Latest news with #APOE4
Medscape
25-06-2025
- Health
- Medscape
Fast Five Quiz: Risk Factors, Symptoms, & Treatments for AD
Alzheimer's disease is the most common form of dementia. Researchers believe that converging environmental, lifestyle, and genetic risk factors trigger a pathophysiologic cascade that, over decades, leads to Alzheimer's pathology and dementia. Depending on such risk factors and related symptoms, certain treatments can be utilized to help manage and slow disease progression. Do you know the risk factors, symptoms, and potential treatments for Alzheimer's disease? Test your knowledge with this quick quiz. Midlife hypertension is an established risk factor for Alzheimer-type dementia. Further, a brain autopsy study evaluating the link between hypertension and Alzheimer's disease found that patients using beta-blockers to control blood pressure had fewer Alzheimer-type brain lesions on autopsy compared with patients taking no drug therapy. Other risk factors for Alzheimer-type dementia include: Advancing age Family history APOE4 genotype genotype Obesity Insulin resistance Vascular factors Dyslipidemia Inflammatory markers Down syndrome Traumatic brain injury Caffeine is generally not a recognized risk factor for Alzheimer-type dementia or Alzheimer's disease. In fact, some studies have demonstrated a lower incidence of Alzheimer's disease in patients who consume caffeinated coffee. Similarly, moderate alcohol consumption is generally not recognized as a risk factor. In the 1960s and 1970s, exposure to aluminum was thought to be a possible risk factor for the development of Alzheimer's disease, leading to concerns about the use of cookware, antiperspirants, foil, antacids, and beverage cans in everyday life. Although studies have shown the neurotoxic effects of aluminum, particularly via exposure through dietary sources, they have failed to confirm a direct correlation between aluminum exposure and the development of Alzheimer's disease. Learn more about the risk factors for Alzheimer's disease. A 2025 report from the Alzheimer's Association indicated that older Black males and females are twice as likely to develop dementias, including Alzheimer's disease, compared with older White patients. Further, the same report noted that older Hispanic patients are at an increased risk for dementia and Alzheimer's disease when compared with older White, non-Hispanic patients. Specifically, the report states this population is 'one and one-half times as likely to have Alzheimer's or other dementias as White older adults.' Modifiable health factors include midlife obesity, which has been associated with the largest proportion of Alzheimer's disease cases in Black individuals, as well as physical inactivity. Additionally, cardiovascular and metabolic conditions, all of which elevate risk for dementia, disproportionately affect this demographic. Socioeconomic and psychosocial factors that correlate with dementia risk among older Black individuals include limited access to education, financial stability, and marital status. Missed and delayed diagnoses are more common in Black communities, and cultural bias in screening tools often leads to under-detection. Learn more about the epidemiology of Alzheimer's disease. By the time Alzheimer's disease reaches the moderate stage, damage has spread further to the areas of the cerebral cortex that control language, reasoning, sensory processing, and conscious thought. Affected regions continue to atrophy, making signs and symptoms of the disease more prominent, particularly as they relate to memory, judgment, and impulse control. The symptoms of this stage are typically: Increasing memory loss and confusion Shortened attention span Problems recognizing friends and family members Difficulty with language; problems with reading, writing, and working with numbers Difficulty organizing thoughts and thinking logically Inability to learn new things or to cope with new or unexpected situations Restlessness, agitation, anxiety, tearfulness, and wandering, especially in the late afternoon or at night Repetitive statements or movement, and occasional muscle twitches Hallucinations, delusions, suspiciousness or paranoia, and irritability Loss of impulse control (shown through such behavior as undressing at inappropriate times or places or using vulgar language) Perceptual motor problems (such as trouble getting out of a chair or setting the table) Pyramidal tract lesions, also known as upper motor neuron lesions, cause a wide range of motor deficits, including hyperactive reflexes, a