Latest news with #neurodegenerativeDiseases
Yahoo
4 days ago
- Business
- Yahoo
Annovis Announces NYSE Acceptance of Plan to Regain Listing Compliance
MALVERN, Pa., June 19, 2025 (GLOBE NEWSWIRE) -- Annovis Bio, Inc. (NYSE: ANVS) ("Annovis" or the 'Company'), a late-stage clinical drug platform company pioneering transformative therapies for neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD), today announced it received notification (the "Acceptance Letter") from the New York Stock Exchange ("NYSE") that the NYSE has accepted the Company's previously-submitted plan (the "Plan") to regain compliance with the NYSE's continued listing standards relating to minimum market capitalization and stockholders' equity. In the Acceptance Letter, the NYSE granted the Company an 18-month period from the Company's receipt of the NYSE's Notice of Noncompliance dated March 26, 2025 (the "Plan Period") to regain compliance with the continued listing standards. As part of the Plan, the Company is required to provide the NYSE quarterly updates regarding its progress towards the goals and initiatives in the Plan. The Company expects its stock will continue to be listed on the NYSE during the Plan Period, subject to the Company adherence to the Plan and compliance with other applicable NYSE continued listing standards. The Company's receipt of such notification from the NYSE does not affect the Company's business, operations or reporting requirements with the U.S. Securities and Exchange Commission. Forward-Looking StatementsThis press release contains, and oral statements made from time to time by our representatives may contain, 'forward-looking statements.' Forward-looking statements include statements identified by words such as 'could,' 'may,' 'might,' 'will,' 'intends,' 'plans,' 'seeks,' 'believes,' 'estimates,' 'expects,' 'continues,' 'projects' and similar references to future periods, or by the inclusion of forecasts or projections. Forward-looking statements are based on our current expectations and assumptions regarding capital market conditions, our business, the economy and other future conditions. Because forward-looking statements relate to the future, by their nature, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict. As a result, our actual results may differ materially from those contemplated by the forward-looking statements. Important factors that could cause actual results to differ materially from those in the forward-looking statements include, but are not limited to, the Company's ability to develop a plan to regain compliance with the continued listing criteria of the NYSE; the NYSE's acceptance of such plan; the Company's ability to execute such plan and to continue to comply with applicable listing standards within the available cure period; risks arising from the potential suspension of trading of the Company's common stock on the NYSE; regional, national or global political, economic, business, competitive, market and regulatory conditions, including risks regarding our ability to manage inventory or anticipate consumer demand; changes in consumer confidence and spending; our competitive environment; our failure to open new profitable stores or successfully enter new markets and other factors set forth under 'Risk Factors' in our Annual Report on Form 10-K for the fiscal year ended December 31, 2024. Any forward-looking statement made in this report speaks only as of the date on which it is made. The Company undertakes no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future developments or otherwise. About Annovis Headquartered in Malvern, Pennsylvania, Annovis is dedicated to addressing neurodegeneration in diseases such as AD and PD. The Company is committed to developing innovative therapies that improve patient outcomes and quality of life. For more information, visit and follow us on LinkedIn, YouTube, and X. Contact Information:Annovis Bio Inc.101 Lindenwood DriveSuite 225Malvern, PA Investor Contact:Alexander Morin, Strategic CommunicationsAnnovis Bioir@ in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
Yahoo
5 days ago
- Health
- Yahoo
How rogue jumping genes can spur Alzheimer's, ALS
