Latest news with #APOE
Yahoo
16-07-2025
- Business
- Yahoo
Voyager Adds Fourth Wholly-Owned Alzheimer's Disease Program to Pipeline, Complementing Existing Tau and Amyloid Assets with New APOE Approach
- New program combines IV-delivered TRACER™ capsid with bifunctional payload to silence APOE in carriers of the high-risk APOE4 variant while delivering the protective APOE2 variant - - Voyager's wholly-owned Alzheimer's disease franchise now includes clinical-stage anti-tau antibody VY7523 as well as gene therapies targeting tau, amyloid, and APOE - LEXINGTON, Mass., July 16, 2025 (GLOBE NEWSWIRE) -- Voyager Therapeutics, Inc. (Nasdaq: VYGR), a biotechnology company dedicated to leveraging genetics to treat neurological diseases, today continued the expansion of its Alzheimer's disease (AD) franchise with the introduction of a wholly-owned program that modulates the expression of apolipoprotein E (APOE), the strongest genetic risk factor for AD.i The program uses a proprietary intravenous (IV)-delivered, blood-brain barrier (BBB)-penetrant TRACER capsid to deliver a bifunctional payload that is designed to decrease expression of APOE in carriers of the variant APOE4, while delivering the variant APOE2. APOE4 has been strongly linked with a higher risk of developing AD, with almost all APOE4 homozygotes exhibiting AD pathologyi, while APOE2 has been associated with a lower risk of developing AD. In preclinical studies, a single IV injection of a TRACER capsid carrying the single bifunctional vector resulted in significant reductions of endogenous APOE4 in key AD-relevant brain regions of APOE4 knock-in mice, while significantly increasing expression of the APOE2 isoform to maintain overall APOE levels. Voyager anticipates presenting early data on this program at an upcoming scientific meeting in 2025. 'The Voyager team is leveraging our deep expertise in Alzheimer's disease biology and drug development to advance multiple programs against what we believe to be the three most-promising targets: tau, amyloid, and APOE,' said Alfred W. Sandrock, Jr., M.D., Ph.D., Chief Executive Officer of Voyager. 'We believe each of these approaches will have an important role to play in the treatment of Alzheimer's disease, particularly as the field begins to understand how best to sequence and combine treatments to improve outcomes for patients. We look forward to near-term data on some of these targets expected from third parties, which we expect will continue to inform our Alzheimer's disease franchise and approach.' Voyager's AD franchise is now comprised of four wholly-owned assets: VY7523, a pathologic-specific anti-tau antibody, which is being evaluated in a multiple ascending dose (MAD) clinical trial in AD patients, with initial tau positron emission tomography (PET) data expected in the second half of 2026. VY1706, an IV-delivered tau silencing gene therapy that has shown up to 73% knockdown of tau mRNA in non-human primates following a single IV dose and is advancing towards IND in 2026. A vectorized anti-Aβ antibody gene therapy, which demonstrated over 15-fold greater brain-to-plasma ratio after a single IV dose compared to a passively administered antibody over 4 weeks in a murine model, as presented at the American Society of Gene & Cell Therapy's (ASGCT) 28th Annual Meeting. The APOE gene therapy program, which is designed to knock down APOE in APOE4 carriers while delivering APOE2 and maintaining total APOE levels. About the TRACER™ Capsid Discovery Platform Voyager's TRACER™ (Tropism Redirection of AAV by Cell-type-specific Expression of RNA) capsid discovery platform is a broadly applicable, RNA-based screening platform that enables rapid discovery of novel AAV capsids to enable gene therapy. Voyager has leveraged TRACER to create multiple families of novel capsids that, following intravenous delivery in preclinical studies, harness the extensive vasculature of the central nervous system (CNS) to cross the blood-brain barrier and transduce a broad range of CNS regions and cell types. In cross-species preclinical studies (rodents and multiple non-human primate species), intravenous delivery of TRACER-generated capsids resulted in widespread payload expression across the CNS at relatively low doses, enabling selection of multiple development candidates in Voyager's wholly-owned and partnered gene therapy programs for neurologic diseases. About Voyager Therapeutics Voyager Therapeutics, Inc. (Nasdaq: VYGR) is a biotechnology company dedicated to leveraging the power of human genetics to modify the course of – and ultimately cure – neurological diseases. Our pipeline includes programs for Alzheimer's disease, Friedreich's ataxia, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple other diseases of the central nervous system. Many of our programs are derived from our TRACER™ AAV capsid discovery platform, which we have used to generate novel capsids and identify associated receptors to potentially enable high brain penetration with genetic medicines following intravenous dosing. Some of our programs are wholly owned, and some are advancing with partners including Alexion, AstraZeneca Rare Disease; Novartis Pharma AG; and Neurocrine Biosciences, Inc. For more information, visit Voyager Therapeutics® is a registered trademark, and TRACER™ is a trademark, of Voyager Therapeutics, Inc. Forward-Looking Statements This press release contains forward-looking statements for the purposes of the safe harbor