Understanding dementia

Why we wrote this

We at BNS Neuro want to share as much of our knowledge on this topic as we can. Understanding this condition can help you, a relative, or a partner. Below, we describe the various types of dementia, who they affect, the current screening guidelines and recommendations, current therapies, modifiable risk factors, and current research.

We are confident that you can take action today to reduce your risk. Learn more by reading further.

What is dementia, and who can be affected?

Dementia is a general, umbrella term for a group of conditions characterized by cognitive impairment. That can include memory loss, difficulty with language, decreased problem-solving ability, and other symptoms that interfere with daily activities. In other words, dementia is not just a memory disorder. It can present as atypical symptoms of language, vision or behavior, not just memory complaints.

Dementia can affect any adult; however, it is most frequently associated with aging. A recent nationally representative study estimated that about 1 in 10 Americans aged 65 and older have dementia. This number increases to roughly 1 in 3 for Americans aged 90 and older.1

Depending on a person’s age, they are more or less likely to develop specific types of dementia. These conditions include Alzheimer’s disease, vascular dementia, Lewy body dementia, frontotemporal dementia, and others.5

When is it dementia?

Clinically, dementia is called major neurocognitive disorder (DSM-5).2 It is defined as a significant acquired decline from a person’s previous level in one or more cognitive domains, severe enough to interfere with independence in daily activities. The cognitive domains are:

• Learning & memory
• Language
• Executive function
• Complex attention
• Perceptual-motor function
• Social cognition

The spectrum of cognitive impairment

Dementia is, first and foremost, a problem of function: cognitive, behavioral, emotional and physical. Memory comes second. It sits at one end of a spectrum that begins with normal aging and passes through mild cognitive impairment (MCI).3

What are the general differences?

Alzheimer’s disease, vascular dementia, and Lewy body dementia are all most likely to occur in adults over the age of 65. Alzheimer’s disease can affect people younger than 65, but this is unlikely unless there is a genetic component (e.g., mutations in APP, PSEN1/PSEN2, or ABCA7, or the APOE ε4 risk variant).

Frontotemporal dementia (FTD), on the other hand, is somewhat different: it is more frequently diagnosed in adults aged 45 to 64. This is considered early onset (<65 years of age), and it may be influenced by other environmental and genetic risk factors. Importantly, Alzheimer’s disease and frontotemporal dementia together account for nearly half of all early-onset dementia cases.

The ages at which these conditions are most likely to occur reflect, in part, our understanding of what causes them. Most forms of dementia are associated with the build-up of abnormal proteins within the brain. These can include amyloid-β plaques, tau tangles, and Lewy bodies.

Toxic tau tangles are potentially involved in, or present in, Alzheimer’s disease, Lewy body dementia, frontotemporal dementia, and other tauopathies such as chronic traumatic encephalopathy (CTE). The build-up of these proteins can be associated with genetic mutations (for example, in the MAPT gene that encodes tau, in some inherited forms of FTD), with repeated head trauma (CTE), and with other environmental and lifestyle factors (see modifiable risk factors).

Unlike the other forms of dementia, vascular dementia is primarily related to cardiovascular problems (e.g., high blood pressure, stroke, atherosclerosis, diabetes). Its risk can therefore be addressed with lifestyle changes and with medications that improve blood pressure, manage diabetes, and so on.

Genes that increase the risk of Alzheimer’s disease

The most important common genetic risk factor is the apolipoprotein E ε4 allele (APOE4):

• About 25% of people carry one copy of APOE4, and roughly 2–3% carry two copies.
• Carrying one copy raises Alzheimer’s risk roughly three-fold; carrying two copies raises it substantially more.
• Carrying two copies also increases the risk of side effects (ARIA) from anti-amyloid therapies. This is one reason APOE testing is considered before treatment.9
• Direct-to-consumer tests can report APOE status. Because results also carry implications for biological children and siblings, consider genetic counseling before and after testing.

Other genes are associated with Alzheimer’s disease, some of them with early-onset forms:

• Presenilin 1 / Presenilin 2
• Amyloid precursor protein (APP)
• ABCA7
• CLU (clusterin)
• CR1
• BIN1
• PICALM
• SORL1

Polygenic risk scores, which combine many small genetic effects, are an active area of research and may become clinically available in the future.

What is tau, and what is amyloid?

Amyloid

Amyloid proteins are found throughout nature. Recent research suggests that normal, soluble amyloid proteins confer an evolutionary advantage in animals and are required for normal development and function. In Alzheimer’s disease, however, plaques formed from misfolded, insoluble amyloid-β are found in many affected brains, and for a long time they were considered the hallmark of the disease. Plaques form when misfolded amyloid proteins aggregate, or “stack,” into insoluble deposits. The brain struggles to clear these deposits, and they can disrupt tissue architecture and harm neurons.

