NESSA.

The Search for a Cure

The search for a cure

A family’s loss, an inventor’s mission, and the science that could stop this disease. Here is why we fight for earlier detection, and 20 plain-language articles on where the research stands today.

These articles are for education and awareness only. They are not medical advice and cannot replace a doctor. If you’re worried about yourself or someone you love, please speak with a qualified healthcare professional.

Why This Foundation Exists

Finding it earlier is how we find a cure

My mother’s dementia was found late, the way it is for almost everyone. By the time the disease had a name, it had already taken years from her. That single fact, that we saw it too late, is what this foundation is built to change.

I am a co-inventor on an issued US patent, “AI-Driven System and Methods for 3D Medical Image Disease Detection”, technology built to read medical scans and catch the earliest signatures of disease, with dementia among the conditions it is designed to detect, long before it takes hold. Four related patents are being issued. The idea behind it is simple, and it is personal. The sooner the disease can be seen, the more can be done, and the closer we come to stopping it for good.

That belief, that earlier detection is the road to a cure, is the reason the Nessa Foundation exists. We fund independent research into detecting dementia sooner and treating it better: the scientists, studies, and institutions across the whole field working toward the same goal. Every gift funds that shared mission, not any single company or product.

The articles below are where that science stands today, from the first blood tests and newest treatments to what still has to be discovered. This is the search for a cure, and you are part of it.

Sajed Khan, Founder

What’s inside

Part One

Recognizing the Signs

Dementia rarely arrives all at once. It begins with small changes that are easy to explain away. Knowing what to watch for is the first step toward an early diagnosis, and earlier care means more time, more options, and more life.

01

The 10 early warning signs of dementia

The changes that are worth paying attention to

Dementia is not a single disease but a group of symptoms caused by changes in the brain that interfere with everyday life. The most recognized early signs include: memory loss that disrupts daily routines (especially forgetting recently learned information); difficulty planning or solving familiar problems; trouble completing everyday tasks; confusion about time or place; problems judging distance or interpreting what the eyes see; new struggles with words, in speech or writing; misplacing things and being unable to retrace steps; declining judgment; withdrawal from work or social life; and noticeable shifts in mood or personality.

The key word is change. Everyone forgets a name now and then. What matters is a clear difference from how a person used to function, a pattern that is getting worse rather than a one-off lapse. When several of these appear together, or steadily deepen, it is worth a conversation with a doctor rather than a wait-and-see.

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02

Normal aging vs. dementia

Telling ordinary forgetfulness from something more

Forgetfulness is a normal part of getting older. The healthy aging brain might briefly misplace keys, blank on a word, or need a moment to recall a name, and then the information comes back. Aging may slow recall, but it does not erase the ability to function independently.

Dementia looks different. A person may forget the entire event, not just a detail. They might repeat the same question minutes apart, get lost on a familiar route, or struggle to follow a recipe they have made for decades. Where normal aging is occasionally forgetting where you parked, dementia is forgetting that you drove. The distinction lies in whether the lapses interrupt daily life and whether they are progressing. A useful rule of thumb: if changes are frequent, worsening, and affecting independence, they deserve a professional evaluation rather than reassurance.

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03

What is mild cognitive impairment (MCI)?

The gray zone between normal aging and dementia

Mild cognitive impairment is a stage where thinking or memory is measurably weaker than expected for someone’s age, but not yet severe enough to disrupt independent daily living. A person with MCI can still manage their own affairs, even if they notice they are working harder to do so.

MCI matters because it is often where the newest treatments and the most meaningful planning happen. Not everyone with MCI goes on to develop dementia, some remain stable, and a portion have causes that can be treated and reversed, such as medication side effects, thyroid problems, depression, or sleep disorders. But MCI caused by Alzheimer’s pathology is exactly the early window in which today’s amyloid-targeting drugs are designed to work. That makes recognizing MCI, and getting it properly assessed, genuinely valuable rather than alarming.

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04

The main types of dementia, explained

Alzheimer’s, vascular, Lewy body, and frontotemporal

Alzheimer’s disease is the most common form, typically beginning with short-term memory loss and tied to the buildup of amyloid plaques and tau tangles in the brain. Vascular dementia, the next most common, results from reduced blood flow, often after strokes, and tends to affect planning, judgment, and speed of thinking more than memory at first.

Lewy body dementia involves abnormal protein deposits and is marked by fluctuating alertness, visual hallucinations, and movement changes similar to Parkinson’s. Frontotemporal dementia tends to strike younger and shows up first as changes in personality, behavior, or language rather than memory. Many people, especially later in life, have mixed dementia, where more than one type is present at once. The type matters because each progresses differently and responds to different care, which is why an accurate diagnosis is worth pursuing.