positive Babinski sign (toe extension when stroking the sole of the foot), and spasticity. These can occur from any damage to the brain or spinal cord as a result of a stroke, trauma, tumors, meningitis, multiple sclerosis, or neurodegenerative disease, such as amyotrophic lateral sclerosis. While these lesions do occasionally occur in patients with Alzheimer's disease, their appearance is uncommon in this patient population. Hypothyroidism and hyperthyroidism can affect cognitive function and should be assessed during the initial workup for Alzheimer's disease. Although it is possible for either one to co-occur in patients, neither is a common symptom of moderate-stage disease. Seizures are not a common symptom associated with moderate Alzheimer's disease but are possible, particularly in late-stage disease and are potentially owing to poor disease course. Learn more about the clinical presentation of Alzheimer's disease. Structural neuroimaging with MRI (or noncontrast CT) to detect lesions that might cause cognitive impairment (eg, stroke, small vessel disease, and tumor) is typically most appropriate during the initial evaluation of patients with dementia or Alzheimer's disease. Imaging studies are part of initial diagnosis and are particularly important to assess for and rule out potentially treatable causes of progressive cognitive decline, such as chronic subdural hematoma or normal pressure hydrocephalus. Brain scanning with single-photon emission CT or PET is usually not recommended for the workup of patients with typical presentations of Alzheimer's disease. EEG is also not generally recommended but is valuable when Creutzfeldt-Jakob disease or another prion-related disease is a likely diagnosis. However, imaging studies are no longer the only method used in the initial evaluation of patients suspected of having Alzheimer's disease. In May 2025, the FDA approved the use of the Lumipulse G pTau217/Beta-Amyloid 1-42 Plasma Ratio for the early detection of amyloid plaques associated with Alzheimer's disease in adult patients, aged 55 years and older, who are exhibiting signs and symptoms of the disease. Although not intended as a stand-alone diagnostic test, it serves as an additional resource to clinicians in a specialized setting as a less invasive diagnostic option. The test increases diagnostic accessibility to patients who might not have easy access to imaging. Learn more about the workup of Alzheimer's disease. Early detection combined with timely treatment enables patients with Alzheimer's disease to preserve their cognition and functional capacities at optimal levels. Cholinesterase inhibitors, along with mental exercises, are prescribed to help prevent or delay the deterioration of cognition in patients with Alzheimer's disease. Cholinesterase inhibitors that have been approved in the US and Europe for the treatment of Alzheimer's disease include donepezil, galantamine, and rivastigmine. Further, certain antiamyloid monoclonal antibody treatments have been approved to slow disease progression as well. According to the Alzheimer's Association, nonpharmacological treatments used to initially and routinely manage symptoms include 'physical activity, reminiscence exercises, music ‐ and art ‐ based therapies, pet therapy, and light therapy.' Some studies suggest that long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) might have a protective effect against Alzheimer's disease, potentially through their anti-inflammatory effects and possible ability to reduce amyloid. However, findings from observational studies and short-term randomized controlled trials have been mixed, and optimal dosage and duration of (NSAIDs) for this purpose remain unclear. Studies suggest that long-term (but not cumulative) use of NSAIDs might be associated with decreased dementia risk. However, further investigation is warranted. Neuroleptic agents are not generally used to prevent or delay deterioration of cognition in patients with Alzheimer's disease. Some data have indicated that they are linked to an increased risk of cognitive decline. While some studies have shown that vitamin E can reduce amyloid-beta oxidative stress, as well as improve memory and cognitive deficits, conflicting results were noted in clinical trials assessing the efficacy of vitamin E as a preventive or treatment for Alzheimer's disease. Further, they are not typically used as an initial therapy to prevent or delay deterioration of cognition in patients with Alzheimer's disease. Learn more about the treatment and management of Alzheimer's disease.
