Doctors Say This Easy Habit Can Protect Your Brain As You Age—And Might Prevent Alzheimer's Disease
New research suggests being curious can protect brain health as you age.
Older adults who stay curious and learn new things may be able to offset Alzheimer's disease.
By tapping into your senses, you can easily experience newness in a known environment.
Little kids ask questions about absolutely everything: why you have to flush the toilet, what the backstory is for a stranger's tattoo, what love means. The list goes on and nothing is off-limits. But that curiosity tends to drop off as we grow up and get older. And apparently, recent research says that's not a good thing for your brain.
A new study suggests that older adults who maintain a healthy dose of curiosity and try to learn new things may be able to help offset or even prevent Alzheimer's disease. And yes, that almost sounds too easy to be true.
So, what's behind this curiosity-dementia link? Women's Health tapped neurologists for more.
Meet the experts: Clifford Segil, DO, is a neurologist at Providence Saint John's Health Center in Santa Monica, CA; Amit Sachdev, MD, MS, is the medical director in the Department of Neurology at Michigan State University
The study, which was published in PLOS One, recruited more than 1,200 people between the ages of 20 and 84, and asked them to fill out an online questionnaire with the goal of figuring out how curious they were in general.
The researchers then asked participants to guess the answers to hard trivia questions that most people likely wouldn't know. For example, What was the first country to give women the right to vote? (Answer: New Zealand!) After they guessed the answer, participants were asked how interested they were to know the answer before they were shown it.
The researchers discovered that people who have more "state curiosity" (which is a fleeting desire to know something) also have more "trait curiosity" (i.e. they're naturally curious), and vice versa. But the researchers also discovered that the drive to learn new things dropped in early adulthood, increased sharply after middle age, and continued upward into older age.
The researchers said in a press release that older adults who are able to stay curious and want to learn new things may be able to offset or even prevent Alzheimer's disease (even though the study didn't explicitly look at data to support this conclusion). But those who aren't interested in learning new things may be at risk for dementia.
This conclusion isn't groundbreaking, by the way: Other studies suggest that older adults who are highly curious have better long-term memory retention than their less-curious counterparts.
There are a few things going on that make your curiosity protective to your brain health. 'New interests develop robust connections in the brain,' says Amit Sachdev, MD, MS, medical director in the Department of Neurology at Michigan State University. 'This network of connections is what builds a more resilient brain.'
Doing the same thing repeatedly also gets old, points out Clifford Segil, DO, a neurologist at Providence Saint John's Health Center in Santa Monica, CA. 'As we age, trying to avoid this repetition is healthy,' he says. 'Reading a new book is likely better for your brain than reading an old book again.'
Ultimately, Dr. Segil says that seeking out new things 'may create new brain pathways rather than strengthening old pathways.'
Dr. Segil recommends that you try to touch on your five senses (vision, hearing, touch, smell, and taste) while experiencing new things.
That means eating new foods, looking at new art, and going to a concert and hearing something different, he says.
A lot of the scientific findings on this topic have similar conclusions when it comes to supporting good brain health:
Don't smoke.
Do moderate to vigorous exercise for at least 150 minutes a week.
Limit how much alcohol you have.
Try to do brain-stimulating activities, like reading, playing games, and visiting museums, regularly.
Eat a healthy, varied diet, like the MIND diet.
Oh, and of course, stay curious. You never know where it can lead you—and your mind.
