Is Alzheimer’s Disease Preventable?

Some think so. But, of course, it’s complicated. Here’s an overview of what you should know, from the basics and 14 factors for risk reduction to the latest research, current treatments and a new promising clinical trial.

By Gia Miller

Artwork by Justin Negard

Imagine you’re driving home from work, listening to your favorite podcast. You’re lost in thought, and suddenly, you realize you missed your turn. Sound familiar? It can happen to anyone. But what if you turned onto your street, looked around and had no idea where you were? That, researchers say, is the difference between a normal mistake and one of the earliest signs of Alzheimer’s disease.

“Once we’ve been somewhere several times, our brain naturally forms connections of the path you took, and it creates a mental map—think of it as a Google Map in your mind,” explains Abid Hussaini, Ph.D., a neurophysiologist and the director of the Laboratory for Systems Neuroscience of Cognition and Dementia at Burke Neurological Institute in White Plains. “Making these maps is second nature to us; we don’t even think about it. And when you miss your turn because you’re engaged in a podcast, but then you say, ‘Oh shoot, I forgot my turn,’ that’s okay—you obviously know where you are. The problem becomes when you make that turn and then ask yourself, ‘Where am I?’ That’s an indication that something is wrong.”

Hussaini’s lab is studying the area of the brain that’s responsible for spatial navigation (called the entorhinal cortex, located behind the ears). They want to learn exactly what happens when the naturally occurring proteins and tau, which are designed to support and protect the brain, begin to malfunction, misfold and clump together, harming you instead. His team is also working to devise an even earlier way to detect the disease, and it involves reading and listening to the brain (more on that later).

But before we go any further into the fascinating research and discoveries, many of which are happening in our own backyard, a brief Alzheimer’s primer is in order. If you’re well-versed on the topic, you can skip to “The anatomy of forgetting” section. And if your knowledge comes from helping someone close to you, you have our deepest sympathies.

Alzheimer’s 101

Alzheimer’s disease (AD) is a form of dementia; however, dementia is not considered a disease. Dementia is an umbrella term used to describe different conditions that feature a group of symptoms affecting memory, thinking and social abilities, which interfere with a person’s daily life. Alzheimer’s is the most common cause of dementia, and the Alzheimer’s Foundation of America (AFA) defines it as “a progressive brain disorder that impacts memory, thinking and language skills, and the ability to carry out the simplest tasks.” Nearly seven million Americans currently live with Alzheimer’s disease. Signs of AD include:

• Changes in decision-making and judgement
• Confusion about time and place
• Difficulty multitasking
• Finding it challenging to complete familiar tasks (brushing teeth, cooking and meal prep, managing medications, etc.)
• Mood and personality changes
• Repeating questions or stories shortly after they were asked or said
• Short-term memory loss
• Trouble finding the right word to use in a sentence or to describe something

There are three stages of Alzheimer’s disease. In the early/mild stage, many of the symptoms listed above will begin to appear. In the middle/moderate stage, these symptoms worsen, and the person may also have trouble recognizing family and friends, struggle to perform more complex tasks and show less concern for their personal hygiene and appearance. In the late/severe stage, they experience almost total memory loss, making it difficult to recognize people and even perform basic functions such as eating and walking.

Most people diagnosed with AD are 65 and older, but it can occur in people younger than 65, which is appropriately called younger-onset Alzheimer’s. Although age is the greatest known risk factor, Alzheimer’s is not a normal part of aging. Everyone’s brain will change as they age, and eventually, most people will experience occasional problems remembering certain things as well as slower thinking. That is considered a natural part of aging. It’s when a person experiences confusion and serious memory loss, along with the other symptoms listed above, that they might have Alzheimer’s disease.

The anatomy of forgetting

“Many people believe that Alzheimer’s disease is defined by a build-up of plaques (amyloid beta proteins) and tangles (tau), as well as neurodegeneration,” explains Gary Gibson, Ph.D., a neuroscientist and the director of the Laboratory for Mitochondrial Biology and Metabolic Dysfunction in Neurodegeneration at Burke Neurological Institute.

