Pick Disease of the Brain

– Performances by Jay Allen and Kylie Morgan, Melinda Doolittle, Charles Esten, Paul Freeman, Paul Greene, Ginna Claire Mason, MaRynn Taylor, Noah Thompson, Alicia Witt, and more covering hits from the early 2000s – – Event raises awareness and funds for the Alzheimer's Association research grant program – *Photos available* NASHVILLE, Tenn., Nov. 13, 2023 /PRNewswire/ -- Hallmark stars Ashley Williams and Nikki DeLoach hosted the sixth annual Dance Party to End ALZ on Sunday, November 12 at Nashville's Wildhorse Saloon, which raised more than $300,000 for the Alzheimer's Association research grant program. The event founded by Kimberly Williams-Paisley was emceed by Apple Music radio host Kelleigh Bannen. Williams and DeLoach opened the evening with a surprise performance of "Party In the U.S.A." The dynamic duo welcomed guests and shared why co-hosting the event meant so much to them after both losing a parent to dementia. Williams' mom, Linda, passed away with Alzheimer's in 2016, and DeLoach's dad, David, passed away with Pick's disease, a rare form of dementia, in 2021. Dressed in 2000s fashion, performers took to the stage covering throwback hits from the era. Accompanied by Wildhorse Saloon's house band Three Lane, performances included: Jay Allen's take on "Kryptonite." Allen was then joined by wife and country music artist Kylie Morgan to perform his song on "No Present Like The Time" Melinda Doolittle's versions of "Crazy In Love" and "Since You've Been Gone" Charles Esten's channeled Billie Joe Armstrong for "Wake Me Up When September Ends" Paul Freeman's rendition of "Mr. Brightside" Paul Greene's spin on "Seven Nation Army" Ginna Claire Mason's version of "Before He Cheats" MaRynn Taylor's rendition of "Complicated" Noah Thompson's take on "Move Along" Alicia Witt channeled Britney Spears for "Lucky" Hallmark stars group number to "I Gotta Feeling" And a group finale to "Beautiful Day" "We are beyond grateful to the Nashville community, performers, generous sponsors and attendees near and far who joined us at the sixth annual Dance Party to End ALZ," said co-hosts Ashley Williams and Nikki DeLoach. "Everyone coming together for this cause means the world to us and our families. Together, we raised awareness and funds to support the Alzheimer's Association's research grant program, which is helping us get one step closer to ending Alzheimer's and all other dementia." Event committee included: Ashley Williams, actor and director Nikki DeLoach, actor, producer and writer Annie Howell, chief communications officer, Hallmark Media Blake McDaniel, music touring agent, CAA Andrew Walker, actor, producer, co-founder of Little West Jay Williams, CEO & apiarist of Williams Honey Farm Generous sponsors included: Hallmark Media Kimberly Williams-Paisley & Brad Paisley Boot Barn Sidekick Therapy Partners The Buffaloe Family DeBartolo Family Foundation Denise Cummins Rosenthal Family Foundation Andrew & Cassandra Walker Nikki DeLoach & Ryan Goodell The Graham Family Charitable Trust Brandon and Karen Jondle family and Tom and Beth Jost family Michael and Sarah Lorance family In Loving Memory of Micheal MacDowell, beloved Husband, father and friend Harley Neuman & Daniel Lam "Paisley Park Girls" in honor of Beth Machado Michael Yu & Erin Zervos Yu R3 Stem Cell/R3 Anti Aging Romance University Southbound Tequila Vanderbilt Memory & Alzheimer's Center, Vanderbilt University Medical Center Williams Honey Farm The Ken and Beth Dunn Family Foundation CAA Empathy Studios Paul Greene & Kate Austin McKellar/Sveslosky & Hart Lillie Pawluk Sandy & Doug Paisley Jennifer Wayne Celebrities in attendance included: Benjamin Ayres Brooke D'Orsay Cindy Busby Danica McKeller Erich Hover Erin Cahill Jen Lilley Jesse Hutch Kimberly Williams-Paisley Kristoffer Polaha Melissa Joan Hart Riley Weston Sarah Drew Trevor Donovan Funds raised through the Dance Party to End ALZ will directly support the Alzheimer's Association's research grant program. To date, Dance Party to End ALZ has raised more than $2.1M to fund diverse and exciting Alzheimer's research — from studying the impacts of genetics and sleep on the brain, to developing a smartwatch-based intervention for dementia risk reduction. For more information and to donate, visit alz.org/DanceParty. About the Alzheimer's Association® The Alzheimer's Association leads the way to end Alzheimer's and all other dementia — by accelerating global research, driving risk reduction and early detection, and maximizing quality care and support. Our vision is a world without Alzheimer's and all other dementia®. For more information, visit alz.org or call the 24/7 Helpline at 800.272.3900. SOURCE Alzheimer's Association

