Worried about Alzheimer's? Start walking, according to a new 10-year study
A new study shows that walking daily can reduce the risk of cognitive decline — especially among those with a genetic predisposition for Alzheimer's disease.
Almost 3,000 participants between the ages of 70 and 79 reported their daily walking habits over the course of 10 years, according to research that will be presented Tuesday at the annual Alzheimer's Association International Conference. Those who reported maintaining or increasing their walking habits over the years showed greater improvements in processing speed and executive function.
The benefits of walking were especially noticeable among those with a genetic predisposition for developing Alzheimer's disease, according to the preprint, which has not been peer-reviewed or published in a professional journal.
'We know sedentary behavior increases as you get older, and physical activity decreases,' said senior study author Dr. Cindy Barha, an assistant professor of kinesiology at the University of Calgary in Alberta. 'So we recommend reducing your sedentary behavior by introducing small bouts of walking in between those times you have to be sitting down.'
How does Alzheimer's disease work?
Alzheimer's disease is a severe form of dementia thought to be caused by a buildup of harmful plaques in the brain that interfere with how the nerve cells communicate, eventually leading to their death, Barha said.
As more nerve cells die, people with Alzheimer's can develop progressive memory loss, confusion, personality changes and physical decline. Eventually, the disease can be fatal, and there is no known cure.
Genetics are thought to play a major role in the disease. Specifically, genotypes called APOE affect the metabolism of plaque and other fats throughout the bloodstream. One specific kind, APOE4, is known to make it harder for the brain to clear the plaques and is linked to a higher risk of cognitive decline.
About 15% to 25% of people have this version of the APOE gene, and the only way to find out is from a genetic test, according to data from the US National Institutes of Health.
The mind-body connection
Although the new study did not test a uniform walking regimen, Barha suggests walking multiple times daily to break up sedentary behavior and maintaining consistent walking habits year to year to prevent cognitive decline.
'More research is really needed to determine how many steps that really takes, but more is definitely going to be better,' she said. 'The next steps would be to actually try to figure out the minimum amount of walking for different subgroups, (such as) females versus males, APOE4 carriers versus non-carriers.'
A 2022 study found that even people who walked about 3,800 steps per day at any speed cut their risk of dementia by 25%.
What might be going on between the brain and the rest of the body? Experts have several theories.
For one, regular exercise has been shown to help the body produce more of a protein called brain-derived neurotrophic factor, or BDNF, which is like fertilizer for your brain, helping it grow more cells and form new connections, Barha explained.
'We're thinking there's proteins released from the muscle that travel to the brain and, either across the blood-brain barrier or at the blood-brain barrier, start a reaction that eventually leads to increases in BDNF within the brain,' she said.
Another theory is that exercise reduces neuroinflammation, a common symptom of Alzheimer's disease.
The brain sends immune cells called microglia to attack plaque buildup, but this can backfire, explained Dr. Christiane Wrann, an associate professor of medicine at the Cardiovascular Research Center at Massachusetts General Hospital and Harvard Medical School. Chronic inflammation can lead microglia to begin attacking healthy brain cells as well, damaging the brain's connections.
'If you exercise, you actually strengthen the gene expression program that microglia need to function properly,' Wrann said.
Does greater risk mean greater reward?
The researchers were surprised to find that walking provided the greatest benefit to those with the APOE4 gene compared to those without it. To understand why this is, more research will be needed — but Barha has a theory.
'Before the study started, we think APOE4 carriers had more room to grow in terms of cognition, since they may already have been experiencing some cognitive decline,' she said. 'They also have more room to show improvement.'
It's possible that the study itself also motivated participants with APOE4 genes to walk more than they had been beforehand, slowing their rate of decline.
'This is a very strong example (that) it's never too late to start exercising,' Wrann said. 'Every step counts, and it's much better to do an exercise regimen that you actually like, that you can actually stick to.'