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2 hours ago
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Why getting rid of belly fat is key to a longer, healthier life
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A good method is to briskly walk for at least 30 minutes a day —'but when I say briskly, I mean fast enough to lose your breath and not be able to hold a conversation. Keep that up for a half hour at a minimum.' The critical next step is to add resistance, otherwise known as strength training, he added. 'When I tell people to go walking or biking or swimming or jogging, I usually recommend that they do resistance concurrently,' Freeman said. 'Carry some weights with them, or put on a weighted backpack, put resistance on the bike or bike uphill, and put fins on their hands when they swim so that there's resistance in the water. Do whatever they need to try to combine the cardio with strength training.' Some of the most effective resistance exercises for building lean muscle and losing fat require multiple joints in the body to work together, according to the nonprofit American Council on Exercise. Dead lifts, lunges, planks, presses, pull-ups and push-ups require many muscles that elevate oxygen use and the release of hormones such as adrenaline that increase blood flow to muscles and boost overall heart rate — both key goals. As you build lean muscle mass, try to add weight, increase sets and repetition, and reduce the breaks you take between exercises. If you're unsure how to do that without injuring yourself, seek out the advice of a physical trainer, the council suggests. 'If you're doing all the right things and you're not building muscle mass, talk to your doctor to rule out issues such as low testosterone that may be hindering your progress,' Dr. Richard Isaacson, director of research at the Institute for Neurodegenerative Diseases, told CNN previously. Plant-based diets are excellent ways to improve nutrition and lose belly fat, experts say. 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A May 2024 study found the Mediterranean dietary pattern cut the risk of death for women by about 25% for more than 25 years, with reductions in both cancer and cardiovascular mortality. Changing when you eat may also help. Try a pattern of eating called intermittent fasting or time-restricted eating, Freeman said. However, he added, it doesn't work for everyone. 'People who are struggling with weight loss have to get their bodies out of its routine, and that's very hard to do,' Freeman said. 'Some people, not everyone, respond by some degree to time-restricted eating. 'You eat breakfast at 11 o'clock, you eat dinner by five o'clock — so six hours a day you're eating, and 18 hours a day you're not. Combine that with strength and cardio training and change the type of fuel to whole foods. You put all those together, and magic things start to happen.'

Boston Globe
3 hours ago
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Yahoo
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AB Science - New peer-reviewed data provide strong evidence supporting masitinib potential for the treatment of Alzheimer's disease
PRESS RELEASE NEW PEER-REVIEWED DATA PROVIDE STRONG EVIDENCE SUPPORTING MASITINIB'S POTENTIAL FOR THE TREATMENT OF ALZHEIMER'S DISEASE THROUGH A DUAL MECHANISM OF COGNITIVE ENHANCEMENT AND NEUROPROTECTION THIS PUBLICATION CORROBORATES NEW ANALYSIS FROM THE CLINICAL PHASE 2B/3 STUDY SHOWING COGNITIVE IMPROVEMENT UNDER MASITINIB TREATMENT PHASE 3 CLINICAL STUDY WITH MASITINIB AS A DISEASE-MODIFYING THERAPY FOR ALZHEIMER'S DISEASE HAS BEEN AUTHORIZED BY THE FDA AND KEY EU COUNTRIES Paris, June 23, 2025, 8am CET AB Science SA (Euronext - FR0010557264 - AB) today announced that a new peer-reviewed study from an independent research team based in China (Guangdong Pharmaceutical University and Sun Yat-sen University) presents new evidence showing that masitinib offers a promising new approach to treating Alzheimer's disease, specifically the most common form, sporadic Alzheimer's disease (sAD), which accounts for over 95% of all cases. 