San Francisco Chronicle
04-06-2025
- General
- San Francisco Chronicle
How a neurologist faces the disease that is slowly stealing his cognitive powers
It was 2006 when Dr. Daniel Gibbs first noticed he was losing his sense of smell. But it wasn't what he didn't smell that tipped him off that something might be wrong. It was what he did smell: perfume, mixed with baked bread. "The same thing, every time." Gibbs, a neurologist in Portland, Oregon, knew this was an olfactory hallucination. And that meant something wasn't working properly in his brain. "I attributed it to getting older, which is a common cause of decreased ability to smell," he said. But Gibbs was just 57 – not so old that he should be losing his sense of anything. "I also knew losing your sense of smell was an early sign of Parkinson's disease, so I thought it might be that." It wasn't. Gibbs was experiencing an early symptom of Alzheimer's disease. But it would be another six years before he knew it. He has since written a book about his experience, which was turned into a documentary. He also keeps a regular blog to help people understand what it's like to live with Alzheimer's. These days, he spends a lot of his time learning and talking about how to slow progression of the disease, something he's been trying to do since he got his diagnosis more than a decade ago. Gibbs and his wife, Lois Seed, discussed what he's learned about Alzheimer's dementia and how he navigates the condition for " The Experts Say," an American Heart Association News series in which specialists explain how they apply their professional knowledge to their own lives. Their remarks have been edited. In 2012, Lois was doing a genealogical project, so we did some genetic testing. Mine came back showing I had two copies of APOE4, a gene known to influence the risk of developing Alzheimer's disease, which totally gobsmacked me. Having two copies means it is almost certain to eventually cause Alzheimer's. I had no measurable cognitive impairment at that time. I was in charge of the neurology resident training program at Oregon Health and Science University in Portland, and I was seeing patients in the clinic, so it was a very busy year for me. Even though it was difficult, I was still able to get all the balls to balance in the air. What did you do once you knew your genetic risk for Alzheimer's? The first thing I did was to go to one of my colleagues and have some cognitive testing done. It was essentially normal with the caveat that all of my cognitive domains were in the 90th percentile except verbal memory, which was in the 50th percentile. So there was a strong hint that there was some incipient loss of function of verbal memory. With that in hand, I went to my department chair and explained the situation. I had no impairment but did not feel it was safe for me to continue to practice. I retired in 2013. Lois: You also went looking for studies you could join, because it's a big deal to see people before they experience symptoms. That's right, I went to the University of California in San Francisco, because they have a ton of studies there. The first study I was involved with was a longitudinal neuroimaging study. I had PET scans of abnormal amyloid and PET scans for tau proteins – two protein clusters in the brain that play a role in the development of Alzheimer's disease. And I had cognitive testing. They loved having me down there because they rarely have people with as early a stage of disease as I showed up with. About a year later, I joined a clinical trial for an anti-amyloid antibody drug that is now approved by the Food and Drug Administration to treat early Alzheimer's disease. What else did you learn about how to slow progression of the disease? This is not rocket science. The sort of things that are good preventive behavior for brain disease are also good for preventing heart and vascular disease. There are evidence-based lifestyle changes that include getting daily aerobic exercise; eating a Mediterranean-style diet, such as the MIND diet; getting mentally stimulating activity; staying socially engaged; getting at least seven hours of sleep nightly; and getting good control of any cerebrovascular risk factors, such as diabetes, high blood pressure, high cholesterol, obesity and smoking. What's good for the heart is good for the brain! How do you put this knowledge into practice? Walking is just built into my day. I do it with my dog, Jack, an 11-year-old English cocker spaniel who is about to age out. He can't keep up with 10,000 steps as easily anymore, so I take some walks by myself. We live in the hills, so I'm getting very good aerobic exercise, short of running. I used to go to the gym, but that stopped at the start of the COVID pandemic. I also have a short workout at home. The first thing I do is I use resistance bands, which is a strength exercise. That takes about 15 minutes and then I do tai chi pretty religiously, something I started six months ago. I can clearly see that it helps my balance, but I can't see if it helps my brain, which is continuing to do more poorly. And thanks to Lois, I've been eating a healthy diet, really forever. Lois: I didn't have control over those french fries you were eating. I don't eat red meat anymore. I closely follow the MIND diet, which is essentially the Mediterranean diet with more berries and nuts. It includes a heavy focus on fruits and vegetables, especially green leafy vegetables, beans, nuts, whole grains, seafood, lean poultry and uses olive oil to cook. I'm quite happy with it. Because I lost my sense of smell, which is totally gone now, I have virtually no taste either. I eat the same thing for lunch and breakfast every day. I enjoy it. I make a sandwich on whole wheat bread that has tuna salad and garbanzo beans, avocado and arugula to get the dark leafy greens. Then some