A gene encoding a protein linked to tau production -- tripartite motif protein 11 (TRIM11) -- was found to suppress deterioration in small animal models of neurodegenerative diseases similar to Alzheimer's disease (AD), while improving cognitive and motor abilities, according to new research. A gene encoding a protein linked to tau production -- tripartite motif protein 11 (TRIM11) -- was found to suppress deterioration in small animal models of neurodegenerative diseases similar to Alzheimer's disease (AD), while improving cognitive and motor abilities, according to new research from the Perelman School of Medicine at the University of Pennsylvania. Additionally, TRIM11 was identified as playing a key role in removing the protein tangles that cause neurodegenerative diseases, like AD. The findings are published today in Science. AD is the most common cause of dementia in older adults, with an estimated 6 million Americans currently living with the disease. It is a progressive brain disorder that slowly destroys memory and thinking skills. Foundational research at Penn Medicine led by Virginia M.Y. Lee, PhD, the John H. Ware III Professor in Alzheimer's Research in Pathology and Laboratory Medicine, and the late John Q. Trojanowski, MD, PhD, a former professor of Geriatric Medicine and Gerontology in Pathology and Laboratory Medicine, reveals that one of the underlying causes of neurodegenerative diseases is neurofibrillary tangles (NFTs) of tau proteins, which cause the death of neurons, leading to the symptoms of AD, like loss of memory. In addition to AD, aggregation of tau proteins into NFTs is associated with over 20 other dementias and movement disorders including progressive supranuclear palsy, Pick's disease, and chronic traumatic encephalopathy, collectively known as tauopathies. Nevertheless, how and why tau proteins clump together and form the fibrillar aggregates that make up NFTs in patients with these diseases remains unclear. This major gap in knowledge has made the development of effective therapies challenging for researchers. "Most organisms have protein quality control systems that remove defective proteins, and prevent the mis-folding and accumulation of tangles -- like the ones we see with tau proteins in the brain of those with taupathies -- but until now we didn't know how this works in humans, or why it malfunctions in some individuals and not others," said senior author, Xiaolu Yang, PhD, a professor of Cancer Biology at Penn. "For the first time, we have identified the gene that oversees tau function, and have a promising target for developing treatments to prevent and slow the progression of Alzheimer's disease and other related disorders." Yang and his team, including first author Zi-Yang Zhang, PhD, a postdoctoral researcher in Yang's lab, previously found that TRIM proteins play an important role in protein quality control in animal cells. After examining over 70 human TRIMs, they found that TRIM11 has a major role in suppressing tau aggregation. TRIM11 possesses three main functions related to the quality control of tau proteins. First, it binds to tau proteins, especially the mutant variants that cause disease, and helps eliminate them. Second, it acts as a "chaperone" for tau, preventing the proteins from mis-folding. Finally, TRIM11 dissolves pre-existing tau aggregates. Using postmortem brain tissues of 23 individuals with AD and 14 health controls from the Center for Neurodegenerative Disease Research tissue bank -- created and maintained by Lee and Trojanowski -- researchers validated these findings, and found that levels of TRIM11 protein are substantially reduced in the brains of individuals with AD, compared to healthy control individuals. To determine the potential utility of TRIM11 as a therapeutic agent, researchers used adeno-associated viral vector (AAV), a tool commonly used in gene therapy, to deliver the TRIM11 gene into the brain of multiple mouse models. Researchers found that mice with tau pathologies receiving the TRIM11 gene exhibited a marked decrease in the development and accumulation of NFTs, and had much improved cognitive and motor abilities. "Not only do these findings tell us that TRIM11 could play an important role in protecting people from Alzheimer's and similar diseases, but we also see that we might be able to develop future therapies that replenish TRIM11 in individuals with lower levels," said Yang. "We are eager to work with our colleagues to explore the possibility of developing gene therapies that halt the progression of neurodegenerative disease." This study was supported by the National Institutes of Health (R01CA243520, UL1TR000003) and funding received by Penn under a sponsored research agreement with Wealth Strategy Holding Limited. Note:Yang is an inventor on patents and patent applications owned by the University of Pennsylvania related to TRIM proteins, and is a co-founder and equity holder of Evergreen Therapeutics LLC, which received investments from Wealth Strategy Holding Limited. Penn and Yang have either received, or may receive in the future, financial consideration related to the licensing of certain Penn intellectual property to Evergreen Therapeutics LLC.

