Lecanemab For Early-Stage Alzheimer's Disease

  • Duyen Nguyen Master in Science - MSci Human Biology, University of Birmingham


Dementia is one of the leading causes of death and disability globally. With more than 55 million people reported to have dementia worldwide, the need for effective treatment is undeniable. Alzheimer's disease is the most common form of dementia, contributing to approximately 60-70% of cases.1 

Presently, there is no cure for Alzheimer’s and current treatments fail to address the underlying cause of the disease. However, recent research progress has demonstrated promising results with the approval of novel Alzheimer’s drugs. One drug that has been approved is lecanemab (also known by the brand name Leqembi). Lecanemab differs from current Alzheimer’s treatments as it is one of the first drugs proven to slow cognitive decline and directly target the disease. 

What is alzheimer’s disease?

Dementia is an umbrella term referring to the impaired neurological symptoms that affect a person’s ability to perform daily activities. Alzheimer’s is the most common form of dementia, affecting around 1 in 14 people over the age of 65 in the UK.2 

Symptoms vary between individuals and may include:3

  • Confusion and disorientation (e.g. getting lost in a familiar place)
  • Communication difficulties (e.g. struggling to follow conversations or forgetting words)
  • Difficulties solving problems or making decisions
  • Personality changes (e.g. aggression, inappropriate behaviour, withdrawal from social activities and work) 
  • Low mood and anxiety 
  • losing track of time

What is lecanemab?

As previously stated, there is currently no cure for Alzheimer’s. The mainstay of treatment is palliative and supportive care, which does not treat the underlying cause of the disease. This means they do not slow the rate of disease progression, they only help to alleviate the symptoms.

Alzheimer's research focuses on discovering treatments that can achieve the following aims:

  • Directly target the underlying causes of disease
  • Slow the rate of disease progression and brain damage

Lecanemab is the first US Food and Drug Administration (FDA)-approved drug that achieves both of these aims. This drug will be used to treat patients with early Alzheimer’s disease (referred to as ‘mild cognitive impairment’). Its approval marks a revolutionary breakthrough in Alzheimer’s therapeutics, being the first drug to slow brain damage in patients.4 

Eisai, based in Tokyo, and Biogen, based in Cambridge, Massachusetts are the pharmaceutical companies that developed lecanemab. The clinical study’s results were published in the New England Journal of Medicine.

How does lecanemab work?

Lecanemab is a monoclonal antibody that works similarly to the antibodies produced naturally in our bodies to fight disease and infections. It helps remove amyloid plaques commonly found in high abundance in Alzheimer’s patients.4

Amyloid is a protein found in the space between neurons in the brains of Alzheimer’s patients. These proteins accumulate and form clusters referred to as ‘plaques’. Amyloid plaques are hypothesised to be a key characteristic of Alzheimer’s and one of the underlying causes of the disease. These plaques contribute to brain toxicity and dementia symptoms.5

Lecanamab binds to the plaques and recruits other immune cells within your body to aid in the removal of the amyloid proteins. The decrease in amyloid plaques enables slower cognitive decline, which is measured by a reduction in symptoms. 

How is lecanemab given?

Lecanemab is administered fortnightly via an intravenous infusion (IV). Each IV lasts one hour and you will be monitored during and after the infusion by a healthcare professional. Before the infusion, you may be given preventative medications to reduce your risk of infusion-related side effects. Preventative medications may include, non-steroidal anti-inflammatory drugs, antihistamines, or glucocorticoids (a class of corticosteroids).  

Considerations and limitations 

“Controversial results” – how effective is lecanemab?

Despite the promising results from clinical trials, lecanemab’s approval has not been entirely met with positive responses. This is due to safety concerns and uncertainty over the significance of lecanemab’s efficacy. 

