The way Alzheimer's disease is diagnosed and treated, a long-standing challenge in medicine, is changing.
Until now, positron emission tomography (PET) or cerebrospinal fluid tests have mainly been used to check for the accumulation of amyloid beta, known as a causative substance of Alzheimer's disease. These tests are costly and place a considerable burden on patients. Against this backdrop, biomarker tests that identify Alzheimer's-related proteins in blood are set to be introduced in Korea's clinical settings.
According to the medical community on the 13th, the domestic clinical use of tests employing phosphorylated tau protein (p-tau) in blood is expected to expand in the Alzheimer's diagnosis field. As blood testing expands, it will open a way to more easily confirm pathological changes of Alzheimer's compared with conventional PET or cerebrospinal fluid tests.
Therapies are also emerging one after another. While Leqembi (ingredient name lecanemab), jointly developed by Japan's Eisai and U.S. Biogen, is being used in Korea, the approval process is underway domestically for Kisunla (ingredient name donanemab), developed by Eli Lilly and Company.
Analysts say the center of gravity in treatment is shifting from "treating after dementia symptoms appear" to "checking what changes are occurring in the brain before symptoms appear and intervening earlier to slow disease progression."
◇ Amyloid that accumulates before dementia symptoms… confirmed by blood
Moon So-young, a neurology professor at Ajou University Hospital, said, "In the past, amyloid could only be confirmed with a PET scan, but blood tests have now advanced to a stage where they can substantially complement PET," and added, "There is a possibility that the p-tau181 assay will be approved in Korea within this year." Moon projected that the p-tau217 test will be introduced next year.
P-tau is a biomarker that measures changes in tau protein associated with Alzheimer's disease in blood. In particular, p-tau217 is drawing attention because it can be used to determine whether amyloid beta has accumulated in the brain.
If blood tests are fully introduced into clinical practice, it is expected that all patients will first be screened for the possibility of Alzheimer's by blood test before undergoing expensive PET or cerebrospinal fluid tests.
Global diagnostics companies are also speeding up development and commercialization of blood-based Alzheimer's tests. Roche Diagnostics, following "Elecsys pTau181," co-developed with Eli Lilly and Company, won Europe's CE mark for "Elecsys pTau217" in May this year.
The pTau test is an in vitro diagnostic that measures phosphorylated tau in blood to help confirm amyloid pathology. It can be used to sort patients who need additional PET or cerebrospinal fluid tests by positive or negative results.
◇ After Alzheimer's drug "Leqembi," "Kisunla" lands
The advent of blood testing is also expected to affect the use of treatments such as "Leqembi" and "Kisunla." Both drugs are antibody therapies targeting amyloid beta, the core pathology of Alzheimer's disease. Currently, administering these drugs requires a process to confirm the presence of amyloid pathology.
If blood biomarkers are sufficiently validated clinically, blood tests can be used to preselect treatment candidates ahead of PET or cerebrospinal fluid tests, which could help reduce the time from diagnosis to treatment and the patient burden.
Moon Hyun-sil, a neurology professor at Konkuk University Hospital, said, "Amyloid beta begins to accumulate 20 to 30 years before symptoms appear," and explained, "After amyloid beta accumulates first, abnormalities in tau protein, neuronal damage, inflammation, and vascular abnormalities act in combination, leading to cognitive decline."
Because of these characteristics, experts say it is more important to intervene when pathological changes are in the early stages rather than to treat after dementia symptoms become pronounced.
◇ Domestic corporations also speed up development of dementia treatments
Both Leqembi and Kisunla are treatments that slow the progression of Alzheimer's disease. If tau pathology and neuronal damage are already significantly advanced after amyloid accumulates, it is difficult to reverse neuronal damage that has already occurred even if amyloid is removed. In other words, there are limits to restoring memory or cognitive function that has already declined.
Experts project that because various factors such as vascular disease, inflammation, and lifestyle affect the progression of dementia, future treatments are likely to evolve to target not only amyloid but also tau, vasculature, and inflammation together.
Domestic corporations are also taking on the challenge of developing various treatments from this perspective.
Aribio is set to announce the results of a global phase 3 trial of the oral Alzheimer's treatment candidate "AR1001." AR1001 improves cerebral blood flow through PDE5 inhibitory action that dilates blood vessels, suppresses neuronal cell death, and even induces clearance of toxic proteins. The premise is that because the causes of dementia onset are multifactorial, a multifront attack rather than a single target is needed.
According to the company, dosing for 52 weeks was completed at the end of June, and the study is currently in the 52-week efficacy and safety analysis phase. As soon as the analysis is completed, the topline results will be disclosed, and the detailed results will be presented at the Clinical Trials on Alzheimer's Disease (CTAD 2026) conference in Boston on Nov. 16. Aribio previously signed an exclusive distribution agreement with China's Fosun Pharma Group for 10 ASEAN countries. The contract is worth about 630 billion won.
Oscotec(039200) and Adel jointly developed "ADEL-Y01," a candidate targeting toxic tau protein, and last year transferred the technology to the French pharmaceutical company Sanofi in a deal worth up to 1.53 trillion won. D&D Pharmatech(347850) is developing NLY01, a candidate therapy for neurodegenerative diseases, and recently has expanded indications from Parkinson's disease to multiple sclerosis, conducting clinical studies.
This means Alzheimer's treatments are expanding beyond removing amyloid beta to target various pathological mechanisms such as tau, inflammation, and neuronal damage.