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Duritect-AD™ test for Alzheimer’s disease
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Duritect-AD™ test for Alzheimer’s disease

A rapid and reliable disease risk assessment test for patients with suspected Alzheimer’s disease, to help you arrive at a diagnosis earlier.1

Try Duritect-AD™ for Alzheimer’s disease
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Assess the risk of Alzheimer’s
with Duritect-AD™

When signs or symptoms of cognitive impairment indicate that a patient might have Alzheimer’s disease (AD), a Duritect™ blood test could help streamline the diagnostic process.1

Duritect-AD™ provides a reliable risk score for AD, allowing you to quickly rule out other conditions with similar symptoms.1  This reduces uncertainty, improves the efficiency of diagnostic resources,
and ensures patients receive timely and appropriate care.1

Earlier diagnosis could make earlier intervention and treatment possible, to improve your patients’ outcomes and quality of life.2,3

Learn more on this page
  • Features and benefits
  • Key facts about Duritect-AD™
  • Try Duritect™ in your clinical practice

About the test

Duritect-AD™ is a disease "risk assessment" test. It combines a simple blood test with machine learning analysis to assess the patient’s risk of having AD.1

Duritect-AD™ is for prescription use only.

The test looks for the presence of specific autoantibodies in the patient’s blood as biomarkers of the disease.1 It combines the measurement of autoantibody signatures detected in serum isolated from peripheral whole blood into a numeric Alzheimer’s Disease Risk Score (ADRS).

The risk score indicates a higher or lower likelihood that the patient’s symptoms are due to AD.1 Test results should be interpreted by healthcare professionals in conjunction with other clinical assessments and diagnostic tools, consistent with professional standards of clinical practice.1

Features and benefits

Duritect-AD™ helps you to categorize patients by risk level and make swift, informed decisions.
detact early
Highly accurate4
The highly accurate risk score indicates the probability of AD-related pathology being present.
Clear and easy to understand
Clear and easy to understand
Each patient gets a report that shows either an increased or typical risk that can easily be interpreted.1
simple admin
Simple to administer
The test is easy to carry out. It involves a blood draw and no specific timing or preparation is needed.
min invasive
Minimally invasive
Collecting a blood sample is a quick and least invasive way to assess your patient’s risk of having AD.
Rapid
Rapid
The test results are generally available 48 to 72 hours after the laboratory receives your blood sample.*
affordable
Affordable
The test is a cost-effective way to assess the risk of AD as part of your initial evaluations.

Key facts about Duritect-AD™

This information is intended for medical professionals and covers the clinical use of the test.

Indications for use

Duritect-AD™ is intended for use as an aid in diagnostic evaluation of adult patients:1

  • Age 55+
  • Presenting with signs/symptoms of cognitive impairment that could indicate AD or other causes of cognitive decline.

The test is not intended for:1

  • Screening asymptomatic patients
  • Stand-alone diagnostic purposes
  • Definitively confirming/excluding a diagnosis of AD or other cognitive conditions.

The performance of the risk score has not been established for:1

  • Predicting development of dementia due to AD or other neurologic conditions
  • Monitoring responses to therapies.
The testing process

The Duritect-AD™ test process is simple:

  • Order: Order the test using the requisition form online or in the sample collection kit.
  • Payment: The patient can pay for the test online.
  • Sample collection: Carry out a blood draw according to the instructions for use.
  • Packaging and shipping: Use the labeled envelope to send the sample to our laboratory for processing.
  • Analysis: The sample is analyzed using a combination of scientific approaches.
  • Results: A report is generally available to view 48–72 hours after the laboratory receives the patient’s blood sample.*
What the test looks for

Duritect-AD™ measures levels of specific autoantibodies in the blood to assess a patient’s risk of having ongoing AD pathology.1

Autoantibodies are immune proteins that respond to the production of disease-specific debris generated as a result of ongoing disease pathology. When ongoing disease pathology results in cellular death and debris, the immune system increases production of disease-specific autoantibodies to bind and clear this antigenic debris.

Research has identified several antigen targets associated with Alzheimer’s disease pathology:5-21

Antigen target Amyloid desposition Neurodegeneration Neuroinflammation Blood-brain
barrier integrity
Marker 1 Group 291 x Group 291 x
Marker 2
 x Group 291 x x
Marker 3
 x Group 291 Group 291 x
Marker 4
 x x Group 291 Group 291

 

Duritect-AD™ looks for the autoantibodies that bind to these antigens as biomarkers of the disease.