Back in 2008, neurovirologist Renée Douville observed something weird in the brains of people who'd died of the movement disorder ALS: virus proteins. But these people hadn't caught any known virus. Instead, ancient genes originally from viruses, and still lurking within these patients' chromosomes, had awakened and started churning out viral proteins. Our genomes are littered with scraps of long-lost viruses, the descendants of viral infections often from millions of years ago. Most of these once-foreign DNA bits are a type called retrotransposons; they make up more than 40 percent of the human genome. Many retrotransposons seem to be harmless, most of the time. But Douville and others are pursuing the possibility that some reawakened retrotransposons may do serious damage: They can degrade nerve cells and fire up inflammation and may underlie some instances of Alzheimer's disease and ALS (amyotrophic lateral sclerosis, or Lou Gehrig's disease). The theory linking retrotransposons to neurodegenerative diseases — conditions in which nerve cells decline or die — is still developing; even its proponents, while optimistic, are cautious. 'It's not yet the consensus view,' says Josh Dubnau, a neurobiologist at the Renaissance School of Medicine at Stony Brook University in New York. And retrotransposons can't explain all cases of neurodegeneration. Yet evidence is building that they may underlie some cases. Now, after more than a decade of studying this possibility in human brain tissue, fruit flies and mice, researchers are putting their ideas to the ultimate test: clinical trials in people with ALS, Alzheimer's and related conditions. These trials, which borrow antiretroviral medications from the HIV pharmacopeia, have yielded preliminary but promising results. Meanwhile, scientists are still exploring how a viral reawakening becomes full-blown disease, a process that may be marked by what Dubnau and others call a 'retrotransposon storm.' A retrotransposon is a kind of 'jumping gene.' These pieces of DNA can (or once could) move around in the genome by either copying or removing themselves from one spot and then pasting themselves into a new spot. Retrotransposons are copy-and-pasters. Many retrotransposons are old companions: Some predate the evolution of Homo sapiens or even the split between plants and animals, Dubnau says. Their predecessors may have alternated between riding along stitched into a host chromosome and existing outside of it, he suggests. Some retrotransposons, after all that time, retain their ability to hop around human DNA. To do so, they copy themselves with the enzyme reverse transcriptase, which is also used by some viruses like HIV to copy RNA sequences into DNA. Once they're copied, the remnant viruses can pop into new locations on chromosomes. If it's terrifying to think of a genome littered with retroviral genes, some capable of bouncing around the genome, don't fret, says Douville, now at the University of Manitoba in Winnipeg. Remarkably, some retrotransposons have taken on helpful jobs, assisting the body with tasks like maintaining stem cells and development of the embryo and nervous system. And many retrotransposons are dormant or broken, and the cell has means to keep them (mostly) quiet. One technique is to stash them in DNA regions that are wound up so tight that the molecular machines needed to copy genes can't get near them. In essence, the cell shoves them into a closet and slams the door shut. But evidence is building that as people age, that closet door can creak open, letting retrotransposons spill out. Exactly what they do then isn't certain. Some scientists think it's not so much that they are jumping around and mutating DNA, but that their viralesque RNAs and proteins can screw up normal cellular activities. 'I think what's actually driving toxicity when transposons are activated is they're making all these factors that look like a virus to the cell,' says Bess Frost, a neurobiologist at Brown University in Providence, Rhode Island. The cell reacts, quite reasonably, with defensive inflammation, which is commonly associated with neurodegeneration. Retrotransposons also seem to team up with rogue proteins classically linked to neurodegeneration, damaging or killing nerve cells, and perhaps even setting off the disease in the first place. Scientists long suspected a link between viruses and ALS, which causes degeneration of the motor neurons that control movement. But the connection, when it was finally found, wasn't quite what anyone predicted. In the early 2000s, scientists reported that some people with ALS had the viral enzyme reverse transcriptase in their blood and, more rarely, spinal fluid. Some had as much reverse transcriptase as a person with an HIV infection. But at the time, says Dubnau, 'Nobody could find a virus.' Finally, Douville and colleagues discovered evidence for one of those leftover viruses, a kind of retrotransposon called HERV-K, in the brains of some people who had died of ALS. From there, scientists began to build a case linking jumping genes to ALS in people, lab animals and