
Eating eggs weekly may lower Alzheimer's risk by nearly 50 percent: Study
Published in The Journal of Nutrition, the study followed more than 1,000 U.S. adults and found that those who consumed more than one egg weekly had a 47 percent reduced risk of Alzheimer's.
Over an average follow-up of 6.7 years, 280 participants, or 27.3 percent, were diagnosed with Alzheimer's dementia. Researchers found that 39 percent of the 'total effect of egg intake' was linked to choline, a nutrient found in egg yolks known to support memory and brain function.
Egg yolks also contain omega-3 fatty acids, which have neuroprotective benefits, further supporting brain health.
This research builds on an earlier study that found that even limited egg consumption, around one per week, was associated with slower memory decline compared to little or no egg intake.
While the findings are promising, researchers emphasize that the study shows an association, not a direct cause-and-effect relationship.

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Yahoo
10 minutes ago
- Yahoo
FIRST ON CNN: Fighting early-stage Alzheimer's with intensive lifestyles changes works, study finds
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It was really good — like I was prior to the disease being diagnosed,' Maida, now 68, told a researcher on the study. 'An older but better version of me.' Maida's cognition showed additional improvement, however, after she completed a total of 40 weeks of intensive lifestyle changes, said principal investigator Dr. Dean Ornish, a clinical professor of medicine at the University of California, San Francisco, and creator of the Ornish diet and lifestyle medicine program. Ornish gave a study update on Tuesday at the 2025 Alzheimer's Association International Conference in Toronto. While not everyone in the 26-person interventional group benefited, 46% showed improvement in three of four standardized tests, he said, including one that measures changes in memory, judgment and problem-solving as well as the ability to function at home, practice hobbies and practice personal hygiene. 'An additional 37.5% of people showed no decline in cognition during those 40 weeks,' Ornish said. 'Thus, over 83% of patients improved or maintained their cognition during the five-month program.' The new findings mirrored those of other studies on lifestyle interventions, he said, including the recent US POINTER study, the largest clinical trial in the United States to test moderate lifestyle interventions over two years in people who are at risk but do not yet have Alzheimer's disease. 'Our study complements these findings by showing, for the first time, that more intensive lifestyle changes may often stop or even begin to reverse the decline in cognition in many of those who already have Alzheimer's disease, and these improvements often continue over a longer period of time,' Ornish told CNN. And unlike available medications for Alzheimer's, he added, lifestyle changes have no side effects, such as bleeding and swelling in the brain that may occur with the newest class of drugs. EmblemHealth, a New York-based insurance company, announced Tuesday that it will be the first health insurer to cover the Ornish lifestyle medicine program for patients who have early-stage Alzheimer's disease. 'Eat well, move more, stress less and love more' The lifestyle intervention Ornish created — which he calls 'eat well, move more, stress less and love more' — has been tested before. In 1990, Ornish showed for the first time in a randomized clinical trial that coronary artery disease could often be reversed with nothing more than diet, exercise, stress reduction and social support. The US Centers for Medicare and Medicaid Services, or CMS, declared in 2010 that Ornish's program for reversing heart disease was an 'intensive cardiac rehabilitation' and that it would be eligible for reimbursement under Medicare. Additional research has shown the same four-part program can lower blood sugars and heart disease risk in patients with diabetes, reduce prostate cancer cell growth, improve depression and even lengthen telomeres, the protective caps of chromosomes that are worn away by aging. During the Ornish intervention, one group of people consumed a strict vegan diet, did daily aerobic exercise, practiced stress reduction and engaged in online support groups. The rest of the participants were in a control group and were asked to not make any changes in their daily habits. Therapists led hour-long group sessions three times a week in which participants were encouraged to share their feelings and ask for support. Meditation, deep breathing, yoga and other ways to reduce stress took up another hour every day. The program also encouraged participants to prioritize good-quality sleep. 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Working harder pays off People in the intervention group who put the most effort into changing their lifestyle have the most improvement in their cognition, said Ornish, founder and president of the nonprofit Preventive Medicine Research Institute and coauthor of 'Undo It! How Simple Lifestyle Changes Can Reverse Most Chronic Diseases.' 'There was a statistically significant dose-response relationship between the degree of adherence to our lifestyle changes and the degree of improvement we saw on measures of cognition,' Ornish said. The 25 people in the study's original 20-week control group — who did not receive the intervention — had shown further cognitive decline during the program. They were later allowed to join the intervention for 40 weeks and significantly improved their cognitive scores during that time, Ornish said. It all makes sense, said co-senior study author Rudy Tanzi, an Alzheimer's researcher and professor of neurology at Harvard Medical School in Boston. 