Plaques

A healthy brain regularly produces, breaks down and clears out protein fragments called amyloid beta (Aβ), but with Alzheimer’s, too much Aβ is made or not cleared well, especially a “stickier” form called Aβ42. These sticky pieces began clumping together, forming plaques that sit in the spaces between brain cells and can cause inflammation and oxidative stress, blocking blood vessels and starving the brain of necessary blood flow.

Tangles

Each brain cell contains “tracks” that carry nutrients and messages from one end of the cell to the other. In a healthy brain, tau connects those tracks, keeping them straight and stable so things can move along smoothly. With Alzheimer’s, tau undergoes a chemical transformation that causes it to begin sticking to itself and twisting into long fibers inside the neuron. Those twisted clumps are called tau tangles, and they interfere with the neuron’s ability to move nutrients and signals. Eventually that cell becomes sick and dies.

Neurodegeneration

Neurodegeneration is precisely what it sounds like: “neuro” means brain cells (neurons), and “degeneration” means breaking down and eventually dying. With Alzheimer’s, the brain’s wiring gradually short-circuits, so messages don’t travel properly, leading to problems with memory, thinking and everyday tasks. As more cells die, remembering recent events, following conversations, recognizing people and staying organized become more challenging.

However, while plaques, tangles and neurodegeneration have been the working theory on why AD occurs for decades, Gibson says this theory doesn’t explain everything. “One third of people diagnosed with Alzheimer’s by [physicians using] the best methods have no plaques on their brain, so we don’t know the real significance of these,” he explains. “And neurodegeneration is not that easy to measure in a living person.”

“It’s still a little unclear as to whether these pathologic changes cause the cognitive issue or if they’re a marker of the cognitive issue,” explains Dr. Anna Hohler, chair of neurology at Northern Westchester Hospital and the chief of neurology at Phelps Hospital. “However, research shows that the more we can reduce the buildup of these toxins, the better people do and the slower their disease progresses.”

So what causes AD? Decades of research have shown that an early sign of Alzheimer’s is a significant and measurable drop in the brain’s ability to use glucose—a major source of energy for our cells. (A quick high school biology refresher: Once glucose is broken down into smaller molecules elsewhere in the cell, mitochondria—the “powerhouse” of the cell—further process those smaller molecules to create the cell’s usable energy. Or, in very simple terms, mitochondria help your cells turn glucose from food into usable energy.) This notable decrease in glucose use indicates the brain’s mitochondria aren’t functioning properly. And because researchers have discovered this change begins to occur in people in their 20s who are predisposed to develop Alzheimer’s, Gibson theorizes that the decrease in glucose is what drives the formation of plaques and tangles, eventually causing Alzheimer’s. “These changes don’t happen five months before [symptoms appear],” he says. “They’re happening years before. It changes earlier than anything else.” That, of course, means there isn’t a reason to test for early signs of neurodegeneration, especially in your 20s, if there are no visible symptoms.

And for some people, even after significant neurodegeneration has occured, it’s still difficult to accurately test for Alzheimer’s. “Highly educated people are very good at masking these symptoms, and they’ll ace the standardized cognitive tasks very easily, which gives the perception that they are not impaired,” Hussaini explains. “Our brains are so plastic that another region can take over the missing function. This ‘cognitive reserve’ helps them mask their symptoms, so to an outside observer, their behavior appears normal, making it even more difficult for them to receive a diagnosis. But the problem is that once all the other brain regions are exhausted, the decline is so sharp because everything falls apart quickly.”

Reading the brain

For years, researchers have used PET scans to identify the build-up of proteins and tangles in the brain by measuring the amount of glucose, but that test isn’t performed when a person or family member is concerned about Alzheimer’s. And because some people can mask their symptoms, that’s not always a reliable test either. So Hussaini’s team is trying to identify a different way to diagnose Alzheimer’s in its early stages. To do this, “you have to read the brain directly with microwires or probes that record brain signals or activity directly from regions involved in Alzheimer’s disease,” he says. This “reading” also involves listening to the brain because the electrical activity the probes record can be converted into sound.