provisions under The Private Securities Litigation Reform Act of 1995 and other federal securities laws. The use of words such as 'will,' 'expect,' 'believe,' 'anticipate,' 'potential,' or 'continue,' and other similar expressions are intended to identify forward-looking statements. For example, all statements Voyager makes regarding Voyager's continued expansion of its AD franchise by advancing multiple programs against tau, amyloid and APOE to treat AD and the potential to sequence and combine such treatments to improve therapeutic outcomes for patients; Voyager's ability to advance its AAV-based gene therapy programs and tau antibody program, including expectations for Voyager's achievement of preclinical and clinical development milestones for its potential development candidates such as the IND filings, the initiation of clinical trials, clinical trial enrollment, and the generation of clinical data; Voyager's ability to advance preclinical programs (i) against ApoE using a single IV-injected TRACER capsid to deliver a bifunctional payload to reduce endogenous ApoE4, as well as (ii) against amyloid by its vectorized anti-Ab antibody gene therapy. Voyager's plans to present scientific data at future conferences; the commercial potential for VY7523 and VY1706; the importance of tau as a target for the treatment of AD; and the potential for third-party clinical data to inform Voyager's clinical development plans are forward looking. All forward-looking statements are based on estimates and assumptions by Voyager's management that, although Voyager believes such forward-looking statements to be reasonable, are inherently uncertain and subject to risks and uncertainties that may cause actual results to differ materially from those that Voyager expected. Such risks and uncertainties include, among others, the expectations and decisions of regulatory authorities; the timing, initiation, conduct and outcomes of Voyager's preclinical and clinical studies; the availability of data from clinical trials; the availability or commercial potential of product candidates under collaborations; the success of Voyager's product candidates; the willingness and ability of Voyager's collaboration partners to meet obligations under collaboration agreements with Voyager; the continued development of Voyager's technology platforms, including Voyager's TRACER platform and its non-viral discovery platform; Voyager's scientific approach and program development progress, and the restricted supply and increased costs of critical research components; the development by third parties of capsid identification platforms that may be competitive to Voyager's TRACER capsid discovery platform; Voyager's ability to create and protect intellectual property rights associated with the TRACER capsid and non-viral discovery platform, the ligands identified by the platform, and development and clinical candidates for Voyager's pipeline programs; the possibility or the timing of Voyager's receipt of program reimbursement, development or commercialization milestones, option exercise, and other payments under Voyager's existing licensing or collaboration agreements; the ability of Voyager to negotiate and complete licensing or collaboration agreements with other parties on terms acceptable to Voyager and the third parties; the success of programs controlled by third-party collaboration partners in which Voyager retains a financial interest; the ability to attract and retain talented directors, employees, and contractors; and the sufficiency of Voyager's cash resources to fund its operations and pursue its corporate objectives. These statements are also subject to a number of material risks and uncertainties that are described in Voyager's most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission. All information in the press release is as of the date of this press release, and any forward-looking statement speaks only as of the date on which it was made. Voyager undertakes no obligation to publicly update or revise this information or any forward-looking statement, whether as a result of new information, future events or otherwise, except as required by law. Contacts Trista Morrison, tmorrison@ Investors: Sarah McCabe, smccabe@ Media: Adam Silverstein, adam@ ____________________________________i Fortea, J., Pegueroles, J., Alcolea, D. et al. APOE4 homozygosity represents a distinct genetic form of Alzheimer's disease. Nat Med 30, 1284–1291 (2024). 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
The Independent
15-07-2025
- Health
- The Independent
Biological changes linked to Alzheimer's begin decades before symptoms appear, study says
A Finnish study indicates that signs of Alzheimer's disease, specifically elevated brain-related biomarkers, may be detectable in blood from middle age. The research, involving 2,051 individuals, found these biological changes in adults aged 41 to 56, suggesting they begin decades before typical symptom onset. The study also identified a potential hereditary component, with a parent's biomarker levels, particularly mothers, possibly linked to similar patterns in their children. Factors such as increasing age and kidney disease were associated with higher biomarker levels, and the APOE ε4 gene was linked to higher levels in older individuals. Researchers cautioned that while promising, these blood tests are not yet suitable for routine diagnosis and require further research for standardization.