The clinical study involved 1,795 participants with early Alzheimer’s and lasted 18 months. Lecanemab use was reported to slow cognitive decline by 27%.4 This decline was measured using a scale that quantifies the severity of dementia symptoms. Despite the moderate benefit, these results present a huge step in Alzheimer’s research. Professor Tara Spires-Jones, from the University of Birmingham, states that although the impact was small, the overall results are still "a big deal because we've had a 100% failure rate for a long time."

Moreover, some researchers have expressed concern regarding the high costs of lecanemab use ($26,500 per patient).6 These costs are surmised to be higher, as patients require MRI scans throughout the treatment course to check for brain abnormalities (swelling or bleeding in the brain). In addition to the potential side effects, the high expenses may lead to a disparity in health benefits for patients. Diana Zuckerman, president of the US National Center for Health Research, says “You’re dealing with people with mild cognitive impairment who are functioning, and you’re putting them at risk”, regarding both their health and finances.  

Another caveat is the trial lasted only 18 months. Therefore, it is uncertain whether the health benefits will be sustained with long-term use. Further research is required to determine this and investigate if lecanemab can be used to treat patients with late-stage Alzheimer’s. 

Potential side effects

Just like any other drug, some patients were reported to experience side effects upon lecanemab use. In the clinical trial, 7% of participants withdrew due to side effects. Safety concerns that arose following the release of the trial’s results include:

  • 26.4% of participants had infusion-related reactions (flushing, fever, rash, and body aches)
  • 3 deaths were reported (caused by brain bleeding and seizures)4

It is important to note that 96% of the infusion-related reactions were mild to moderate.

Lecanemab may also cause amyloid-related imaging abnormalities (ARIA), such as swelling or bleeding. ARIA refers to changes in the brain that occur in unusual places and can be observed via MRI scans. In the clinical trial, 20% of participants experienced bleeds and swelling of the brain. Although ARIA does not typically cause additional symptoms, some people were reported to experience:7 

  • Confusion
  • Dizziness
  • Headaches
  • Nausea
  • Seizures
  • Vision changes

Patients taking lecanemab will be monitored throughout treatment for ARIA via frequent MRI scans. Treatment will be discontinued if patients develop ARIA. 


In recent years, prominent advances in Alzheimer's disease research have been made. One of these is the approval of the novel Alzheimer’s drug, lecanemab. Lecanemab is an antibody treatment that specifically targets one of the underlying causes of the disease: amyloid protein build-up. The removal of amyloid proteins leads to a reduction in cognitive decline. Despite its benefits, lecanemab is not a complete cure. Future studies are necessary to determine whether it can be used for late-stage Alzheimer’s and ensure its efficacy with long-term use.

Ultimately, lecanemab still presents a momentous achievement in Alzheimer’s therapeutics and has paved the way for a new era of Alzheimer's drugs. This is evident with the successful results from a trial testing another antibody treatment, donanemab. Donanemab also targets amyloid proteins and is awaiting approval by the FDA. Overall, with the advancements in research and development, we hope to see the continued development of more effective medicines and the optimisation of Alzheimer’s treatments.8,9 


When will lecanemab be available?

At the moment, lecanemab is only available to patients with early Alzheimer’s disease in the USA, Japan, and China. This follows its approval in July 2023 by the FDA

In May 2023, Eisai applied for approval from the Medicines and Healthcare Products Regulatory Agency (MHRA) to enable availability in the UK as well. However, MHRA approval does not substantiate lecanemab use on the NHS, this requires further approval by the National Institute for Health and Care Excellence (NICE). For this reason, lecanemab availability in the UK is expected to be granted in 2025 instead.

Dr Richard Oakley, from the Alzheimer’s Society UK, states significant changes to the NHS are required to improve dementia diagnosis if the UK plans to implement lecanemab. He says, “At least 106,000 people could benefit from lecanemab. But currently, one in six people wait over a year to see a specialist after a GP referral, and one in ten waits over six months for a brain scan.”

How much will lecanemab cost?