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The research also revealed that masitinib: • Reduced toxic brain proteins such as hyperphosphorylated Tau. • Alleviated synaptic dysfunction and morphological damage, i.e., it protected synapses, which are essential for brain cell communication. • Suppressed microglial activation, which in turn inhibited the NF-κB/NLRP3/caspase-1 signaling axis, a key inflammatory signaling cascade linked to Alzheimer's disease, thereby suppressing inflammation in the brain of sAD mice. The authors emphasized that this is the first study to demonstrate that masitinib attenuates sporadic Alzheimer's disease pathology through dual mechanisms of cognitive enhancement and neuroprotection. Professor Olivier Hermine, MD, President of the Scientific Committee of AB Science and member of the Académie des Sciences in France said, 'These new, independent findings provide strong evidence supporting masitinib as a promising disease-modifying therapy for sporadic Alzheimer's disease and perfectly compliment previously published clinical and preclinical data for masitinib in this indication.' New data from phase 2B/3 study in patients with mild Alzheimer's disease It has previously been shown that masitinib enhances cognitive function and synaptic integrity in a familial Alzheimer's disease mouse model [2]. Moreover, randomized, placebo-controlled, phase 2 and phase 2B/3 studies demonstrated that masitinib (4.5 mg/kg/day) can effectively delay or mitigate the progression of dementia [3,4]. Clinical and preclinical study findings have also been summarized in a review article [5], with the authors concluding that 'all research studies revealed positive effects concerning the cognitive functions in Alzheimer's disease and generally with good safety and tolerability'. New analysis from the completed phase 2B/3 study (AB09004), shows that masitinib treatment may not only slow down worsening of cognition in patients with mild Alzheimer's disease, but actually improves it over the treatment period of 24 weeks. Indeed, study AB09004 included patient with both mild and moderate AD (MMSE [12 - 25]). In the overall study population, which included patient with both mild and moderate AD (MMSE [12 - 25]), masitinib 4.5 mg/kg/day plus standard of care (memantine and anticholinesterase) demonstrated a significant reduction in cognitive impairment (ADAS-Cog LS Mean Diff = -2.15; p=0.0003) compared with standard of care alone. However, the clinical benefit on ADAS-Cog was greater in patients with mild impairment (LS Mean Diff = -2.89 ; p=0.0008) than in patients with moderate impairment (LS Mean Diff = -1.74; p=0.0284). Notably, there was a meaningful improvement in cognitive function between baseline and week 24 in the mild AD subgroup under masitinib treatment (LS Mean = -2.47), while it remained stable in the control arm (LS Mean = -0.42), as presented in the table below. ADAS-COG Change from Baseline to Week 24 N LS Mean LS Mean Diff.(97.51% CI) p-value Mild and moderate AD patients Masitinib 4.5 mg/kg/day + SoC 182 -1.45 -2.15(-3.48, -0.81) 0.0003 Placebo + SoC 176 0.69 ADAS-COG Change from Baseline to Week 24 N LS Mean LS Mean Diff.(97.51% CI) p-value Mild patients [MMSE (21-25)] Masitinib 4.5 mg/kg/day + SoC 63 -2.47 -2.89(-4.80, -0.99) 0.0008 Placebo + SoC 61 0.42 Moderate patients [MMSE (12-20)] Masitinib 4.5 mg/kg/day + SoC 119 -1.04 -1.74(-3.52, 0.04) 0.0284 Placebo + SoC 115 0.70 SoC = Standard of care = memantine and anticholinesteraseNote : Negative change in LS Mean of ADAS-COG means an improvement of cognition. Positive change in LS Mean of ADAS-COG means a worsening of cognition. Authorized phase 3 to support New Drug Application in case of success AB Science previously received an Investigational New Drug (IND) approval letter from the FDA and similar authorizations from several European countries to initiate Phase III study (AB21004) in patients with Alzheimer's disease. Study AB21004 is a randomized, double-blind phase 3 study to evaluate the safety and efficacy of masitinib in patients with mild Alzheimer's disease, as an add-on therapy to standard of care, cholinesterase inhibitors and/or memantine. The study will enroll 600 patients. The objective of study AB21004 is to confirm results from the first phase 2B/3 study, AB09004, which showed that masitinib administered at 4.5 mg/kg/day significantly slowed cognitive deterioration relative to placebo and also reduced loss of functional ability in activities of daily living in the targeted AD population. Study AB21004 will evaluate the effect of masitinib on absolute change from baseline in cognition (ADAS-Cog-11) as primary endpoint and integrated AD rating scale (iADRS) and daily living (ADCS-ADL) as secondary endpoints. Expected patent protection until 2041 