Medscape
15-07-2025
- Health
- Medscape
APOE4 May Raise Brain Bleed Risk in Apixaban Users With AF
TOPLINE: Carriers of the apolipoprotein E epsilon 4 (APOE ε4) allele had a threefold higher risk for intracranial hemorrhage (ICH) when taking apixaban for atrial fibrillation (AF) compared with noncarriers, a new study suggested. METHODOLOGY: The study included data for more than 2000 participants (mean age, 71 years; 55% men; 84% with European ancestry) from the All of Us Research Program, collected between 2017 and 2022. The median follow-up duration was 2.9 years. Individuals older than 50 years who were taking apixaban for AF were included in the study, which excluded those with prior ischemic stroke or ICH. After APOE ε4 status was determined, carriers (n = 483) were defined as those having one or two alleles and noncarriers (n = 1555) as those without alleles. The primary outcome was incident ICH after initiating apixaban therapy, including any nontraumatic intraparenchymal, subdural, or subarachnoid hemorrhage. Secondary outcomes included incidences of intraparenchymal hemorrhage, ischemic stroke, and a composite of ischemic stroke and ICH. Also used was a HAS-BLED score, which includes factors such as age, hypertension, stroke, and history of or predisposition for bleeding, to predict risk for major bleeding. TAKEAWAY: About 26 participants developed ICH during the study, with cumulative ICH incidence significantly higher among APOE ε4 carriers than noncarriers (3.1% vs 1%; P = .007). Carrying the APOE ε4 allele was associated with a threefold increase in risk for ICH (hazard ratio [HR], 3.1; P = .004) and intraparenchymal hemorrhage (HR, 3.7; P = .002) compared with not carrying the allele. There were no significant differences between carriers and noncarriers in the other two secondary outcomes. APOE information improved the predictive power of the HAS-BLED score, with C statistics of 0.74 and 0.68 for models with and without APOE information, respectively (P = .03). IN PRACTICE: The findings 'underscore the importance of genetics in personalizing pharmacological therapy, aiding clinicians in identifying high-risk patients and tailoring anticoagulant strategies,' the investigators wrote. 'Further research is needed to evaluate whether cerebral amyloid angiopathy mediates the observed association and whether APOE ε4 information improves clinical decision-making about anticoagulation therapy' in patients with AF, they added. SOURCE: This study was led by Santiago Clocchiatti-Tuozzo, MD, Yale School of Medicine, New Haven, Connecticut. It was published online on June 23 in JAMA Neurology LIMITATIONS: This study could not distinguish between lobar and deep hemorrhages because of its reliance on electronic health record data, limiting the ability to determine the relative contributions of hypertension and cerebral amyloid angiopathy to each hemorrhage type. The predominant European ancestry of participants may have limited the generalizability of the findings. Additionally, external validation of the prediction analyses was not possible because of the lack of other genetic studies in the US evaluating patients with AF treated with apixaban. DISCLOSURES: This study was funded by the National Institutes of Health and the American Heart Association. Several investigators reported having financial ties with various organizations and companies. Full details are provided in the original article. This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Scottish Sun
14-07-2025
- Health
- Scottish Sun
Two common infections may trigger Alzheimer's, scientists warn – are you at risk?