grapes or bananas and half a dark chocolate bar. Breakfast is homemade granola, and I add cranberries or blueberries. I throw walnuts in as well. Dinner is whatever Lois picks that I can eat. I stopped drinking alcohol. There's no safe amount of alcohol if you are on this trajectory. So I got rid of it, but I used to love red wine. Do you know what to expect as the disease progresses? That's a difficult question to answer. In the old days, when people got a diagnosis of Alzheimer's, they were only living three to five years after that because we made the diagnosis so late. There's less information out there about people who have known they have the disease for a long time and how they will do going forward. Lois: There's a lot of confusion and misconception because there are different types of dementia. Alzheimer's tends to progress more slowly. The early stage can last 20 years. Here we are 13 years after his diagnosis and Dan's really doing well. I'm a little more of a caregiver than I was a few years ago, but not by much. He dresses himself and monitors medications, and people who talk to him casually wouldn't even know. We've been at that plateau for quite some time. How would you describe the stage you're at right now? Right now, I have mild Alzheimer's dementia. To say you have dementia is to say you are having trouble managing your personal affairs. I'm just at a stage now where I can't balance a checkbook. And as things go along, I will have more problems with memory and the ability to recognize people and remember their names. I've lost my train of thought. Lois: You were talking about what stage you're at. When I'm not remembering where I am, then I will have severe dementia. There are memories I have going back through my whole life. They tend to be events that are emotionally laden. I'm terrible with names. I know my immediate family members. My neighbors, I forget their names. Lois is taking over the things I can't manage anymore, like the financial part of our lives, anything that involves planning ahead, scheduling, calendars, remembering all the family stuff, managing the household. She also goes with me when I have a talk to give. Lois: He gives talks on Alzheimer's, but almost every time that Dan is getting ready to speak to a group, he gets frustrated and says, "This is the last time I'm doing this," because getting his thoughts together is challenging. He writes out notes. Most of the talks he gives now are screening events for the film with question-and-answer sessions. It works well if Lois is there to find … Lois: Words. That makes it easier.
Daily Mirror
03-06-2025
- General
- Daily Mirror
Lip sign could mean you're '80% more likely to get dementia'
A study has found that a certain virus that can manifest on the lips could indicate a heightened risk of developing Alzheimer's disease. A symptom appearing on the lips could potentially signal an increased risk of developing dementia, according to recent research. This viral symptom has been linked with an 80 per cent increased risk of Alzheimer's disease. The study, published in the British Medical Journal, suggests that the herpes simplex virus type 1 (HSV-1), a common virus responsible for herpes and cold sores, may contribute to the onset of Alzheimer's. While previous studies have hinted at a link between HSV-1 and Alzheimer's, this research aimed to delve deeper into this association. As part of the study, researchers analysed the medical records of over 300,000 individuals aged 50 and above. As reported by SurreyLive, participants were split into two equal groups, distinguished by those diagnosed with Alzheimer's disease and those without such a diagnosis. Alzheimer's Research UK detailed how the study found that 1,507 (0.44 per cent) of participants diagnosed with Alzheimer's disease had a history of HSV-1 infection, compared with 823 (0.22 per cent) without an Alzheimer's diagnosis. The conclusion drawn was that individuals with an HSV-1 infection had an 80 per cent increased risk of Alzheimer's. This remained true even when other factors, such as carrying two copies of the APOE4 gene, a known risk factor for Alzheimer's, were taken into account. Furthermore, individuals who had been prescribed medication to treat the virus were found to be 17 per cent less likely to develop Alzheimer's compared to those not on any medication. Limits of the study Nevertheless, it's essential to consider some constraints of this study. Dr Sheona Scales, director of Research at Alzheimer's Research UK, highlighted: "Despite the large sample size, this research is based on information gathered from using health records and administrative claims data, which often are based on people self-reporting their conditions. "Most people infected with HSV-1 don't have any symptoms so some infections might not have been recorded. Infections predating the information recorded are also not available. Although cases were matched with controls, diagnosing Alzheimer's disease, especially in the early stages, remains a challenge." While HSV-1 is common, contracting the virus does not guarantee that an individual will develop Alzheimer's disease. The precise relationship between HSV-1 and a heightened risk of Alzheimer's is still under investigation, with current hypotheses suggesting that infections may trigger brain inflammation, potentially leading to damage. Dr Scales further stated: "We know there are 14 lifestyle and environmental risk factors for dementia, and there's not enough evidence to include infections in this list. "This study doesn't tell us if infections are causing the risk, it only shows an association. Further research is needed to understand what the underlying biology around this is." Alzheimer's disease is the most prevalent form of dementia worldwide, accounting for an estimated 80 per cent of all dementia cases.