'If you picture a brain full of damage as a sink full of water, when you just turn off the tap, it takes a long time for that sink to slowly drain, right?' Tanzi told CNN in 2024. 'If you want the amyloid to go down in 20 weeks, as we found on one blood test, you're going to need a Roto-Rooter.' Additional blood testing may offer insights In the 2024 study, a blood test called plasma Aβ42/40 showed a significant improvement in the original intervention group. Aβ42/40 measures the level of amyloid in the blood, a key symptom of Alzheimer's. Tests that measure amyloid in different ways, however, did not show improvement, Dr. Suzanne Schindler, an associate professor of neurology at Washington University School of Medicine in St. Louis who specializes in blood biomarkers told CNN at the time. There was no significant change in a test for amyloid called p-tau 181, considered to be a superior measure of Alzheimer's risk, said Schindler, who was not involved in the study. 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'So often when people get a diagnosis of dementia or Alzheimer's, they are told by their doctors that there is no future, 'It's only going to get worse, get your affairs in order.' That's horrible news and is almost self-fulfilling,' Ornish said. 'Our new findings empower patients who have early-stage Alzheimer's disease with the knowledge that if they make and maintain these intensive lifestyle changes, there is a reasonably good chance that they may slow the progression of the disease and often even improve it,' he said. 'Our study needs to be replicated with larger, more diverse groups of patients to make it more generalizable,' Ornish said. 'But the findings we reported today are giving many people new hope and new choices — and the only side effects are good ones.' Get inspired by a weekly roundup on living well, made simple. Sign up for CNN's Life, But Better newsletter for information and tools designed to improve your well-being.


Medscape
2 hours ago
- Medscape
Combination CVD Meds Tied to Slower Cognitive Decline
Older adults taking a combination of medications to treat high blood pressure, cholesterol, and diabetes experienced slower cognitive decline and reduced dementia-related brain pathologies than those taking fewer or no such medications, a large analysis showed. 'In individuals simultaneously using two or three medication classes, the decline of cognition was slower, equivalent to the change in cognition of a person 3 years younger than the average age on this sample,' Roshni Biswas, MBBS, PhD, MPH, research scientist, Rush Alzheimer's Disease Center, Chicago, told Medscape Medical News . 'Our findings suggest that early interventions with combination therapies targeting multiple vascular metabolic risk factors could potentially delay or prevent cognitive decline and dementia,' Biswas said. The study was presented on July 27 at Alzheimer's Association International Conference (AAIC) 2025. Heart-Brain Connections Hypertension, dyslipidemia, and diabetes are known risk factors for dementia. Antihypertensives, lipid-lowering, and antidiabetic medications may help reduce the risk for dementia. However, a few studies have examined the association of combination cardiovascular therapies with cognitive decline and dementia-related postmortem neuropathologies. To that end, Biswas and colleagues evaluated 4651 older adults without dementia at baseline who participated in five ongoing longitudinal studies of aging and dementia at the Rush Alzheimer's Disease Center. Participants underwent at least two annual cognitive assessments for an average of 9 years. Use of antihypertensive, lipid-lowering, and antidiabetic medications was documented annually. In a subgroup of 1896 participants who had died and undergone autopsy, the researchers evaluated the extent of Alzheimer's disease (AD) and other dementia-related neuropathologies. Synergistic Effects? Compared with no medication use, treatment with all three medication classes was associated with a slower decline in global cognition ( P = .02), particularly semantic and working memory, the researchers found. Among autopsied participants, treatment with all three medication classes was associated with lower odds of atherosclerosis (odds ratio [OR], 0.47; P < .01) and arteriolosclerosis (OR, 0.53; P = .01); less global AD pathology ( P < .01), specifically amyloid and tangles; and lower odds of hippocampal sclerosis (OR, 0.27; P = .03) and TDP-43 (OR, 0.46; P < .01), a protein increasingly recognized as a key player in AD pathology, particularly in its later stages. Even treatment with just two medication classes was associated with a slower decline in global cognition ( P < .01), as well as lower odds of atherosclerosis (OR, 0.63; P < .01), less global AD pathology ( P = .03) and tangles ( P = .03), and lower odds of TDP-43 (OR, 0.71; P = .02). Use of a single class of medication was associated with more limited but still measurable benefits, especially in preserving semantic memory and reducing tangles. 'Our study raises the possibility for increased beneficial effects of combination vascular metabolic therapies (as opposed to single therapy) in preventing cognitive decline and dementia in aging. However, further study is needed before making clinical recommendations,' Biswas told Medscape Medical News . Reached for comment, Courtney Kloske, PhD, director of scientific engagement at the Alzheimer's Association, said this study supports the 'heart-brain connection' and demonstrates that 'controlling modifiable vascular risk factors could have beneficial impacts on the brain.'