cells in dishes. A team reported in 2017 that numerous jumping genes had been activated in the brains of certain people with ALS. Douville's colleagues also documented damage inflicted by HERV-K: When they put a gene from the retrotransposon into mice, the animals' nerve cell projections shriveled and they exhibited ALS-like symptoms. As the scientists zeroed in on what might be waking up HERV-K, a familiar protein turned up. Called TDP-43, it had already been linked to ALS. But even before that, it was found to be involved in cells' responses to the retrovirus HIV. Scientists discovered in the 1990s that TDP-43 works in the cell's nucleus, where it hinders activation of HIV genes. It also regulates human genes there. But in the neurons of people with ALS or a related condition, frontotemporal dementia (FTD), TDP-43 departs the nucleus and goes on to form abnormal clumps in the cytoplasm. The globs have been associated with a number of neurodegenerative conditions and can spread from cell to cell. And when TDP-43 vacates the nucleus, it also creates a gap in gene regulation, throwing off the activity levels of many genes. TDP-43 gone bad is sufficient to cause neurodegeneration, but studies indicate its desertion of its nuclear role can also wake up retrotransposons. When TDP-43 leaves the nucleus, tightly coiled DNA next to certain retrotransposons starts to loosen up and unravel, a study of cells from the brains of people who died of ALS or FTD revealed. And researchers saw that in cultured cells, this loss of TDP-43 freed certain retrotransposons from their restraints. The closet door was now ajar, in other words, allowing the retrotransposons to jump out and around. Meanwhile, Dubnau and collaborators, were looking at data on TDP-43 and the genes it controls in rats, mice and people. They found that TDP-43 can naturally stick to the RNAs of a variety of jumping genes, suggesting a way that normal TPD-43 might continue to corral them, even if they've managed to get copied into RNA. That interaction was altered in people with FTD and in rodents with abnormally high or low amounts of TDP-43 — very much as if TDP-43 was unable to control the jumping genes anymore. The Dubnau group also turned to fruit flies. Both old age and the human TDP-43 gene caused retrotransposons in the fly brain to sneak out of the chromosomal closet, inducing brain cells to kill their neighbors and prompting neurodegeneration, the group reported in a series of papers from 2013 to 2023. Moreover, activation of certain retrotransposons also caused TDP-43 to clump together outside of the nucleus, creating a vicious cycle whereby TDP-43 and the retrotransposons reinforce each other's abnormal behaviors. Past a certain point, says Dubnau, 'It just takes off.' Based on the sum of all these findings, Dubnau suggests a possible way that ALS could develop: Normally, TDP-43 in the nucleus helps to repress retrotransposons. But if aging or some other disturbance causes TDP-43 to decamp, those once-silenced retrotransposons spring to life, producing virus-like RNAs and proteins. While the retrotransposons might induce disease on their own, by jumping into new DNA locations or spurring inflammation, they also act on TDP-43. They force more TDP-43 to leave the nucleus and clump in the cytoplasm, causing further neurodegeneration that spreads to neighboring cells. This isn't the cause of all kinds of ALS, which is a complex disorder with many possible triggers. But in a 2019 study of postmortem brain samples, Dubnau and colleagues found that about one in five people with ALS had high levels of retrotransposon activation and TDP-43 dysfunction. Stay in the KnowSign up for the Knowable Magazine newsletter today As that ALS story was developing, other scientists were pursuing a connection between retrotransposons and another toxic protein in neurodegeneration: the tau protein, which twists into unruly tangles in the brain cells of people with Alzheimer's disease. It affects retrotransposons because it, like TDP-43, plays a role in keeping retrotransposons quiet, says Frost. That maintenance is a downstream effect of tau's association with the cell's interior skeleton. That skeleton is physically linked to the nucleus's skeletal structure, which in turn anchors the tightly wound-up DNA that silences retrotransposons. When tau goes bad, it changes the structure of the cell's main skeleton, making it more rigid. Frost and colleagues found that this structural defect propagates all the way to the nuclear skeleton and the chromosomes, just like tightening the strands on one side of a net could change the shape of the other side. This structural effect can unlock the tightly wound bits of chromosome in fruit flies, which damages their neurons, Frost reported in 2014. By 2018, she'd shown that tau problems unleashed jumping genes in the flies. 