Click to share on X/Twitter (Opens in new window) Click to share on Facebook (Opens in new window) SCIENTISTS have spent decades trying to understand what causes dementia. Is it alcohol? Obesity? Or are some of us simply genetically predisposed? Sign up for Scottish Sun newsletter Sign up 1 Two common infections may play a role in the development of Alzheimer's Credit: Getty The evidence is mixed - though experts generally agree that there are several factors involved in the abnormal build-up of proteins called amyloid and tau, which are what cause symptoms. A new review by Philadelphia College of Osteopathic Medicine, Pennsylvania, suggests two common infections may play a role. Researchers found both chlamydia pneumoniae and SARS-CoV-2 increase the levels of substances in the brain called cytokines. These trigger inflammation, which can "harm brain cells and may help speed up the buildup of harmful proteins linked to Alzheimer's". Chlamydia pneumoniae is a "very common" type of bacteria that causes lung infections, including pneumonia. It affects about 50 per cent of people by age 20, and 75 per cent by 65, and is passed on by sneezing and coughing, according to Superdrug. It is not the same as the STI chlamydia, though both are highly infectious. SARS-CoV-2 is the virus that causes Covid-19. In 2022, seven in 10 people in England were thought to have been infected. That number is now likely much higher. The report, published in Frontiers in Aging Neuroscience, found chlamydia pneumoniae and SARS-CoV-2 can invade the central nervous system through the blood-brain barrier and, "potentially more importantly", the olfactory route, which is responsible for our sense of smell. Common painkiller used for back pain ups risk of dementia by 29%, scientists warn "The olfactory system is lined with a specialised tissue called neuroepithelium that can serve as an entry point for pathogens to the brain," the authors said. "After initial infection, these microbes can travel along the olfactory nerves, ultimately reaching the brain's olfactory bulbs, which are linked to areas of the brain for memory and cognition. "This pathway is particularly relevant given that loss of smell is an early symptom in both Covid-19 and Alzheimer's disease." We hope to create new avenues for prevention and treatment Dr Brian J Balin They looked at patients with certain genetic factors known to significantly increase a person's risk of developing Alzheimer's - the most common form of dementia. This included APOE - a protein which transports fatty molecules like cholesterol to cells in our brain. Everyone carries two copies of APOE, one inherited from each parent. The three most common variants are APOE2, APOE3 and APOE4. Having at least one APOE4 variant is said to double or triple the risk of developing Alzheimer's, and someone with two variants is eight to 12 times more likely to get it, according to Alzheimer's Research UK. About one in 50 people carry two copies of APOE4. Scientists also examined the cytokines IL-6 and CCL2, which are involved in inflammation and immune responses in the body. Those carrying this gene variant appeared to be "more susceptible" to both chlamydia pneumoniae and SARS-CoV-2, "potentially amplifying" their risk for developing Alzheimer's. Co-author Dr Brian J Balin, a professor of neuroscience and neuropathology and director of the Center for Chronic Disorders of Aging, said: "These findings bring us one step closer to understanding the complex interactions between infections and Alzheimer's disease. "As we continue to learn more about the role infectious agents play in the development of this disease, we hope to create new avenues for prevention and treatment." What causes Alzheimer's disease? ALZHEIMER'S disease is thought to be caused by the abnormal build-up of proteins in and around brain cells. One of these is amyloid, deposits of which form plaques around brain cells. The other is tau, deposits of which form tangles within brain cells. Unfortunately, it's not known exactly what causes this process to begin. However, scientists suggest that the following factors are known to increase your risk of developing Alzheimer's: Age - the single most significant factor. The likelihood of developing Alzheimer's disease doubles every five years after you reach 65. Family history - the genes you inherit from your parents can contribute to your risk of developing Alzheimer's disease. Down's syndrome - the genetic changes that cause Down's syndrome can also cause amyloid plaques to build up in the brain over time. Head injuries - people who have had a severe head injury may be at higher risk of developing Alzheimer's disease, but research is still needed in this area. Lifestyle factors and conditions - smoking, obesity, diabetes, high blood pressure are associated with a higher risk. Other factors - research suggests that hearing loss, untreated depression, loneliness or social isolation and a sedentary lifestyle may also play a role. About 980,000 people in the UK are living with dementia. This number is expected to rise to more than 1.4million by 2040. Alzheimer's is the most common form of dementia, accounting for between 60 and 80 per cent of all cases. Symptoms often develop slowly over several years and they may not be obvious at first. In the early stages, it can be difficult to tell the difference between memory problems caused by Alzheimer's, and mild forgetfulness that happens as we get older. But memory loss is one of the most common early symptoms, and may include losing memories of recent events, asking the same questions repeatedly, or having difficulty following conversation and learning new information. Patients may go on to regularly forget names and faces, repeat the same behaviours and routines, regularly misplace things, become confused about the date or time of day, feel disorientated in unfamiliar places, have problems finding the right words, or become low in mood, anxious or agitated. As Alzheimer's progresses, it can impact other areas of life, including communication, sleep, movement, senses and day-to-day care. If you are worried that you or a loved one are experiencing symptoms of Alzheimer's, speak to your GP. While there is no cure, there are treatment options to help manage your symptoms for a time.