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Protofibrils can cause neuronal and synaptic damage in the brain, which can subsequently adversely affect cognitive function through multiple mechanisms.1 The mechanism by which this occurs has been reported not only by increasing the formation of insoluble Aβ plaques, but also by directly damaging signaling between neurons and other cells. It is believed that reducing protofibrils may reduce neuronal damage and cognitive impairment, potentially preventing the progression of AD. 2 MEDIA CONTACTSEisai Co., Ltd. Public Relations Department TEL: +81 (0)3-3817-5120 Eisai Europe, Ltd. EMEA Communications Department +44 (0) 797 487 9419 Emea-comms@ Eisai Inc. (U.S.) Libby Holman +1-201-753-1945 Libby_Holman@ Biogen Inc. Madeleine Shin +1-781-464-3260 INVESTOR CONTACTSEisai Co., Ltd. Investor Relations Department TEL: +81 (0) 3-3817-5122 Biogen Inc. Tim Power + 1-781-464-2442 IR@ Notes to Editors 1. About lecanemab (generic name, brand name: LEQEMBI®)Lecanemab is the result of a strategic research alliance between Eisai and BioArctic. It is a humanized immunoglobulin gamma (IgG1) monoclonal antibody directed against aggregated soluble (protofibril) and insoluble forms of amyloid-beta (Aβ). Protofibrils are believed to contribute to the brain injury that occurs with AD and are considered to be the most toxic form of Aβ, having a primary role in the cognitive decline associated with this progressive, debilitating condition.1 Protofibrils cause injury to neurons in the brain, which in turn, can negatively impact cognitive function via multiple mechanisms, not only increasing the development of insoluble Aβ plaques but also increasing direct damage to brain cell membranes and the connections that transmit signals between nerve cells or nerve cells and other cells.2 It is believed the reduction of protofibrils may prevent the progression of AD by reducing damage to neurons in the brain and cognitive dysfunction. Lecanemab has been approved in 46 countries and is under regulatory review in 11 countries. In January 2025, the supplemental Biologics License Application (sBLA) for intravenous (IV) maintenance dosing of the treatment was approved in the U.S. After an 18 months initiation phase with once every two weeks of dosing, a transition to the maintenance dosing regimen of 10 mg/kg once every four weeks or continuing 10 mg/kg once every two weeks may be considered. Additionally, the U.S. Food and Drug Administration (FDA) accepted Eisai's Biologics License Application (BLA) for the LEQEMBI subcutaneous autoinjector for weekly maintenance dosing in January 2025 and set a PDUFA action date for August 31, 2025. Since July 2020 the Phase 3 clinical study (AHEAD 3-45) for individuals with preclinical AD, meaning they are clinically normal and have intermediate or elevated levels of amyloid in their brains, is ongoing. AHEAD 3-45 is conducted as a public-private partnership between the Alzheimer's Clinical Trial Consortium that provides the infrastructure for academic clinical trials in AD and related dementias in the U.S, funded by the National Institute on Aging, part of the National Institutes of Health, Eisai and Biogen. Since January 2022, the Tau NexGen clinical study for Dominantly Inherited AD (DIAD), that is conducted by Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU), led by Washington University School of Medicine in St. Louis, is ongoing and includes lecanemab as the backbone anti-amyloid therapy. 2. About the Collaboration between Eisai and Biogen for ADEisai and Biogen have been collaborating on the joint development and commercialization of AD treatments since 2014. Eisai serves as the lead of lecanemab development and regulatory submissions globally with both companies co-commercializing and co-promoting the product and Eisai having final decision-making authority. 3. About the Collaboration between Eisai and BioArctic for ADSince 2005, Eisai and BioArctic have had a long-term collaboration regarding the development and commercialization of AD treatments. Eisai obtained the global rights to study, develop, manufacture and market lecanemab for the treatment of AD pursuant to an agreement with BioArctic in December 2007. The development and commercialization agreement on the antibody lecanemab back-up was signed in May 2015. 4. About Eisai Co., Corporate Concept is "to give first thought to patients and people in the daily living domain, and to increase the benefits that health care provides." Under this Concept (also known as human health care (hhc) Concept), we aim to effectively achieve social good in the form of relieving anxiety over health and reducing health disparities. With a global network of R&D facilities, manufacturing sites and marketing subsidiaries, we strive to create and deliver innovative products to target diseases with high unmet medical needs, with a particular focus in our strategic areas of Neurology and Oncology. In addition, we demonstrate our commitment to the elimination of neglected tropical diseases (NTDs), which is a target (3.3) of the United Nations Sustainable Development Goals (SDGs), by working on various activities together with global partners. For more information about Eisai, please visit (for global headquarters: Eisai Co., Ltd.), and connect with us on X, LinkedIn and Facebook. The website and social media channels are intended for audiences outside of the UK and Europe. For audiences based in the UK and Europe, please visit and Eisai EMEA LinkedIn. 