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05

The stages: early, middle, and late

How dementia typically progresses over time

Dementia is usually described in three broad stages, though everyone’s path is different. In the early stage, a person remains largely independent but notices lapses, forgetting words, misplacing items, struggling with complex tasks or new places. Many continue to work, drive, and socialize with some support.

In the middle stage, often the longest, symptoms become harder to hide. Memory gaps widen, confusion grows, and help is increasingly needed with daily activities like dressing or managing money. Mood and behavior changes are common. In the late stage, individuals need extensive, often around-the-clock care, lose much of their ability to communicate, and become physically frail. Understanding the stages helps families plan ahead, anticipate needs, and make the most of the time when their loved one is still most themselves.

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06

Early signs of Alzheimer’s specifically

What the most common dementia looks like at the start

Because Alzheimer’s first affects the brain regions tied to forming new memories, its earliest hallmark is usually difficulty holding on to recent information. Someone may ask the same question repeatedly, rely heavily on notes and reminders, or forget appointments and conversations while still recalling events from decades ago with clarity.

Other early Alzheimer’s signs include misplacing objects in unusual places, losing track of dates and seasons, trouble finding the right words, and growing difficulty with tasks that require several steps, such as cooking a familiar meal or managing finances. People often develop subtle workarounds, withdrawing from activities that have become hard, or letting a spouse take over tasks they used to handle. Recognizing these patterns early opens the door to a confirmed diagnosis through today’s biomarker tests and to treatments that work best in the earliest stages.

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07

Changes in mood, personality & behavior

When the shift shows up in who someone seems to be

Dementia is not only about memory. For many families, the most painful changes are in temperament, a warm, outgoing person growing anxious, irritable, suspicious, or withdrawn. Apathy is especially common: a loss of interest and initiative that can be mistaken for laziness or depression.

Some people become uncharacteristically blunt, restless, or socially inappropriate, particularly in frontotemporal dementia, where behavior change can precede memory loss entirely. Others experience confusion that worsens in the evening, sometimes called sundowning. These shifts are caused by changes in the brain, not by choice or stubbornness, a distinction that can ease a family’s frustration and guilt. Noticing personality change as a possible medical sign, rather than simply “getting older and crankier,” can lead to earlier help and better support.

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08

When language starts to slip

The subtle erosion of words and conversation

Trouble with language is one of the more telling early signs. It often begins as occasional word-finding difficulty, pausing mid-sentence, substituting a vague term like “that thing” for a specific word, or calling objects by the wrong name. Following or joining group conversations may become tiring.

As changes progress, a person may repeat themselves, lose the thread of what they were saying, or struggle to read and write as easily as before. In certain dementias, language is the very first system to fail, while memory stays relatively intact, a pattern known as primary progressive aphasia. Because we lean on words constantly, language changes can be among the earliest things a family notices, even before formal memory problems appear. Naming the pattern out loud, and raising it with a doctor, is a meaningful first step.

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09

Younger-onset dementia (before 65)

When symptoms arrive in the prime of life

Dementia is most common in older adults, but it does occur earlier, younger-onset (or early-onset) dementia refers to symptoms appearing before age 65, sometimes in a person’s 40s or 50s. Because it is unexpected at that age, it is frequently misread at first as stress, depression, burnout, or menopause, and diagnosis can take longer.

Younger-onset dementia carries its own challenges: people may still be working, raising children, or financially responsible for a household. Frontotemporal dementia and certain genetic forms of Alzheimer’s are more represented in this group. The signs are similar to later-life dementia, memory, language, judgment, personality, but the stakes and the disruption can be especially heavy. Awareness matters, because younger people and their doctors may not think of dementia, delaying the answers and support that an accurate diagnosis brings.

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10

When to see a doctor, and what happens

Taking the first step, and what to expect

If memory or thinking changes are persistent, worsening, or affecting daily life, it is time to see a doctor, sooner rather than later. Early evaluation matters because some causes of cognitive symptoms are treatable and reversible, and because the newest dementia therapies are designed for the earliest stages.

A typical assessment starts with a conversation about symptoms and history, often with a family member present, followed by brief memory and thinking tests. Doctors check for other explanations, medications, vitamin deficiencies, thyroid issues, depression, sleep problems, through blood work and physical examination. Depending on findings, they may order brain imaging or, increasingly, a blood biomarker test that can detect the changes of Alzheimer’s. A diagnosis can feel frightening to pursue, but it also brings clarity, access to treatment and trials, and the chance to plan while a person can still take part in the decisions.