Phase 2a publication entitled “Combined Regulatory T-Lymphocyte and IL-2 Treatment is Safe, Tolerable, and Biologically Active for One Year in Persons with Amyotrophic Lateral Sclerosis” has been published in peer-reviewed journal Neurology, Neuroimmunology & Neuroinflammation COYA 101 was well tolerated and increased Treg suppressive function The majority (6 out of 8) of patients either slowed or stopped progression (mean change of -2.7 points on ALSFRS-R score) during the open label extension over a 24-week period while 2 out of 8 patients did not benefit from treatment Assessment of biomarkers of inflammation and oxidative stress over the course of the study correlated with ALS disease severity and may serve to prospectively evaluate and/or monitor treatment response HOUSTON, Sept. 01, 2022 (GLOBE NEWSWIRE) -- Coya Therapeutics, Inc. (“Coya”), a clinical-stage biotechnology company developing multiple approaches that aim to enhance regulatory T cells (Tregs) function, including allogeneic Treg-derived exosome therapeutics and novel biologics, today announced the publication of the Phase 2a clinical trial data for its first-in-class Treg cell therapy product candidate, COYA 101. Coya has an exclusive worldwide license from Houston Methodist Hospital to develop, manufacture, and commercialize COYA 101. The article entitled “Combined Regulatory T-Lymphocyte and IL-2 Treatment is Safe, Tolerable, and Biologically Active for One Year in Persons with Amyotrophic Lateral Sclerosis” has been published online in the peer-reviewed journal Neurology, Neuroimmunology, & Neuroinflammation. Subjects enrolled in the Phase 2a trial were initially randomized into a double-blind portion to receive active Treg cells or matching placebo every four weeks over 24 weeks. After completion of the 24-week double-blind (DB) portion, subjects entered an open-label extension (OLE) during which all patients received active Treg cells every four weeks for additional 24 weeks. The DB portion of the trial was curtailed due to COVID-19-related restrictions, and the limited number of patients enrolled made statistical analysis not feasible. However, the eight patients included in the OLE completed the 24-week study, and 75% (n=6) of them exhibited slow to no progression as measured by the ALSFRS-R (mean decline of -2.7 points). A sub-analysis of these six patients showed that four of them (50% of the intention-to-treat [ITT] patient population, n=8) exhibited no decline over the 24-week treatment period. The two remaining patients in the OLE did not experience a treatment benefit. The Revised Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS-R) is a validated rating instrument that gauges the progression of disability in patients with amyotrophic lateral sclerosis (ALS) on a 48-point scale. In addition to the benefit experienced by the majority of patients in clinical function, Treg suppressive function was higher following infusions, compared to baseline values at screening. An unbiased proteomics assay of the OLE specimens documented that the two rapidly progressing patients had markedly higher levels of biomarkers of inflammation (IL-17F and IL-17C) and oxidative stress (OLR1 and ox-LDL) compared to the other six patients who exhibited amelioration or halting of disease progression, representing important findings that may provide new tools to identify the most suitable ALS patients for the next well-powered and well controlled trial. Overall, treatment with COYA 101 was well tolerated. No deaths were reported and no patient receiving Treg infusions were discontinued from the study. Howard Berman, Ph.D., Chief Executive Officer of Coya, stated, “We believe this Phase 2a study, with the limitations of a small sample size, supports that COYA 101 was well tolerated and biologically active in ALS patients and may slow or halt disease progression in the right patient population. We believe the findings that high levels of inflammation and oxidative stress may limit the effectiveness of Tregs, resulting in shorter cell half-lives and impacting their downstream suppressive anti-inflammatory effects, may help to better enhance the signal by prospectively identifying the patients with the higher likelihood to respond,” concluded Dr. Berman. “We are encouraged by the results from this study, which are consistent with the positive outcomes of the previous Phase 1 trial in ALS patients. We believe these results are relevant, as they provide information we need to design our next double-blind controlled study to assess the efficacy and safety of COYA 101,” added Adrian Hepner, M.D, Ph.D., President and Chief Medical Officer of Coya. Stanley H. Appel, M.D., the Chair of the Scientific Advisory Board of Coya, stated, “Although the double-blind portion of the Phase 2a study was compromised by COVID-19, we believe the Open Label Extension supports the findings of our Phase 1 study that COYA 101 infusions are well tolerated, may enhance suppressive functions and may have the potential to slow disease progression.” The online publication can be accessed at About Coya Therapeutics, Inc. Headquartered in Houston, TX, Coya Therapeutics, Inc. (Coya) is a clinical-stage biotechnology company developing approaches utilizing Treg modifying therapeutics to target systemic and neuro inflammation. Coya has pioneered the ability to produce Tregs with a highly suppressive phenotype (“Super Tregs”) from a patient’s own dysfunctional Tregs. "Super Tregs” confer their properties through reproducible upregulated proteins in the expanded/post cryopreserved condition that allow for an off-the-shelf like approach for serial infusion. Coya is also developing exosome therapies derived from “Super Tregs” for allogeneic applications, as well as a biologic that works to upregulate Treg function in vivo. Coya is focused on the advancement of disease modifying approaches to address the significant unmet medical needs of patients with Amyotrophic Lateral Sclerosis (ALS), Frontal Temporal Dementia (FTD), Scleroderma, and Hepatic Inflammation and Fibrosis. For more information, please visit . Contacts Investor Contact David Snyder david@coyatherapeutics.com Media Contact Jessica Starman media@coyatherapeutics.com