Salt Lake so that these water levels come up and we're not getting the dust blowing this way off the lake bottom that's dried, said Cox.

Utah political leaders and state officials tasked with helping the Great Salt Lake reacted with concern in interviews with FOX 13 News.

What can we do to protect ourselves from the already proven risks and the possibility of more found in this study?

Research on its own can't make change, explained Eliza Cowie, Policy Director at O2 Utah.

Cowie encourages people to pay attention, read up on the issues, and show up when it comes time for decisions to be made at the Utah State Capitol that impact the lake and the state's air quality.

Its really important to get people involved to take that information and produce it as a policy solution," she said. "You can't rely purely on researchers and scientists to save us. We need to kind of take the information and produce our own results.

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Startling discovery at Great Salt Lake could lead to damaging health ... - FOX 13 News Utah

Neuropathology

Senolytic therapies suppress long COVID in human organoids … – BioWorld Online

Infection

Researchers from the University of Queensland discovered that senolytic therapies can suppress long-COVID neuropathology and long-term disorders caused by viral infections by reducing senescent cells, thereby reducing inflammation. Published Nov. 13, 2023, in Nature, the study examined the use of human pluripotent stem cells to generate small mini human brain organoids to screen for antiaging interventions called senolytics that selectively eliminate senescent cells that accumulate with age, lead author Julio Aguado told BioWorld.

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Senolytic therapies suppress long COVID in human organoids ... - BioWorld Online

Neuropathology

Eight scientists among most-cited researchers in world – Mirage News

Eight scientists from the University of Freiburg are among the "Highly Cited Researchers" for 2023. A survey by Clarivate Analytics reveals that they are among the most-frequently cited authors worldwide in their fields of research over the past decade. With nine entries - one scientist is recognised for work in two areas - the University of Freiburg holds fifth place among German universities alongside Bonn and Dsseldorf.

The University of Freiburg's Faculty of Environment and Natural Resources is represented in the list by Prof. Dr. Jrgen Bauhus and Prof. Dr. Carsten Dormann. Bauhus' research focuses on the structure and dynamics of forests, nutrient and carbon cycles in forests and ecological interactions in forest ecosystems. Dormann researches and develops statistical ecology methods that are used for example for the analysis of ecological networks.

Dr. Bjrn Grning from the Department of Computer Science is also among the Highly Cited Researchers. Grning is an expert in bioinformatics and heads Freiburg's Galaxy team. Galaxy is an open source platform for the analysis of big data in the life sciences.

Bjrn Grning, Bertram Bengsch, Marco Prinz, Carsten Dormann, Jrg Meerpohl, Jrgen Bauhus, Lukas Schwingshackl and Ori Staszewski. Photos: SFB 1425, Freiburg University Medical Center, Christian Hanner, Jrgen Gocke, Angela Schuberth-Ziehmer.

Five researchers from the Medical Faculty among the most-cited scientists

From the Medical Faculty at the University of Freiburg, the Highly Cited Researchers include Prof. Dr. Bertram Bengsch, Prof. Dr. Jrg Meerpohl, Prof. Dr. Marco Prinz, Prof. Dr. Lukas Schwingshackl, and Dr. Ori Staszewski, who is now a neuropathology consultant at Klinikum Saarbrcken. With the direct involvement of patients, Bengsch, from the Department of Internal Medicine II, undertakes research into the adaptive immune system in chronic disease, specifically virus infections, tumour diseases and diseases brought about by the autoimmune system. Meerpohl is the head of the Institute for Evidence in Medicine at the Freiburg University Medical Center. Together with his team, he develops new ways of making scientific findings accessible to doctors more clearly, more quickly and more convincingly in review papers.