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Part Two

What’s Being Developed

For decades, dementia research delivered mostly disappointment. That has changed. The last few years brought the first drugs proven to slow Alzheimer’s, the first blood test to diagnose it, and a pipeline richer than ever. None of it is a cure yet, but the direction is unmistakable.

11

Lecanemab: the first drug to slow Alzheimer’s

A turning point after years of dead ends

Lecanemab, sold as Leqembi, is an antibody that clears amyloid, the sticky protein that builds up in the Alzheimer’s brain. In a large trial of roughly 1,800 people with early disease, it slowed cognitive and functional decline by about 27% over 18 months compared with placebo. That is modest, not miraculous, but it was the first time a treatment was shown to change the underlying course of Alzheimer’s, and it earned full FDA approval in 2023.

It is meant only for people in the earliest stages, mild cognitive impairment or mild dementia, with confirmed amyloid in the brain. Originally an IV infusion every two weeks, it now has less frequent maintenance dosing and, as of 2025, a once-weekly under-the-skin injection that can be given at home. It is not a cure, and it carries real risks (see article 13), but it represents a genuine shift from managing symptoms to attacking the disease itself.

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12

Donanemab: a second amyloid-clearing therapy

A different schedule, a similar strategy

Donanemab, sold as Kisunla, is the second amyloid-clearing antibody to win FDA approval for early Alzheimer’s. In its main trial of more than 1,700 people, it also slowed decline in those treated in the early stages. Like lecanemab, it targets the amyloid plaques thought to drive the disease, and it is approved only for people with mild symptoms and confirmed amyloid.

One notable feature is that donanemab is given as a monthly infusion, and treatment can sometimes be stopped once brain scans show the amyloid has been cleared, potentially reducing time and cost. In 2025, regulators approved a revised, gradual dosing schedule shown to lower the risk of brain-swelling side effects while preserving benefit. Having two approved options means doctors and families can weigh schedules, risks, and circumstances rather than facing a single take-it-or-leave-it choice.

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13

Understanding ARIA: the risks to weigh

Why these drugs require careful monitoring

The amyloid-clearing antibodies share a significant side effect known as ARIA, amyloid-related imaging abnormalities. As the drugs strip plaque from blood vessel walls, they can cause temporary brain swelling (ARIA-E) or small spots of bleeding (ARIA-H). In the trials, roughly one in five treated patients showed some form of ARIA.

Most cases cause no symptoms and are caught only on routine MRI scans, resolving when treatment is paused. But ARIA can occasionally be serious, and in rare instances fatal. The risk is higher in people who carry a gene variant called APOE ε4, which is why doctors typically test for it and perform brain MRIs before and during treatment. ARIA is the central reason these drugs require specialist oversight and honest risk-benefit conversations, and why so much current research focuses on getting the benefits of amyloid removal with fewer dangers.

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14

The first blood test for Alzheimer’s

A diagnosis that no longer requires a brain scan or spinal tap

In May 2025, the FDA cleared the first blood test to help diagnose Alzheimer’s disease. Until then, confirming the disease meant an expensive PET brain scan or an invasive spinal fluid sample, barriers that left many people undiagnosed or diagnosed late. The new test measures a protein fragment called p-tau217 alongside an amyloid marker, producing a ratio that signals whether Alzheimer’s-type plaques are likely present.

In validation studies, the test agreed with the older gold-standard methods in the large majority of cases, with results available within days from an ordinary blood draw. For now it is approved for adults 55 and older who already show symptoms, used alongside a doctor’s evaluation rather than as a stand-alone answer. But it is a landmark: a simple, accessible, affordable way to catch the disease earlier, exactly the window in which today’s treatments work best.

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15

Detecting dementia earlier: biomarkers & imaging

Seeing the disease before the symptoms

One of the most powerful shifts in the field is the move toward detecting dementia biologically, spotting the disease in the brain or blood before, or alongside, the first noticeable symptoms. Beyond the new blood tests, researchers use PET scans that light up amyloid and tau deposits, and spinal fluid analysis, to confirm what is happening at a molecular level.

The frontier is even earlier detection. Studies suggest p-tau217 in the blood can flag Alzheimer’s changes in people who have no symptoms yet, raising the future possibility of screening at-risk individuals while there is still time to intervene. Advanced brain imaging and artificial intelligence are increasingly used to read scans more precisely and catch subtle patterns the human eye can miss. The goal across all of this work is the same: turn dementia from something diagnosed late, often after years of uncertainty, into something caught early, when action means the most.