“Our brains have these electrical signals that allow the neurons to communicate with each other by transmitting information quickly and efficiently—like electrical circuits,” Hussaini explains. “We want to listen to those signals and patterns so we can translate the way they talk to each other. It’s almost like a doctor putting a stethoscope on your chest and trying to listen to what is going on in your heart. We want to listen in and determine if they are communicating normally and doing what they should be doing.”

Their first goal is to find patterns in the brain that indicate brain dysfunction, and their eventual goal is to search for similar patterns when people perform a task, such as walking down a street and following directions to make a few turns before returning, while wearing something that can track the electrical signals in their brain. Even if the patient returns having successfully completed the task, reading those electrical signals will tell the real story: were they compensating for deficiencies in the entorhinal cortex, or are all parts of the brain working as they should?

Hussaini’s team is also exploring another early indicator of AD—losing a specific sense of smell. “Researchers have given people five pens with different fragrances,” he explains. “The person opens the cap, smells it and then puts the cap back on. Then they mark what they smelled—banana, leather, rose, etc. What they’ve found is that there are some smells that are highly predictive of dementia-related changes, and not being able to smell leather is one of them.” Hussaini’s goal is to read the brain as the person smells each pen, preventing them from using workarounds to get the correct answer.

“In this case, instead of asking what they smelled, we could hook them to the electrodes and let that do the work,” he explains. “To do this, we would need to learn the pattern that each smell creates in the brain so we can match it. So even if they say they smelled leather, if the pattern doesn’t match, we know something is off. Or, ideally, we could just decode the answer by looking at the brain’s electrical pattern. They wouldn’t have to tell me the answer; I could tell them.”

Is avoiding the inevitable possible?

Depending on who you ask, up to 45 percent of dementia cases could potentially be prevented or delayed. The 45 percent comes via a 2024 report published by the Lancet Commission on Dementia Prevention, Intervention, and Care that highlighted 14 factors for dementia risk reduction, which they divided into three life stages:

Early life: educational opportunities build cognitive reserve

Midlife: vascular and metabolic insults (hypertension, high LDL cholesterol, obesity, diabetes, traumatic brain injury) create brain damage

Late life: sensory loss, social isolation, depression, and air pollution lower the threshold at which damage becomes clinical dementia

If that list feels overwhelming, focus on the most important ones first. “What I think about in terms of early prevention for any type of neurologic disease—stroke, Alzheimer’s, Parkinson’s, dementia in general—is optimizing our lifestyle,” says Hohler of Northern Westchester Hospital. “Number one, you want to be healthy in terms of your diet. In the neurodegenerative literature, the Mediterranean diet has been shown to help slow the progression of cognitive decline. Number two is exercise, and there are different forms of exercise that can be helpful. Typically, we want to think about cardiovascular exercise because we’re trying to help the heart-brain connection. We recommend walking two miles three times a week or 10,000 steps a day. Adding weight training to your walking routine is ideal, as it benefits your cognitive functioning, cardiovascular health and bone health. Along with those, there is something people don’t think about as much as we would like them to: hydration. We want to optimize our water and electrolyte consumption to make sure the blood is flowing and going where it needs to.”

“In addition to that,” she continues, “we want to think about cognitive exercises. This is something I preach all the time. How can we optimize our cognition? Reading is the best activity. We also think about puzzles—crossword puzzles, Sudoku, and things like that. But what I have found is that reading out loud is actually even better than reading to ourselves. Passive reading often means we’re skipping words, and we’re not necessarily articulating; we’re not optimizing our hearing associated with it. But reading out loud for 30 minutes a day is something I’ve asked all my patients to do who are concerned about cognitive issues because it’s training your articulation and it’s working on your cognition. And then it’s also working on your sensory input from your hearing. Does it matter what you read? Not necessarily. We want people to enjoy the reading, so sometimes I have people read to their spouse, and sometimes they read by themselves. Whatever works for them, but the 30 minutes is the most important part.”