Yahoo
19-06-2025
- Health
- Yahoo
A Study Has Revealed The Biggest Risk Factors For Getting Early Dementia, And Knowledge Is Power
A recent study by the University of Exeter and Maastricht University published in JAMA Neurology has identified some of the factors that can lead to early cases of dementia ― some of which may surprise you. The data analyzed the behaviors of over 350,000 participants younger than 65 across the United Kingdom to evaluate young-onset dementia, which occurs before age 65. The researchers found there are 15 common issues that can contribute to the early development of the condition. A few have to do with genetics and other elements outside our control, but many others are modifiable. The study is meaningful to experts because it 'looks at young-onset dementia risk factors in a way that has only been done in late-onset dementias previously,' according to Dr. Kevin Bickart, an assistant professor in neurology at the University of California Los Angeles Health's David Geffen School of Medicine. The study features 'a very large sample that was prospectively followed from healthy baseline to a dementia diagnosis with lots of data collection.' Here's what to know: The biggest risk factors for young-onset dementia: Related: "This Has Taken Me Years And Years And YEARS To Figure Out": This Woman's Clever Way To Tell If Someone Is Your Real Friend Is Being Called The Most Accurate Thing Ever Related: 25 Eye-Opening Confessions From A Trauma Therapist That Changed The Way I Think About Mental Health The large-scale study looked at 39 possible risk factors and determined that 15 of them made the biggest difference when it came to developing dementia before the age of 65. Those include: Social isolation Lower formal education Lower socioeconomic status Carrying two copies of the APOE gene (a marker that influences Alzheimer's risk) Vitamin D deficiency Hearing impairment Alcohol use disorder No alcohol use (abstinence) Depression High C-reactive protein levels Lower handgrip strength (physical frailty) Orthostatic hypotension (a form of low blood pressure) Stroke Diabetes Heart disease Although some recognized risks are out of many people's control ― like being a carrier of the APOE gene or your socioeconomic status ― others can be managed through lifestyle changes. What you can do to lower your risk of early-onset dementia. Overall, the study results are consistent with what medical experts have been advising patients for years. Dr. Arman Fesharaki-Zadeh, an assistant professor of psychiatry and of neurology at the Yale School of Medicine, recommended three 'lifestyle measures' that folks may want to consider when trying to lower their risk of young-onset dementia ― starting with physical exercise. 'An active daily exercise practice can have far-reaching benefits, which include enhanced neurocognitive function,' Fesharaki-Zadeh said, adding that physical activity can boost neurogenesis (the formation of new neurons and synapses), vasculogenesis (the creation of new blood vessels) while also providing inherent mood benefits. Next, focus on eating nourishing foods. Fesharaki-Zadeh championed a Mediterranean-based diet, mentioning its well-documented benefits. 'Such dietary practice, which includes food groups such as green leafy vegetables, olive oil, salmon and blueberries, is rich in vitamins, omega-3 fatty acids, as well as antioxidants ― all neuroprotective factors,' he explained. Fesharaki-Zadeh recommended cognitive, mood and social stimulation to keep your mind sharp. For cognitive stimulation, this could look like learning a new language or attending a seminar, listening to music or dancing. Basically, anything that engages your mind will help it stay healthy. Mood stimulation, on the other hand, relates to stress reduction practices, 'such as mindfulness and yoga,' Fesharaki-Zadeh said. As for social stimulation, it's pretty simple: Try to connect with other humans face-to-face and actually talk to them as much as possible. 'In the era of pandemic and now post-pandemic, quality social connections should increasingly be encouraged and practiced,' Fesharaki-Zadeh said. While these habits don't cover the whole list of dementia risk factors, they are a pretty solid article originally appeared on HuffPost. Also in Goodful: Therapists Are Revealing The Moments That Made Them Break Their "No Judgment" Rule, And I'm Honestly Speechless Also in Goodful: 19 "Garbage" Modern Trends People Refuse To Partake In Despite Their Popularity Also in Goodful: Medical Professionals Are Sharing "Mundane" Things That Actually Make So Many People Sick