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16

Beyond amyloid: targeting tau

Going after the other protein behind the damage

Amyloid plaques get the headlines, but a second protein, tau, may track even more closely with the actual loss of brain cells and thinking ability. In Alzheimer’s, tau forms tangles inside neurons, and its spread through the brain mirrors the progression of symptoms. Many researchers believe that targeting tau, alone or together with amyloid, could be key to greater benefit.

Several tau-focused therapies are now in clinical trials, including antibodies designed to stop tangles from forming or spreading, and experimental approaches that aim to lower tau production. Tau-imaging scans also help researchers stage the disease and measure whether treatments are working. Tau therapies are earlier in development than the amyloid drugs and none is approved yet, but they represent one of the most active and promising directions in dementia science, an attempt to hit the disease on a second front.

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17

The pipeline: 180+ trials, new targets

A field that is broader than ever

The amyloid antibodies are just the visible tip of a large and growing research effort. At any given time there are well over a hundred active Alzheimer’s trials underway, spanning more than a dozen different biological targets, not only amyloid and tau, but also brain inflammation, energy metabolism, blood vessel health, and the connections between brain cells.

This breadth matters because Alzheimer’s and related dementias are almost certainly not caused by one thing, and no single drug is likely to be the whole answer. Promising candidates include oral medications that may be easier to take than infusions, drugs aimed at protecting synapses, and therapies that calm the brain’s overactive immune response. Not every trial will succeed, many will fail, as they have before, but the sheer diversity of approaches is itself a reason for hope. Each one tests an idea that, if it works, could become the next breakthrough.

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18

Can lifestyle prevent dementia? The U.S. POINTER study

Evidence that everyday habits move the needle

One of the most encouraging recent findings did not come from a drug at all. The large U.S. POINTER study, reported in 2025, tested whether a structured program of healthy living could protect the aging brain. Participants at risk of decline followed a combination of regular exercise, a brain-healthy diet, mental challenge, social engagement, and monitoring of heart-health numbers like blood pressure.

Both the structured and the self-guided groups improved their cognition over two years, with the more intensive, structured program producing the greater benefit, across different backgrounds and genetic risk levels. It builds on an earlier landmark Finnish study with similar results. The message is powerful and hopeful: while lifestyle is not a guarantee against dementia, the same habits that protect the heart appear to protect the brain, and they are within many people’s reach starting today.

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19

The 14 risk factors you can change

Nearly half of dementia risk may be modifiable

A major expert review concluded that addressing a set of 14 modifiable risk factors across a lifetime could prevent or delay up to 45% of dementia cases worldwide. In other words, a large share of dementia risk is not fixed fate, it is influenced by things that can be changed.

The factors, which shift in importance at different ages, include: less education in early life; hearing loss, high LDL cholesterol, depression, head injury, physical inactivity, diabetes, smoking, high blood pressure, obesity, and excessive alcohol in midlife; and social isolation, air pollution, and untreated vision loss in later life. Many overlap with general health advice, stay active, protect your hearing and vision, manage blood pressure and blood sugar, stay socially connected, don’t smoke. None of this offers certainty, and dementia still strikes people who do everything right. But it reframes the disease as one we can push back against, both individually and through public health.

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20

The frontier: GLP-1s, vaccines & AI

Where the next wave of ideas is coming from

Beyond today’s approved drugs, researchers are pursuing strikingly varied ideas. GLP-1 medications, the same class behind popular diabetes and weight-loss drugs, have been studied in large Alzheimer’s trials on the theory that improving metabolism and reducing inflammation might protect the brain; results so far have been mixed, but the line of inquiry continues. Vaccine-style immunotherapies, including newer designs aimed at amyloid, tau, and inflammation, are being explored to prevent or slow the disease by harnessing the body’s own immune system.

And artificial intelligence is increasingly woven through the field, helping read brain scans, spot disease earlier in imaging and blood data, and accelerate the search for new drugs. This is the frontier the Nessa Foundation cares about most: the work that could one day move dementia from something we merely slow to something we detect at the very start, and finally stop. None of these is proven yet. All of them are reasons not to give up.

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A note on these articles

This content is written for education and awareness and is current as of mid-2026. It draws on public information from sources such as the U.S. Food & Drug Administration, the National Institute on Aging, the Alzheimer’s Association, the Mayo Clinic, and peer-reviewed medical journals. Treatments, approvals, and research findings change quickly, always confirm current details with a healthcare professional.

This is not medical advice. Nothing here can diagnose a condition or replace care from a qualified clinician. If you are concerned about yourself or someone you love, please reach out to a doctor.

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