Hamilton Spectator
2 hours ago
- Hamilton Spectator
ProMIS Neurosciences to Showcase Protein-Misfolding Drug Discovery Platform & PRECISE-AD Trial Design at the 2025 Alzheimer's Association International Conference
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'PRECISE-AD was intentionally designed with a robust framework to assess both the safety and potential signs of efficacy of PMN310. PMN310 is designed to selectively target toxic amyloid-beta oligomers, which are considered a primary driver of Alzheimer's disease, while aiming to reduce the risk of safety issues observed with other therapies. We were encouraged by the recent recommendation from the independent Data and Safety Monitoring Board (DSMB) to proceed to the second dose level, and we have been enrolling patients swiftly into this second cohort.' 'As of this week, more than 50% of the approximately 128 patients planned for the study have been enrolled, reflecting the pace of our clinical progress and the urgent need for new treatment options. To date, we have not observed any cases of amyloid-related imaging abnormalities (ARIA), including brain swelling or microhemorrhages. 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'Additionally, we are pleased to have been invited to share data supporting the design process and validation of our proprietary target discovery engine, EpiSelectTM, which utilizes advanced computational discovery technologies to identify and target toxic misfolded proteins implicated in neurodegenerative and other misfolded protein diseases,' said Neil Cashman, M.D., Chief Scientific Officer and Co-founder, ProMIS Neurosciences. 'This precision targeting approach has enabled us to design novel therapeutic antibodies with a high degree of selectivity for the key underlying drivers of these conditions.' Presentation details Title: Protein misfolding-specific epitope identification for passive and active immunotherapy of neurodegenerative diseases Presenter: Neil Cashman, M.D., Chief Scientific Officer and Co-founder, ProMIS Neurosciences Session: Featured Research Session: Advancing Translational Success by Enhancing Predictive Validity in Neurodegenerative Diseases, Thursday, July 31, 2025: 10:00am – 11:30am Eastern Time Abstract Number: 98670 Title: PRECISE-AD, A Phase 1b, Double-Blind, Placebo-Controlled, Multiple Ascending Dose Study of the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Preliminary Efficacy of PMN310 in Patients with Early Alzheimer's Disease Presenter: Larry Altstiel, M.D., Ph.D., Chief Medical Officer, ProMIS Neurosciences Session: In Person Poster: Drug Development: Human, Wednesday, July 30, 2025: 7:30am – 4:15pm Eastern Time Poster Number: 103159 Title: Leveraging recent advances in biomarkers to optimize early phase drug development in Alzheimer's Disease Joint Presenter: Garret Duncan, Statistician, Pentara Corporation and Johanne Kaplan, Ph.D., Chief Development Officer, ProMIS Neurosciences Session: In Person Poster: Biomarkers: Biomarkers (non-neuroimaging), Monday, July 28, 2025: 7:30am – 4:15pm Eastern Time Poster Number: 103841 Abstracts will be available on the Poster and Publications page of the Company's website at n following the presentations. About PMN310 and the PRECISE-AD Clinical Trial PMN310, the Company's lead product candidate for the treatment of AD, is a humanized monoclonal antibody that has been designed to be differentiated in its ability to selectively target only the toxic oligomers, avoiding plaque, thereby potentially reducing or eliminating ARIA liability. In addition, because PMN310 may not be limited by off-target binding or side effects, PMN310 could potentially offer an improved efficacy profile over other amyloid-directed antibody therapeutics. Based on the encouraging results from the Phase 1a trial ( NCT06105528 ) of PMN310, ProMIS initiated PRECISE-AD, a Phase 1b clinical trial in AD patients. PRECISE-AD ( NCT06750432 ) is a randomized, double-blind, placebo-controlled study to evaluate the safety, tolerability and pharmacokinetics (PK) of multiple ascending doses (5, 10, 20 mg/kg) of intravenous PMN310 in patients with Mild Cognitive Impairment due to AD and mild AD (Stage 3 and Stage 4 AD). PRECISE-AD will be the first study to examine the effects of a monoclonal antibody directed solely against AβO on biomarkers associated with AD pathology and clinical outcomes. Safety will be a primary outcome of the study with particular emphasis on assessing whether, as a non-plaque binder, PMN310 may have a reduced risk of ARIA. The study is powered to provide 95% confidence for detection of ARIA. The study has been designed with a sample size intended to provide sufficient power to provide meaningful insight into effects of PMN310 on biomarkers and clinical outcomes. About ProMIS Neurosciences Inc. ProMIS Neurosciences is a clinical-stage