In January 2023, Eisai announced the launch pricing of lecanemab to be $26,500 (24,766 EUR) per patient. However, actual annualised pricing may vary between patients depending on their prognosis and the costs of additional MRI scans.10 

Who should not take lecanemab?

Lecanemab is not recommended for those taking anti-coagulant medicines (blood thinners). This is due to the potential risk of ARIA. Individuals who have inherited two copies of the APOE-ɛ4 gene also have an increased genetic risk of developing ARIA while taking lecanemab. To prevent this, genetic testing is recommended before starting treatment.

Overall, you should always consult your doctor to ensure the best treatment modality is used for you. Your doctor will help you weigh the benefits and risks.


  1. Dementia [Internet]. [cited 2024 Jan 26]. Available from: https://www.who.int/news-room/fact-sheets/detail/dementia
  2. NHS England » Preparing for a new chapter: disease modifying treatments for early Alzheimer’s disease [Internet]. [cited 2024 Jan 26]. Available from: https://www.england.nhs.uk/blog/preparing-for-a-new-chapter-disease-modifying-treatments-for-early-alzheimers-disease/
  3. nhs.uk [Internet]. 2018 [cited 2024 Jan 26]. Alzheimer’s disease. Available from: https://www.nhs.uk/conditions/alzheimers-disease/ 
  4. Van Dyck CH, Swanson CJ, Aisen P, Bateman RJ, Chen C, Gee M, et al. Lecanemab in early alzheimer’s disease. N Engl J Med [Internet]. 2023 Jan 5 [cited 2024 Jan 26];388(1):9–21. Available from: http://www.nejm.org/doi/10.1056/NEJMoa2212948 
  5. Reiss AB, Arain HA, Stecker MM, Siegart NM, Kasselman LJ. Amyloid toxicity in Alzheimer’s disease. Rev Neurosci. 2018 Aug 28;29(6):613–27. 
  6. Eisai Co., Ltd. [Internet]. [cited 2024 Jan 26]. Eisai’s approach to u. S. Pricing for leqembi™(Lecanemab) , a treatment for early alzheimer’s disease, sets forth our concept of “societal value of medicine” in relation to “price of medicine” | news release:2023. Available from: https://www.eisai.com/news/2023/news202302.html 
  7. Withington CG, Turner RS. Amyloid-related imaging abnormalities with anti-amyloid antibodies for the treatment of dementia due to alzheimer’s disease. Front Neurol. 2022;13:862369.
  8. Sims JR, Zimmer JA, Evans CD, Lu M, Ardayfio P, Sparks J, et al. Donanemab in early symptomatic alzheimer disease: the trailblazer-alz 2 randomized clinical trial. JAMA. 2023 Aug 8;330(6):512–27.
  9. Volloch V, Rits-Volloch S. Effect of lecanemab and donanemab in early alzheimer’s disease: mechanistic interpretation in the amyloid cascade hypothesis 2. 0 perspective. J Alzheimers Dis [Internet]. [cited 2024 Jan 26];93(4):1277–84. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10357217/ 
  10. Jönsson L, Wimo A, Handels R, Johansson G, Boada M, Engelborghs S, et al. The affordability of lecanemab, an amyloid-targeting therapy for Alzheimer’s disease: an EADC-EC viewpoint. Lancet Reg Health Eur. 2023 Jun;29:100657.
This content is purely informational and isn’t medical guidance. It shouldn’t replace professional medical counsel. Always consult your physician regarding treatment risks and benefits. See our editorial standards for more details.

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Duyen Nguyen

Master in Science - MSci Human Biology, University of Birmingham

Duyen is a creative and enthusiastic writer with an MSci in Human Biology. She has an extensive scientific background and is highly proficient in cancer biology and Drosophila genetics. Her research project investigated the importance of calcium transporters, Itpr and SERCA, in the regulation of apoptosis-induced proliferation. She is an aspiring medical writer and strives to create accessible and engaging content that effectively translates research to a range of audiences.

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