Prinz is the head of the Institute of Neuropathology at the Freiburg University Medical Center, and was recognised as a Highly Cited Researcher by Clarivate in two areas: in immunology and in the field of neural and behavioural sciences. Together with Staszewski, Prinz studies the role of the immune system in the healthy brain and its involvement in diseases such as multiple sclerosis, Alzheimer's and brain tumours. They are both researching among other things the influence of nutrition and epigenetics on the formation of the immune system in the brain. Schwingshackl, senior researcher at the Institute for Evidence in Medicine and at Cochrane Germany, analyses studies into the influence of nutrition on health and develops new methods for future dietary guidelines.

About the list

Clarivate Analytics identifies the Highly Cited Researchers from an analysis of the most-cited papers in the Web of Science literature database. The list ranks the authors of research papers that are among the top one percent in their field in the Web of Science citations index. For 2023, the survey looked at papers that were published and cited in the period from January 2012 to December 2022. In total, the list includes more than 6,800 researchers from more than 1,300 institutions across 67 countries and regions.

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Eight scientists among most-cited researchers in world - Mirage News

Neuropathology

UW study links past military service to Alzheimer’s disease – University of Wisconsin School of Medicine and Public Health

The brains of deceased military veterans had higher levels of two abnormal proteins considered hallmarks of Alzheimers disease, suggesting that military veterans face a greater risk for developing Alzheimers, according to a new study from the University of Wisconsin School of Medicine and Public Health.

The study was recently published in Alzheimers & Dementia: The Journal of the Alzheimers Association led byRyan Powell, PhD, MA, assistant professor of medicine, UW School of Medicine and Public Health.

Emily Greendonner 608-516-9154 egreendonner@uwhealth.org

The study found that military veterans who had donated their brains to Alzheimers disease research centers had 26% greater odds of having amyloid plaques in their brains than nonveterans and 10% greater odds of having neurofibrillary tangles made of abnormal tau proteins, according to Powell. The findings, as well as prior research showing higher frequency of Alzheimers disease risk factors among veterans, support a rationale for greater support in disease prevention and treatment interventions for this population.

To our knowledge, this is the first study to link a history of military service to Alzheimers disease neuropathology, the gold standard for diagnosing Alzheimers, said Powell, who is data science director of the UW Center for Health Disparities Research. This has important implications for the Veterans Health Administration since it indicates an urgent need to screen veterans and to target therapies to those at greatest risk.

Powell and his research collaborators looked at brain biopsy data from 597 males who died between 1986 and 2018 and donated their brains to Alzheimers disease research centers at the UW School of Medicine and Public Health and the University of California San Diego.

Genealogical archivists used genealogy databases, census and military records to determine that about 60% of the males had served in the military most likely during World War II, Korean War and Vietnam War eras. The rate of military service was consistent between those who donated brains in San Diego and in Madison, Powell said.

The group of 358 male veterans had higher levels of both amyloid plaques and tau tangles in their brains, both biomarkers of Alzheimers disease. Researching female veteran risk is a key next step but researchers were unable to conduct this analysis given the small number of them represented in the current study, Powell said.

This study is shining new light on data thats been collected over decades some donations date all the way back to the mid-1980s so the donations of these veterans are still yielding valuable new insights after all these years, he said. We identified the who and the what in this study, but we need to narrow in on the why and the when.

Veterans are exposed to many known risks for brain disorders, including chronic stress from physical and psychological pain, physical trauma including traumatic brain injuries and environmental hazards such as Agent Orange, a tactical defoliating agent used in Vietnam. In addition, veterans have higher rates of cardiovascular disease, depression and PTSD, all of which are known risk factors for dementia, Powell said.

Exposures during military service and differences in life both before and after service likely all contribute to the brain disease, he explained. Researchers hope to expand the study to other brain banks to gain a deeper understanding and include younger generations of veterans to unlock the root causes of these brain changes in veterans, he said.

We might be able to uncover other factors and learn where risks can be reduced, Powell said. And with new Alzheimers therapies coming online, theres a need for scientific-based health equity policies to get them to those who might benefit most. Its exciting that this ongoing line of research can inform policy changes that improve the health of veterans.

