Exploring Innovative Therapeutics: When Can We Expect New Treatments for Alzheimer’s Disease?

Alzheimer's disease treatments are changing fast. Learn what’s approved, what’s in phase 3, and when new options may reach care.

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Published: April 21, 2026

Written by

Anoutia Allymohamed

Edited by

Anna MacDonald

Model of the human brain surrounded by an assortment of medicinal pills.

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Alzheimer’s disease (AD) is the most common cause of dementia.¹ It involves the abnormal accumulation of two proteins in the brain, called amyloid beta (Aβ) and tau, which build up to form toxic clumps called amyloid plaques and intracellular neurofibrillary tangles (NFTs).

These toxic formations are thought to damage neurons over time,² leading to the development of symptoms like memory loss, forgetfulness, confusion, communication challenges, and even mood swings.³

Widely used Alzheimer’s disease interventions at present

Currently, medical treatments for AD aim to manage symptoms with medicines like cholinesterase inhibitors and memantine. Cholinesterase inhibitors, such as donepezil, rivastigmine and galantamine,⁴work by boosting the availability of the neurotransmitter acetylcholine to improve communication between neurons, helping with things like memory and learning impairments in mild to moderate AD.⁵

Neurons damaged by AD overproduce a neurotransmitter called glutamate, which can cause further damage to neurons. Memantine works by blocking excessive activity of glutamate in the brain, which protects the nerve cells from further damage, thus improving communication between neurons, and reducing the symptoms of moderate to severe AD.⁶

The need for disease-modifying drugs

While cholinesterase inhibitors and memantine can help alleviate symptoms, improving quality of life for some time, these medications do not slow down or reverse the progression of the disease.⁴ Consequently, a number of new drug interventions are being developed with the aim of modifying the disease course by targeting the root causes of the disease.

Currently, new disease-modifying drugs lecanemab and donanemab have been shown to target amyloid accumulation directly, with positive results showing a reduction in cognitive decline in the early stages of the disease.^7,8

These medications are a type of drug called a monoclonal antibody. They contain synthetic antibodies that bind specifically to the protein Aβ. These antibodies then trigger an immune response, which allows the immune system to clear Aβ. This reduces the risk of neurons becoming damaged by actively clearing the problematic accumulation of Aβ from the brain.^7–10

These drugs have both recently completed large phase 3 trials,^7,8 and have been approved in a number of countries, including Australia, Brazil, Mexico,¹¹ the United States,¹² Germany,¹³ Japan,¹⁴ and the United Kingdom.^9,10

However, their availability depends on the individual national health system decisions regarding cost or insurance coverage, which means that these medications are still not widely in use.^9,10,15

This raises a number of infrastructural and ethical considerations for the future. For example, do we have the capacity to efficiently produce and deliver such medications? Are the clinical benefits significant or modest relative to current therapies? Which communities will be able to access such treatments?

Innovative drug delivery systems

Currently undergoing phase 3 trials is the drug trontinemab.¹⁶ Like lecanemab and donanemab, trontinemab is a monoclonal antibody and works by utilizing the body's immune system to recognize and remove Aβ.

However, it incorporates an innovative delivery system that involves a “shuttle” component that attaches to the antibodies and then binds to specific natural receptors on the blood-brain barrier, allowing the medicine to cross the protective membrane completely and enter deeper parts of the brain.^17,18 This has the potential to provide faster, more efficient Aβ removal than other delivery methods.

Already, this technology has shown promising early results for rapid Aβ plaque clearance and a lower rate of serious side effects such as ARIA (amyloid-related imaging abnormalities),^19,20 which have been observed with lecanemab and donanemab.^7,8

Remternetug is another promising investigational immunotherapy drug targeting Aβ.²¹ It is currently going through multiple phase 3 trials to test the effectiveness and safety of the drug in larger groups of people with “mild” or early symptoms of AD, and in people with early-onset AD caused by genetic mutations.^22–24

One of the trials (TRAILRUNNER-ALZ 1²²) is also comparing a subcutaneous injectable version of remternetug (similar to an autoinjector pen used for insulin) with the intravenous drip method into the arm. This may provide a more practical way of taking the drug compared to other anti-Aβ therapies.