'They were legitimately jumping,' she says, going from their original chromosomal locations to other ones in the fly's brain cells. And the jumping genes contributed to the death of nerve cells. Frost and colleagues also studied mammals — mice — and in 2022 they reported that retrotransposons were also activated in mice with dysfunctional tau. Meanwhile, Frost and others examined brain cells from people who'd died of tau-related diseases such as Alzheimer's, which also revealed activated retrotransposons. 'They were legitimately jumping.' — BESS FROST This awakening of retrotransposons appears to happen early in the disease, according to the work of another team published in 2022. In blood samples from people on their way to developing Alzheimer's disease, the copying of retrotransposon genes into RNAs spiked, creating a 'retrotransposon storm,' just before their symptoms got bad enough to be labeled Alzheimer's. This growing body of evidence suggests that reactivating once-quiet retrotransposons, whether via dysfunctional tau or TDP-43, can create havoc. A potential treatment quickly comes to mind: Since these retrotransposons are a lot like viruses, scientists reason that antiviral drugs could help. Handily, doctors already have medications that stymie retroviruses: Millions of people take antiretroviral drugs to keep HIV in check or prevent it from gaining a foothold in their cells. Indeed, multiple studies over several years have investigated drugs from the HIV treatment playbook that block the enzyme reverse transcriptase. And in cells, flies and mice the drugs have dialed down retrotransposon activity and neurodegeneration. These medications are well understood and generally safe, and are already in trials for neurodegenerative disease. For example, researchers have tested the safety of a 24-week antiretroviral course in 40 people with ALS. Not only did most people safely complete the trial, but the levels of HERV-K in their blood went down, and they seemed to have a delay in progression of their ALS symptoms, the researchers reported in 2019. Frost recently published results from a small trial in which 12 people with early Alzheimer's disease took a reverse transcriptase inhibitor for 24 weeks. Her main goal was to determine if the treatment was safe, and it was — but the researchers also observed a drop in signs of inflammation in the participants' spinal fluid. Both Dubnau and Frost serve on the scientific advisory board for Transposon Therapeutics, which tested its own reverse transcriptase inhibitor in 42 people with ALS and/or FTD. The company says the drug was tolerable and yielded signs of less neurodegeneration and inflammation, plus a delay in the inevitable worsening of symptoms. The company is planning a larger trial; it also plans to test its drug in people with ALS, Alzheimer's and a related tau-based disease, progressive supranuclear palsy. Neither Frost nor Dubnau, who together recently summarized the field for the Annual Review of Neuroscience, believes that antiretroviral drugs alone are the solution to transposon-fueled Alzheimer's or ALS. As Douville notes, the drugs were designed to act only on specific target enzymes — they won't do anything to other retrotransposon genes, RNAs or proteins, which could also spur nerve-damaging inflammation. Meanwhile, scientists are looking beyond ALS and Alzheimer's as evidence accumulates that retrotransposons may contribute to other neurodegenerative and inflammatory conditions, such as Parkinson's disease and multiple sclerosis. 'It's really picking up speed,' Frost says. This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.
Washington Post
28-05-2025
- Health
- Washington Post
Scientists develop gene delivery ‘trucks' that could treat brain diseases
Scores of researchers have produced new tools that can deliver genes and selectively activate them in hundreds of different cell types in the brain and spinal cord, a breakthrough that scientists hope advances them toward developing targeted therapies to treat neurodegenerative diseases such as ALS, Parkinson's disease and Alzheimer's. The discoveries, made through the National Institutes of Health's BRAIN initiative, show with unprecedented clarity and precision how neural cells work together, but also how diseases disrupt their tight choreography. The insight offers the promise that doctors may one day treat diseases by manipulating dysfunctional cells.