Tau

Tau proteins, similarly, are necessary for the proper and healthy function of our brains. They stabilize the microtubules that form the internal structure, or “skeleton,” of our neurons. When tau becomes chemically altered (hyperphosphorylated), or in some inherited conditions mutated, it detaches, misfolds and forms tangles and fibrils that can spread from neuron to neuron. These tangles are considered neurotoxic and may drive neurodegeneration, though the exact details of these processes remain unclear.

A two-way relationship

Some research has shown that these two abnormal proteins may also potentiate each other: the presence of one may make the other more likely to form or spread. Preventing the formation of one of these contributors may therefore help reduce the build-up of the other.

Does the presence of these proteins cause dementia?

Blood tests are beginning to allow physicians to identify these abnormal proteins more easily. In 2025, the FDA cleared the first blood test to aid in diagnosing Alzheimer’s disease, and others are under review.14 However, the presence of these abnormal proteins does not guarantee that a person will develop symptoms of dementia. That’s why a cognitive assessment by a physician is required to diagnose dementia.

There are many reported cases of people with amyloid and tau build-up who show no dementia or severe cognitive decline. There are also people with dementia and cognitive decline without significant amyloid and tau build-up. So while build-up of these proteins is correlated with dementia, scientists do not yet understand the full picture and have not established a complete causal model. In practice, testing for these proteins is mostly used to narrow a diagnosis to a specific form of dementia.

Alzheimer’s disease vs. Alzheimer’s dementia

“Neither the AA nor IWG documents are appropriate to serve as a guide for how to apply biomarkers in a clinical setting. Appropriate use criteria are needed to form a bridge between biological frameworks and real-world clinical practice.”Petersen, Mormino & Schneider, JAMA Neurology, 20244

Cognitive reserve: the brain as a muscle

Some researchers suggest that whether dementia is diagnosed depends on the individual and how much cognitive impairment they actually experience.15 Think of the brain as a muscle that can be trained and strengthened. Instead of lifting weights or running, a person can learn a language, read, or write.

Consider a trained athlete who loses 20% of their muscle. They will most likely still be able to perform all of their daily activities without much difficulty, although they may notice that they are weaker or slower. Now consider someone who has not been physically active and already has underlying health conditions. A further 10–20% loss may leave them unable to take care of themselves, requiring constant skilled nursing. We can think of our brain in the same way.

See current treatment options and modifiable risk factors.

What are the current treatment options?

Several drugs have been approved by the FDA to target amyloid-β, one of the proteins associated with Alzheimer’s disease. This may sound like great news. But these new therapies are extremely expensive, have highly restrictive criteria for who can take them, are prone to significant and sometimes severe side effects, and have shown limited benefits.

The most recent agents are the monoclonal antibodies lecanemab (Leqembi^®) and donanemab (Kisunla^™). They are approved for early, symptomatic Alzheimer’s disease (MCI or mild dementia) with confirmed amyloid pathology. An earlier drug, aducanumab (Aduhelm^®), was discontinued by its manufacturer in 2024.

Key elements of current anti-amyloid therapy

• Only for early symptomatic Alzheimer’s disease, not other dementias
• Amyloid must be confirmed (amyloid PET or cerebrospinal fluid testing)
• Scheduled intravenous infusions
• An MRI at baseline and scheduled “safety” MRIs to watch for ARIA
• Treatment is paused and re-evaluated if ARIA develops
• When to stop, continue or resume therapy is individualized
• Associated with brain-volume loss, sometimes called “amyloid-removal-related pseudo-atrophy”

ARIA stands for amyloid-related imaging abnormalities. These include swelling (ARIA-E, edema/effusion) and small bleeds (ARIA-H, microhemorrhages and superficial siderosis).

Who is eligible?

The American Geriatrics Society summarized general inclusion and exclusion criteria based on the clinical trials:9

Research vs. reality

Trial criteria exclude most real-world patients. Among U.S. Medicare beneficiaries, 92% of people with Alzheimer’s dementia and 85% with MCI had at least one exclusion criterion, most of them several. The most common were cardiovascular or cerebrovascular disease, anticoagulant use, chronic kidney disease, and age over 85.11 In an Italian memory-clinic study, only 6 of 911 patients met the criteria.12

Benefits and risks

What the experts say

“Significant uncertainties remain as to whether the average benefits of lecanemab will exceed the risks.”Institute for Clinical and Economic Review (ICER), Final Evidence Report, April 202310

“The list price of lecanemab exceeds typical thresholds for cost-effectiveness… it is particularly important that therapies for Alzheimer’s disease be priced in line with their value to patients.”ICER, April 202310

“We are particularly concerned for the lack of racial and ethnic diversity in the Clarity AD trial and the lack of data on people who are of advanced age or living with multiple chronic conditions.”American Geriatrics Society, 20239

“The between group difference of 0.45 does not meet the criteria for minimally clinically important difference (MCID).”American Geriatrics Society, 20239

In short, the AGS considered the evidence insufficient to guide many of the prescribing situations its members will face. What matters most to patients, families and care partners is clear benefit to cognition, function and daily life.