TauRx is exploring a new oral tablet option for the treatment of AD.²⁵Their drug, hydromethylthionine mesylate, is a tau aggregation inhibitor which works by targeting tau protein and reducing its accumulation or clumping together in the brain,²⁵ and could potentially become the first oral treatment for AD which targets tau protein pathology.²⁶

At the 2025 AD/PD International Conference on Alzheimer’s and Parkinson’s Diseases, TauRx presented new data from their 12-month phase 3 LUCIDITY study (NCT03446001²⁷), highlighting the efficacy of the drug in early to moderate AD.²⁸ However, the full results from the trial have yet to be released in a peer reviewed publication, so further details are needed before we can fully assess its safety and efficacy.

Beyond Aβ- and tau-targeted approaches

AD is a multifactorial and complex disease, and Aβ and tau accumulation only represent one part of the disease process. For this reason, there are a number of innovative therapies being developed that go beyond Aβ- and tau-targeted approaches.

Therapies in the current research pipeline are targeting a diverse range of abnormal physiological processes, including neuroinflammation, synaptic dysfunction, and microglial dysregulation²⁹ (see Table 1), highlighting the many avenues of treatment possibilities.

Table 1: Emerging drugs for Alzheimer’s disease currently in/recently completed phase 3 trials.

Drug name	Mechanism of action
Masitinib	Inhibition of the c-kit, Ln, Fyn and CSF1R (colony stimulating factor-1-receptor) kinases³⁰
Tricaprilin	Ketosis inducer³¹
Bezisterim	Anti-inflammatory³²
Blarcamesine	Muscarinic receptor modulators: Sigma-1 receptor antagonists³³
Buntanetap	Aβ protein precursor inhibitors, tau protein inhibitors³⁴

The importance of early detection and diagnosis

It is important to note, however, that the majority of new investigational therapies are showing positive results in people with “early” or “mild” to “moderate” onset of the disease. This means that early detection and diagnosis of AD is crucial for patients.

Unfortunately, it is estimated that 75% of all dementia cases globally go undiagnosed,³⁵ with AD contributing to 60–70% of dementia cases worldwide.³⁶ This highlights the importance of early detection and the investment in accessible and accurate diagnostic testing.

Recently, AD biomarker research has focused heavily on developing accessible and accurate blood-based tests and protein panels that measure specific proteins in the blood that reflect brain Aβ and tau pathology.³⁷ The proteins p-tau217, p-tau181, Aβ42/40, MTBR-tau243, glial fibrillary acidic protein (GFAP), and neurofilament light chain (NfL) have been reported as promising markers.^38–42

Notably, the combinations of such markers have been shown to offer greater accuracy in detecting individuals with Aβ and/or tau accumulation. For example, in a new study led by researchers at the Barcelonaβeta Brain Research Center, the researchers found that the ratio between the proteins p-tau217 and Aβ42 was the best-performing biomarker in their blood-based biomarker panel for detecting individuals with Aβ accumulation in the brain.⁴³

The accuracy of this biomarker correlated well with the current gold standard diagnostic methods of cerebrospinal fluid measurements and positron emission tomography (PET) scans, highlighting how such blood-based tests may one day be able to replace costly PET scans and invasive spinal taps for early detection of AD.

A hopeful future for people living with Alzheimer’s disease

AD research is making exciting progress, and despite the complexities of the disease and the challenges ahead, the development of innovative therapies like trontinemab and accessible diagnostic markers like blood-based tests and protein panels all mark an important step towards improving our understanding of AD, and finding better ways to actively treat the disease in the future, rather than just managing the symptoms.

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Meet the Author

Anoutia Allymohamed

Freelance Science Writer

Anoutia Allymohamed is a freelance science writer. She holds a Masters in Mental Health Science, and a Bachelors in Cybernetics and Artificial Intelligence from the University of Reading, UK. Her research interests include neurodegenerative diseases, the glymphatic system, neuroethics and human relevant research, artificial intelligence and disease detection, treatment resistant depression, and psychosis.

Edited By

Anna MacDonald

Senior Science Editor

After obtaining a first-class honors degree in biological sciences from the University of East Anglia, Anna worked as a scientific conference producer before joining Technology Networks. As part of her role, Anna helps to coordinate coverage, working with key opinion leaders from industry and academia to produce content across all communities.

Exploring Innovative Therapeutics: When Can We Expect New Treatments for Alzheimer’s Disease?

Alzheimer's disease treatments are changing fast. Learn what’s approved, what’s in phase 3, and when new options may reach care.

Widely used Alzheimer’s disease interventions at present

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Beyond Aβ- and tau-targeted approaches

The importance of early detection and diagnosis

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A hopeful future for people living with Alzheimer’s disease

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