The study was supported by funding from the National Institutes of Health - National Institute on Aging (grants R21AG079277, R01AG070883, P30AG062715, R01AG079303, and P30AG066530).

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UW study links past military service to Alzheimer's disease - University of Wisconsin School of Medicine and Public Health

Neuropathology

Study reveals no neuroinflammation in long COVID patients with … – News-Medical.Net

In a recent study published in JAMA Network Open, researchers examined cerebrospinal fluid (CSF) markers of neuroinflammation in individuals with post-coronavirus disease 2019 (COVID-19) condition (PCC) and neuropsychiatric symptoms.

PCC, also known as long COVID, represents a diverse group of symptoms that last for months post-acute COVID-19. Some individuals with PCC have neuropsychiatric symptoms (neuro-PCC), and the underlying mechanisms are poorly understood. CSF provides a means to evaluate neuropathology, given that it circulates the central nervous system (CNS) and serves as a window to the brain.

Research Letter: Self-Reported Neuropsychiatric PostCOVID-19 Condition and CSF Markers of Neuroinflammation. Image Credit:Donkeyworx/ Shutterstock

In the present study, researchers assessed CSF markers of neuroinflammation in people with neuro-PCC and COVID-19-nave individuals. Neuro-PCC subjects were recruited to the COVID Mind Study if they reported neuropsychiatric symptoms three months after COVID-19. Asymptomatic individuals recruited before 2020 (pre-COVID-19) served as controls.

The control group also included a COVID-19-nave participant recruited in 2022, with laboratory evidence supporting the seronegative status. Individuals with a history of immunocompromising conditions and psychiatric or neurologic illness and those taking immunosuppressive medications were excluded.

Data on COVID-19 test dates/results and vaccination were obtained from medical records and interviews. Participants provided consent for blood sampling and lumbar puncture. CSF and plasma were evaluated using a multiplex cytokine laser bead assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure neopterin (microglia activation marker).

Ethnicity and race were self-reported by participants. Group comparisons for clinical and demographic data were performed using t-tests, while a two-proportion z-test was used for comparisons of race. Mann-Whitney tests were used to compare cytokine data between controls and neuro-PCC subjects, controlling for false discovery rates.

The study included 37 individuals with neuro-PCC and 22 controls. Neuro-PCC subjects tested positive for COVID-19 from March 2020 to July 2022. Most individuals with neuro-PCC were White (78.4%) and female (73%). Only four participants (11%) in the neuro-PCC group were vaccinated at the time of infection, while 89% remained non-vaccinated. However, 46% were partially or fully vaccinated at the PCC study visit.

A majority of neuro-PCC participants had acute disease when severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Alpha was the predominant variant. Cognitive impairment, brain fog, and excess fatigue were the most common PCC symptoms. The neuro-PCC group did not exhibit elevated protein levels and white blood cell counts. Moreover, the CSF-to-blood albumin ratio, which changes during the breakdown of the blood-brain barrier, was not elevated in the neuro-PCC group.

There was no evidence of intrathecal production of immunoglobulins. However, interleukin-6 (IL-6) and monocyte chemoattractant protein-1 were reduced, while tumor necrosis factor-alpha levels were elevated in the CSF of neuro-PCC subjects relative to controls, albeit not statistically significant when accounted for multiple comparisons. Besides, other chemokines and cytokines in the plasma or CSF were not significantly different. Furthermore, neopterin levels were not elevated in neuro-PCC subjects.

Taken together, the study did not find evidence of neuroinflammation and blood-brain barrier dysfunction in participants with neuro-PCC relative to control participants. The findings suggest persistent CNS immune activation does not drive neurologic long COVID. The studys limitations were the small sample size, increased rates of alcohol use and smoking, reduced rates of antidepressants among controls, and discrepancies in the race and gender of neuro-PCC subjects relative to controls.

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Study reveals no neuroinflammation in long COVID patients with ... - News-Medical.Net