5. About Biogen Founded in 1978, Biogen is a leading biotechnology company that pioneers innovative science to deliver new medicines to transform patient's lives and to create value for shareholders and our communities. We apply deep understanding of human biology and leverage different modalities to advance first-in-class treatments or therapies that deliver superior outcomes. Our approach is to take bold risks, balanced with return on investment to deliver long-term growth. The company routinely posts information that may be important to investors on its website at Follow Biogen on social media – Facebook, LinkedIn, X, YouTube. Biogen Safe HarborThis news release contains forward-looking statements, including about the potential clinical effects of lecanemab; the potential benefits, safety and efficacy of lecanemab; potential regulatory discussions, submissions and approvals and the timing thereof; the treatment of Alzheimer's disease; the anticipated benefits and potential of Biogen's collaboration arrangements with Eisai; the potential of Biogen's commercial business and pipeline programs, including lecanemab; and risks and uncertainties associated with drug development and commercialization. These forward-looking statements may be accompanied by such words as "aim," "anticipate," "assume," "believe," "contemplate," "continue," "could," "estimate," "expect," "forecast," "goal," "guidance," "hope," "intend," "may," "objective," "plan," "possible," "potential," "predict," "project," "prospect," "should," "target," "will," "would," and other words and terms of similar meaning. Drug development and commercialization involve a high degree of risk, and only a small number of research and development programs result in commercialization of a product. Results in early-stage clinical trials may not be indicative of full results or results from later stage or larger scale clinical trials and do not ensure regulatory approval. You should not place undue reliance on these statements. Given their forward-looking nature, these statements involve substantial risks and uncertainties that may be based on inaccurate assumptions and could cause actual results to differ materially from those reflected in such statements. These forward-looking statements are based on management's current beliefs and assumptions and on information currently available to management. Given their nature, we cannot assure that any outcome expressed in these forward-looking statements will be realized in whole or in part. We caution that these statements are subject to risks and uncertainties, many of which are outside of our control and could cause future events or results to be materially different from those stated or implied in this document, including, among others, uncertainty of long-term success in developing, licensing, or acquiring other product candidates or additional indications for existing products; expectations, plans and prospects relating to product approvals, approvals of additional indications for our existing products, sales, pricing, growth, reimbursement and launch of our marketed and pipeline products; our ability to effectively implement our corporate strategy; the successful execution of our strategic and growth initiatives, including acquisitions; the risk that positive results in a clinical trial may not be replicated in subsequent or confirmatory trials or success in early stage clinical trials may not be predictive of results in later stage or large scale clinical trials or trials in other potential indications; risks associated with clinical trials, including our ability to adequately manage clinical activities, unexpected concerns that may arise from additional data or analysis obtained during clinical trials, regulatory authorities may require additional information or further studies, or may fail to approve or may delay approval of our drug candidates; the occurrence of adverse safety events, restrictions on use with our products, or product liability claims; and any other risks and uncertainties that are described in other reports we have filed with the U.S. Securities and Exchange Commission. These statements speak only as of the date of this press release and are based on information and estimates available to us at this time. Should known or unknown risks or uncertainties materialize or should underlying assumptions prove inaccurate, actual results could vary materially from past results and those anticipated, estimated or projected. Investors are cautioned not to put undue reliance on forward-looking statements. A further list and description of risks, uncertainties and other matters can be found in our Annual Report on Form 10-K for the fiscal year ended December 31, 2024 and in our subsequent reports on Form 10-Q and Form 10-K, in each case including in the sections thereof captioned "Note Regarding Forward-Looking Statements" and "Item 1A. Risk Factors," and in our subsequent reports on Form 8-K. Except as required by law, we do not undertake any obligation to publicly update any forward-looking statements whether as a result of any new information, future events, changed circumstances or otherwise. References Amin L, Harris DA. Aβ receptors specifically recognize molecular features displayed by fibril ends and neurotoxic oligomers. Nat Commun. 2021;12:3451. doi:10.1038/s41467-021-23507-z Ono K, Tsuji M. Protofibrils of Amyloid-β are Important Targets of a Disease-Modifying Approach for Alzheimer's Disease. Int J Mol Sci. 2020;21(3):952. doi: 10.3390/ijms21030952. PMID: 32023927; PMCID: PMC7037706. View original content to download multimedia: SOURCE Eisai Inc.