Dr. Hohler’s three tips for optimizing your lifestyle:

• Eat a healthy diet, preferably the Mediterranean diet.
• Get adequate cardiovascular exercise (walk two miles three times a week or 10,000 steps a day). Add some weight training. And  don’t forget to hydrate to maximize your blood flow.
• Engage in cognitive exercises, preferably by reading aloud for 30 minutes a day.

Hohler also recommends paying attention to nutritional deficiencies, particularly vitamin D, vitamin B12, and iron. Low levels, which can be determined through routine bloodwork, could cause cognition difficulties. Ask your physician for the appropriate supplement dosage that will help you build and maintain neural health.

And then there’s sleep. During deep sleep, the cerebrospinal fluid flushes the brain, removing toxins. “The deeper you sleep, the better the flush and the more toxins will get removed,” says Hussaini. “If you continuously accumulate a sleep deficit, then they won’t get removed.” The current hypothesis is that poor sleep, along with stress over time, is considered a risk factor and possible contributor to tau accumulation and spread.

In recent years, several sleep studies have concluded that sleep duration is not as important as sleep hygiene, especially going to bed and waking up around the same time each day. A 2025 study published in the journal Sleep Medicine found that maintaining moderate-to-regular daily sleep patterns is the best way to support your cognitive health, whereas “rigid or highly regular sleep patterns are not optimal” for reducing the risk of AD. “You just have to treat it like any hygiene,” Hussaini recommends. “Just like brushing your teeth, sleep hygiene is something we need to follow very carefully. It’s linked to Alzheimer’s and many other diseases.”

As you’ve probably heard or read before, the earlier you can begin living a healthy lifestyle, the better. And, as you’ve also probably heard or read before, it’s never too late to start. “We should think about this probably no later than our thirties,” Hohler recommends. “That’s when we should get into a routine where we’re exercising our minds and our bodies to try and push off these cognitive impairments to as late as possible.”

And to address the “up to” part from the first sentence of this section, both Hussaini and Gibson believe science doesn’t support the theory that addressing those 14 risk factors can prevent dementia. However, they do believe it’s possible to delay symptoms by following that list. Plus, it contains good health advice to reduce your risk for other diseases as you age.

Treating Alzheimer’s

There is no cure for AD, but treatments include medications that can temporarily and moderately improve memory, thinking and daily functioning for a period of time. There are also new antibody drugs, mainly infusions, that are designed to slow disease progression in people with early Alzheimer’s. These treatments are targeted at Aβ and mainly designed to prevent them from clumping, but they might also remove existing plaques. They are only given to select patients, require an IV for administration as well as regular monitoring, and do have risks. Unfortunately, these treatments are unable to stop the decline, and eventual death, of brain cells, so AD will continue to progress.

“AD is such a complex disease with multiple facets to it, and there are no clear solutions yet,” says Hussaini. “Scientists are working hard to solve this puzzle, but after many decades, some drugs still barely work. However, there is hope; many drugs are in different stages of clinical trial, but it will take some time until the results are published.”

Meanwhile, medications to manage vascular health and lifestyle may be prescribed to control conditions like blood pressure, diabetes, exercise, sleep and social engagement, as these can impact AD’s progression. And several non-drug approaches are recommended to help people function as well as they can for as long as possible. These include cognitive and physical therapy, managing heart and metabolic health, and strong caregiver and environmental support. “Often, what we find is the patients who have Alzheimer’s do so much better when they’re involved in different types of group activities,” notes Hohler. “I recommend my patients get involved in their senior center or their local groups, where they can participate in either exercise programs or other types of social interactions, whether it be dancing, singing, bingo, etc. That socialization helps improve not just their cognitive speed and processing, but it also improves mood as well, which has a significant impact on cognition.”