Based on the results from AB09004 study, AB Science filed a patent application relating to methods of treating Alzheimer's disease (i.e. a medical use patent) with its lead compound masitinib (WO2022129410A1). If granted, this patent will provide intellectual property protection for masitinib in this indication until 2041. A similar strategy was successfully applied in Amyotrophic Lateral Sclerosis, with medical use patent for masitinib in ALS being granted worldwide (press release dated June 1st 2023). References : Jia K, Shen Q, Zhang Z, et al. Masitinib attenuates neuropathological changes in acrolein-induced sAD mouse model via NF-κB/NLRP3/Caspase-1 signaling pathway. Neurosci Lett. Volume 862, 27 July 2025, 138300. Published online June 10, 2025. Li T, Martin E, Abada YS, et al. Effects of Chronic Masitinib Treatment in APPswe/PSEN1dE9 Transgenic Mice Modeling Alzheimer's Disease. J Alzheimers Dis. 2020;76(4):1339-1345. doi:10.3233/JAD-200466 Dubois B, López-Arrieta J, Lipschitz S, et al. Masitinib for mild-to-moderate Alzheimer's disease: results from a randomized, placebo-controlled, phase 3, clinical trial [published correction appears in Alzheimers Res Ther. 2023 Apr 22;15(1):85. doi: 10.1186/s13195-023-01230-9.]. Alzheimers Res Ther. 2023;15(1):39. Piette F, Belmin J, Vincent H, et al. Masitinib as an adjunct therapy for mild-to-moderate Alzheimer's disease: a randomised, placebo-controlled phase 2 trial. Alzheimers Res Ther. 2011;3(2):16. Published 2011 Apr 19. doi:10.1186/alzrt75 Ettcheto M, Cano A, Sanchez-López E, et al. Masitinib for the treatment of Alzheimer's disease. Neurodegener Dis Manag. 2021;11(4):263-276. doi:10.2217/nmt-2021-0019 About AB ScienceFounded in 2001, AB Science is a pharmaceutical company specializing in the research, development and commercialization of protein kinase inhibitors (PKIs), a class of targeted proteins whose action are key in signaling pathways within cells. Our programs target only diseases with high unmet medical needs, often lethal with short term survival or rare or refractory to previous line of treatment. AB Science has developed a proprietary portfolio of molecules and the Company's lead compound, masitinib, has already been registered for veterinary medicine and is developed in human medicine in oncology, neurological diseases, inflammatory diseases and viral diseases. The company is headquartered in Paris, France, and listed on Euronext Paris (ticker: AB). Further information is available on AB Science's website: Forward-looking Statements - AB ScienceThis press release contains forward-looking statements. These statements are not historical facts. These statements include projections and estimates as well as the assumptions on which they are based, statements based on projects, objectives, intentions and expectations regarding financial results, events, operations, future services, product development and their potential or future performance. These forward-looking statements can often be identified by the words "expect", "anticipate", "believe", "intend", "estimate" or "plan" as well as other similar terms. While AB Science believes these forward-looking statements are reasonable, investors are cautioned that these forward-looking statements are subject to numerous risks and uncertainties that are difficult to predict and generally beyond the control of AB Science and which may imply that results and actual events significantly differ from those expressed, induced or anticipated in the forward-looking information and statements. These risks and uncertainties include the uncertainties related to product development of the Company which may not be successful or to the marketing authorizations granted by competent authorities or, more generally, any factors that may affect marketing capacity of the products developed by AB Science, as well as those developed or identified in the public documents published by AB Science. AB Science disclaims any obligation or undertaking to update the forward-looking information and statements, subject to the applicable regulations, in particular articles 223-1 et seq. of the AMF General Regulations. For additional information, please contact: AB ScienceFinancial Communication & Media Relations investors@ Attachment Alz sAD Model PreClin vENG VFError while retrieving data Sign in to access your portfolio Error while retrieving data Error while retrieving data Error while retrieving data Error while retrieving data