biotechnology company committed to the discovery and development of therapeutic antibodies selective for toxic oligomers associated with the development and progression of neurodegenerative and other misfolded protein diseases. The Company's proprietary target discovery engine, EpiSelect™, predicts novel targets known as Disease Specific Epitopes (DSEs) on the molecular surface of misfolded proteins that cause neurodegenerative and other misfolded protein diseases, including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), multiple system atrophy (MSA), and Parkinson's Disease (PD). ProMIS has offices in Cambridge, Massachusetts (USA) and Toronto, Ontario (CAN). Forward-Looking Statements This press release contains forward-looking statements that are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Certain information in this news release constitutes forward-looking statements and forward-looking information (collectively, 'forward-looking information') within the meaning of applicable securities laws. In some cases, but not necessarily in all cases, forward-looking information can be identified by the use of forward-looking terminology such as 'plans', 'pleased to', 'look forward to', 'potential to', 'targets', 'expects' or 'does not expect', 'is expected', 'excited about', 'an opportunity exists', 'is positioned', 'estimates', 'intends', 'assumes', 'anticipates' or 'does not anticipate' or 'believes', or variations of such words and phrases or state that certain actions, events or results 'may', 'could', 'would', 'might', 'will' or 'will be taken', 'occur' or 'be achieved'. In addition, any statements that refer to expectations, projections or other characterizations of future events or circumstances contain forward-looking information. Specifically, this news release contains forward-looking information relating to the Company's progress and expectations for its Phase 1b clinical trial in AD patients, including planned timing for completion and anticipated data readout of interim and full results in the second and fourth quarters of 2026, repsectively, the potential for such studies to provide the first proof-of-concept data for PMN310, the potential for PMN310 to positively benefit patients with AD and to be a more effective and well-tolerated option, the targeting of toxic misfolded proteins in neurodegenerative diseases that the Company believes may directly address fundamental AD pathology (including the belief and understanding that toxic oligomers of Aβ are a major driver of AD) and have greater therapeutic potential due to reduction of off-target activity and the Company's expectations regarding the benefits of Fast Track Designation and management's belief that its proprietary target discovery engine can predict and identify toxic misfolded proteins implicated in the development and progression of neurodegenerative and other misfolded protein diseases. Statements containing forward-looking information are not historical facts but instead represent management's current expectations, estimates and projections regarding the future of our business, future plans, strategies, projections, anticipated events and trends, the economy and other future conditions. Forward-looking information is necessarily based on a number of opinions, assumptions and estimates that, while considered reasonable by the Company as of the date of this news release, are subject to known and unknown risks, uncertainties and assumptions and other factors that may cause the actual results, level of activity, performance or achievements to be materially different from those expressed or implied by such forward-looking information, including, but not limited to, the risk that enrollment may not continue at the current rate, that clinical results or early results may not be indicative of future results, the Company's ability to retain and recognize the incentives conferred by Fast Track Designation for PMN310, the Company's ability to fund its operations and continue as a going concern, its accumulated deficit and the expectation for continued losses and future financial results. Important factors that could cause actual results to differ materially from those indicated in the forward-looking information include, among others, the factors discussed throughout the 'Risk Factors' section of the Company's most recently filed Annual Report on Form 10-K for the year ended December 31, 2024 and in its subsequent filings filed with the United States Securities and Exchange Commission. Except as required by applicable securities laws, the Company undertakes no obligation to publicly update any forward-looking information, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise. For further information: Visit us at Please submit media inquiries to info@ For Investor Relations, please contact: Kaytee Bock Zafereo