The promising news is that novel therapies are currently being tested that may reduce the development of AD. Remember when we explained that Gibson believes the drop in the brain’s ability to use glucose and the mitochondria’s diminished ability to metablize glucose are what causes plaque and tangle formation? Gibson also theorizes that a thiamine (vitamin B1) deficiency is the root cause. “We’ve known since the 1930s that if you reduce thiamine in a human, you severely impair recent memory,” Gibson explains. “In the 1990s, they showed that the change in glucose metabolism in the human brain in Alzheimer’s patients and in thiamine-deficient humans is somewhat similar. They also showed that memory deficits in a thiamine-deficient human are similar to those in Alzheimer’s disease. So the idea is that thiamine is involved in memory.” Thiamine is essential for the mitochondria to convert glucose into usable energy, but scientists have discovered that thiamine does not enter the brains of people with early AD even though they have a sufficient amount of thiamine in their blood. So Gibson is currently testing a treatment that will increase the levels of thiamine in the brain. But this approach is tricky for several reasons:

• Blood tests in the U.S. don’t regularly or accurately do the proper testing to detect a thiamine deficiency.
• A thiamine deficiency can occur in the brain but not the body.
• Simply taking vitamin B1 won’t necessarily improve your brain’s thiamine levels enough to make a difference—you need what’s called a transporter to pass through the blood-brain barrier.

“Research has proven that thiamine deficiency exaggerates plaque and tangle formation, so we wondered, ‘What if you could raise thiamin in the brain?’” says Gibson. “Animal research showed us that if you give them the compound benfotiamine, and you raise blood thiamine a lot, you greatly reduce plaques in the brain by more than 80 or 90 percent. And benfotiamine has been proven very safe in humans. This compound was used in Germany to treat diabetics, and they saw no safety problems.”

Gibson and his team at Burke received FDA approval for a pilot trial involving 70 patients—35 received a placebo and 35 received benfotiamine. The medication was given in two capsules that patients took at home twice a day—no needles, no infusions, no monitoring while receiving treatment. “In the pilot trial, the most important thing was patient safety,” says Gibson. “In older people, there can be other serious problems, but, like in the Germany trial, the benfotiamine group experienced fewer adverse events than the placebo group.”

Gibson’s team presented the results to a group at U.C. San Diego that runs an AD cooperative study. “They set up this amazing process for clinical trials,” he explains. “That’s what they’re the world’s best at.” His team convinced the leadership to run a larger trial,  and they have partnered with Dr. Jose Luchsinger from Columbia University and Howard Feldman, MDCM, from the University of California, San Diego, to run this trial in 46 sites around the U.S. The trial, which began in April 2024, will enroll 406 participants, and each participant will remain in the trial for 18 months. “It’s a gold standard Alzheimer’s study,” says Gibson. “In this trial, we’re testing a dosage twice as high, and we designed it so that we could monitor safety very carefully. Right now, all the patients are on the higher dosage because it’s so safe.”

“The other thing that’s novel about this trial,” Gibson continues, “is that it’s now well documented that the proper blood test can provide a pretty good estimate of plaques, tangles, inflammation and oxidative stress in the brain. And we know how to measure glucose in the brain as well.” As of deadline, 90 percent of patients needed have been recruited, and recruitment will end in June 2026, with the last patient completing the trial 18 months later. There are nine sites within New York State, including three in Manhattan. Patients must have mild cognitive impairment or early Alzheimer’s disease. To learn more or enroll in the trial, visit benfoteam.org.

“Right now,” Gibson adds, “it’s hard to imagine a cure for Alzheimer’s, but it’s easy to imagine that we can extend the length of a healthy lifespan.”

Want to learn more? Check out our podcast, available on Spotify, where you can hear and watch the full interviews from some of the experts in this article.

This article was edited by Meryl Kay and Julie Schwietert Collazo, and it was fact-checked by Gia Miller. The artist used acrylic paints on canvas.

This article was published in the May/June 2026 edition of Connect to Northern Westchester.