Live longer, live smarter: modifiable risk factors

In 2024, the Lancet Commission on dementia prevention, intervention and care identified 14 modifiable risk factors across the life course. Together they account for around 45% of dementia cases worldwide. That is up from 12 factors and 40% in its 2020 report, after high LDL cholesterol and untreated vision loss were added.56

Supplements, and where research is heading

Research into dementia is moving on several fronts: understanding the underlying causes, better and earlier blood-based diagnostics, and new therapies, including those that target tau rather than amyloid.

Nutrition and dietary supplements are an active area of study. The NIH’s National Center for Complementary and Integrative Health notes that, so far, no dietary supplement has been proven to prevent cognitive decline or dementia in rigorous human trials, and research is ongoing.16 We believe that honesty matters. It is why we ground our work in laboratory evidence, show you exactly where that evidence stands, and follow the literature closely.

References

1. Manly JJ, Jones RN, Langa KM, et al. Estimating the prevalence of dementia and mild cognitive impairment in the US: the 2016 Health and Retirement Study Harmonized Cognitive Assessment Protocol Project. JAMA Neurol. 2022;79(12):1242–1249. doi:10.1001/jamaneurol.2022.3543
2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). 2022.
3. Albert MS, et al. The diagnosis of mild cognitive impairment due to Alzheimer’s disease. Alzheimers Dement. 2011;7(3):270–279; and McKhann GM, et al. The diagnosis of dementia due to Alzheimer’s disease. Alzheimers Dement. 2011;7(3):263–269.
4. Dubois B, et al. Alzheimer disease as a clinical-biological construct: an International Working Group recommendation. JAMA Neurol. 2024; and Petersen RC, Mormino E, Schneider JA. Alzheimer disease: what’s in a name? JAMA Neurol. 2024.
5. Livingston G, Huntley J, Liu KY, et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. Lancet. 2024;404(10452):572–628. doi:10.1016/S0140-6736(24)01296-0
6. Livingston G, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet. 2020;396(10248):413–446.
7. van Dyck CH, et al. Lecanemab in early Alzheimer’s disease. N Engl J Med. 2023;388(1):9–21. doi:10.1056/NEJMoa2212948
8. Sims JR, et al. Donanemab in early symptomatic Alzheimer disease: the TRAILBLAZER-ALZ 2 randomized clinical trial. JAMA. 2023;330(6):512–527. doi:10.1001/jama.2023.13239
9. American Geriatrics Society. Position statement and guidance on lecanemab and anti-amyloid therapies. J Am Geriatr Soc. 2023.
10. Institute for Clinical and Economic Review. Lecanemab for Early Alzheimer’s Disease: Final Evidence Report. April 2023.
11. Anderson TS, Ayanian JZ, Souza J, Landon BE. Representativeness of participants eligible to be enrolled in clinical trials of aducanumab for Alzheimer disease compared with Medicare beneficiaries with Alzheimer disease and mild cognitive impairment. JAMA. 2021;326(16):1627–1629. doi:10.1001/jama.2021.15286
12. Canevelli M, et al. “Real world” eligibility for aducanumab. J Am Geriatr Soc. 2021. doi:10.1111/jgs.17390
13. Review of amyloid-related imaging abnormalities with anti-amyloid antibodies. BioDrugs. 2024;38:5–22. doi:10.1007/s40259-023-00633-2
14. U.S. Food and Drug Administration. FDA clears first blood test used in diagnosing Alzheimer’s disease. May 2025.
15. Stern Y. Cognitive reserve in ageing and Alzheimer’s disease. Lancet Neurol. 2012;11(11):1006–1012.
16. National Center for Complementary and Integrative Health. Dietary supplements and cognitive function, dementia, and Alzheimer’s disease.
17. Alzheimer’s Society (UK). Two new dementia risk factors identified in Lancet Commission study. July 31, 2024.
18. Alzheimer’s Research & Prevention Foundation. 4 Pillars of Prevention, Pillar 1: Diet & Supplements.