Yahoo
29-05-2025
- Business
- Yahoo
Halia Therapeutics CEO Dr. David Bearss to Deliver Keynote Address at Med Investment Forum 2025 in Abu Dhabi
ABU DHABI, UAE, May 28, 2025 /PRNewswire/ -- Halia Therapeutics, a clinical-stage biopharmaceutical company pioneering therapies that target the innate immune system, announces that CEO Dr. David Bearss will serve as keynote speaker at the Med Investment Forum 2025. The event will take place on May 29, 2025, at the Rotana Beach Hotel in Abu Dhabi, UAE. Dr. Bearss will present: "Pioneering a New Era of Medicine by Unlocking the Body's Power of Genetic Resilience." The keynote will explore how insights from resilient individuals—those who remain disease-free despite genetic risk—are reshaping therapeutic development. Halia's research, grounded in population-scale genomic data, is enabling breakthrough treatments for inflammatory and neurodegenerative diseases. "The key to solving medicine's toughest challenges lies in understanding why certain individuals are protected from disease," said Dr. Bearss. "At Halia, we're using that insight to design therapies that reprogram the body's immune response at the molecular level, ushering in a new era of precision immunology." Advancing Precision Immunology Through Genetic Resilience Halia Therapeutics is redefining how inflammation drives severe medical conditions through cutting-edge science and a robust development pipeline. The company's lead programs include HT-6184, a NEK7 allosteric modulator in clinical trials for myelodysplastic syndromes (MDS) and obesity, and HT-4253, designed to replicate the protective genetic effect of RAB10 loss-of-function in APOE4 homozygotes who show resilience to Alzheimer's disease. The Med Investment Forum, held under the patronage of the UAE Ministry of Health and Prevention in partnership with the World Health Organization (WHO), serves as a premier global platform connecting health ministers, investors, biotech leaders, and healthtech innovators. Halia's keynote participation underscores the innovation and global impact the Forum champions. The event offers an opportunity to discover transformative biotech solutions and connect with investors and decision-makers who are shaping the future of healthcare. Event Details Date: May 29, 2025 Location: Rotana Beach Hotel, Abu Dhabi, UAE Website: About Halia Therapeutics Halia Therapeutics is a clinical-stage biopharmaceutical company developing therapies that modulate the innate immune system to treat inflammation-driven diseases. By uncovering the biology behind genetic resilience, Halia designs breakthrough treatments for neurodegeneration, hematological disorders, and metabolic diseases. Learn more at Media Contact Taylor AveiDirector of Business DevelopmentHalia Therapeuticsinfo@ View original content to download multimedia: SOURCE Halia Therapeutics Error 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
20-05-2025
- Health
- Yahoo
New Study Finds This Common Supplement Cuts Dementia Risk by 40 Percent
New research offers promising hope in the battle against cognitive decline. Biochemist Rhonda Patrick shared a study published in Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring, which found a strong link between vitamin D supplementation and a lower risk of developing dementia. Researchers followed over 12,000 people for a decade and discovered that those who took vitamin D supplements were 40 percent less likely to develop dementia compared to non-users. Within the first five years alone, 84 percent of supplement users remained dementia-free, while only 68 percent of non-users did. The protective effects of vitamin D were especially strong in those with mild cognitive impairment or who carried the APOE4 gene, a well-known genetic risk factor for Alzheimer's. Carriers of this gene can have an increased Alzheimer's risk, but vitamin D supplementation still appeared to reduce dementia risk by about 33 percent in this group. Once processed by the body, vitamin D becomes a steroid hormone that influences over 1,000 genes, including many involved in brain health. It regulates nearly 5 percent of the human genome by entering cell nuclei and turning genes on or off, which plays a key role in everything from inflammation to neural communication. Vitamin D deficiency is shockingly common, with about 70 percent of Americans falling into the deficient or insufficient range. Fortunately, supplementation can easily correct this. Some small trials have also indicated that vitamin D supplementation may improve cognition in individuals with mild cognitive impairment or early Alzheimer's, though results in healthy adults are mixed. If you're not getting enough sun, are over 50, or carry extra body fat, a daily vitamin D supplement could help bridge the gap. As always, consult with a healthcare provider to check your levels and determine the right dosage.