Associated Press
27-05-2025
- Business
- Associated Press
VectorY Therapeutics Appoints Jessica Atkinson as Chief Business Officer
AMSTERDAM & BOSTON--(BUSINESS WIRE)--May 27, 2025-- VectorY Therapeutics, a biotechnology company developing innovative vectorized antibody therapies for the treatment of neurodegenerative diseases, today announced the appointment of Jessica Atkinson as Chief Business Officer (CBO). In this newly created role, Atkinson will partner with the Chief Executive Officer and management team to develop long-term business and commercial strategies that support company growth, and will also drive strategic partnerships. This press release features multimedia. View the full release here: Jessica Atkinson, New CBO at VectorY Therapeutics Atkinson brings over two decades of business development and commercialization experience across biopharmaceutical companies and innovative startups. She has held leadership roles at ImmuneID, Glympse Bio, and Foundation Medicine, where she spearheaded strategic partnerships and corporate strategy initiatives. She also held roles of increasing responsibility over seven years in the U.S. commercial organization of Merck & Co. Most recently, Atkinson served as a fractional CBO or strategic advisor to multiple early-stage biotech companies through her consulting firm, TwoStep Advisors. 'I'm delighted to welcome Jessica to VectorY,' said Jim Scibetta, chief executive officer of VectorY Therapeutics. 'Her proven expertise in shaping strategy and driving successful transactions across all stages of drug development will be invaluable as we advance our pipeline and pursue new opportunities. Jessica's collaborative approach and strategic vision make her an ideal addition to our leadership team.' 'VectorY's pioneering approach to developing vectorized antibody therapeutics holds immense promise for patients with neurodegenerative diseases,' said Atkinson. 'I look forward to working closely with the management and research teams to further develop our corporate strategy and to create transformative alliances and business collaborations that support the company's mission and long-term success.' Atkinson holds a Bachelor of Science degree in Molecular Biology from the University of Texas, Austin. She has been an advocate for encouraging women to pursue careers in science and volunteers with Mass General Cancer Center's Peer Mentoring program that offers patients and family members the opportunity to speak by telephone one-to-one with an experienced patient. About VectorY VectorY is on a mission to provide people with neurodegenerative diseases a longer, better life by creating transformative vectorized antibody treatments. Our platform combines the promise of precise therapeutic antibodies with one-time AAV-based delivery to the CNS. Unique in-house expertise in antibodies, AAV vectors, protein degradation, manufacturing and neuroscience drives the rapid development of much needed disease-modifying therapies for neurodegenerative diseases such as ALS and Huntington's disease. For more information, see View source version on CONTACT: VectorY Therapeutics B.V. E-mail:[email protected] Tel: +31 20 226 8020 Vigo Consulting (Media) Melanie Toyne-Sewell / Rozi Morris E-mail:[email protected] Tel: +44 207 390 0237 / +44 20 7390 0231 KEYWORD: MASSACHUSETTS EUROPE UNITED STATES NETHERLANDS NORTH AMERICA INDUSTRY KEYWORD: SCIENCE NEUROLOGY OTHER SCIENCE BIOTECHNOLOGY RESEARCH PHARMACEUTICAL HEALTH CLINICAL TRIALS SOURCE: VectorY Therapeutics Copyright Business Wire 2025. PUB: 05/27/2025 07:05 AM/DISC: 05/27/2025 07:05 AM
Globe and Mail
07-05-2025
- Business
- Globe and Mail
This Biotech Found Mid-Week Success Following Analyst Upgrade
A biotech company based out of Massachusetts found a tremendous amount of success on Wednesday after Leerink Partners upgraded the stock from market perform to outperform, raising their price target for the stock from $4 to $10. Traders wasted no time buying up shares of Amylyx Pharmaceuticals Inc. (Nasdaq:AMLX), pushing the small cap to close up at $4.87/share (+4.73%) on the day. This doesn't come at too much of a surprise given the bullish price target versus yesterday's close at just $4.65. This move was a strong continuation of the success this stock has had over the last month. Amylyx Pharmaceuticals Inc is a clinical-stage pharmaceutical company working on developing a novel therapeutic for amyotrophic lateral sclerosis and other neurodegenerative diseases. Copyright © 2025 All rights reserved. Republication or redistribution of content is expressly prohibited without the prior written consent of shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. View more of this article on About Media, Inc.: Founded in 1999, is one of North America's leading platforms for micro-cap insights. Catering to both Canadian and U.S. markets, we provide a wealth of resources and expert content designed for everyone—from beginner investors to seasoned traders. is rapidly gaining recognition as a leading authority in the micro-cap space, with our insightful content prominently featured across numerous top-tier financial platforms, reaching a broad audience of investors and industry professionals. Want to showcase your company's story to a powerful network of investors? We can help you elevate your message and make a lasting impact. Contact us today. Contact: Media, Inc.