You can read more about using autoantibodies as biomarkers on the Science and Research page.

The test results

The Duritect-AD™ test determines the Alzheimer’s Disease Risk Score (ADRS):1

  • Patients with a higher score (60 or greater) are considered to be at an increased risk of AD pathology. They should be referred for additional diagnostic, cognitive, and physiological examinations consistent with professional guidelines for AD diagnosis.1
  • Patients with a lower score (40 or lower) are considered to be at a typical risk of AD pathology. They should be monitored and evaluated for other conditions that mimic early symptoms of AD, consistent with professional clinical guidelines.1
  • Patients with an intermediate score (between 40 or 60) are considered to be inconclusive of AD pathology. The test should be repeated and if same result is obtained, the patient should be retested within 6-12 months.1

Test results should be interpreted in conjunction with other clinical assessments and diagnostic tools, consistent with professional standards of clinical practice.1

Try Duritect-AD™ 
in your clinical practice

Are you passionate about advancing the diagnosis and treatment of Alzheimer’s disease? Do you thrive on innovation and the opportunity to shape the future of healthcare?

If you’re involved in diagnosing and treating neurodegenerative diseases, we invite you to join our Early Adopters Program and try Duritect™ now.

Find out more
Duritect™ embodies our dedication to innovation in healthcare – delivering a fast and highly accurate test, to help you detect the presence of a particular disease and begin treating your patients much earlier
Prof. Robert Nagele, PhD
CSO Durin Life Sciences

Abbreviations and references

  1. [Duritect-AD™. Indications for use. Durin Life Sciences. 2024.]
  2. DeMarshall CA, Viviano J, Emrani S, et al. Early detection of Alzheimer’s disease-related pathology using a multi-disease diagnostic platform employing autoantibodies as blood-based biomarkers. J Alzheimer’s Dis. 2023;92:1077–1091.
  3. Rasmussen J, Langerman H. Alzheimer’s disease – why we need early diagnosis. Degen Neurol Neuromusc Dis. 2019;9:123–130.
  4. Duritect™'s analytical and clinical validation results, company internal, 2025.
  5. Sonoda Y, Yashige H, Fujii H, Maekawa T, Abe T. Treatment of idiopathic neutropenia in the elderly with recombinant human granulocyte colony-stimulating factor. Acta Haematol. 1991;85(3):146–152.
  6. Kametani F, Tanaka K, Sato M, et al. A monoclonal antibody Hy20-54-16-3L to lambda (lambda) light chain of human immunoglobulin reacts with amyloid in Alzheimer's disease brain. Neurosci Lett. 1990;117(1-2):62–67.
  7. Kaya ZZ, Tuzuner MB, Sahin B, et al. Kappa/Lambda light-chain typing in Alzheimer's disease. Curr Alzheimer Res. 2022;19(1):84–93.
  8. Buxbaum J. Mechanisms of disease: monoclonal immunoglobulin deposition. Amyloidosis, light chain deposition disease, and light and heavy chain deposition disease. Hematol Oncol Clin North Am. 1992;6(2):323–346.
  9. Absmeier RM, Rottenaicher GJ, Svilenov HL, Kazman P, Buchner J. Antibodies gone bad - the molecular mechanism of light chain amyloidosis. FEBS J. 2023;290(6):1398–1419.
  10. Brenner DA, Jain M, Pimentel DR, et al. Human amyloidogenic light chains directly impair cardiomyocyte function through an increase in cellular oxidant stress. Circ Res. 2004;94(8):1008–10.
  11. Kuçi H, Ebert MP, Röcken C. Anti-lambda-light chain-peptide antibodies are suitable for the immunohistochemical classification of AL amyloid. Histol Histopathol. 2007;22(4):379–387.
  12. Maury CP, Teppo AM. Immunodetection of protein composition in cerebral amyloid extracts in Alzheimer's disease: enrichment of retinol-binding protein. J Neurol Sci. 1987;80(2-3):221–228.
  13. Broer L, Ikram MA, Schuur M, et al. Association of HSP70 and its co-chaperones with Alzheimer's disease. J Alzheimer’s Dis. 2011;25(1):93–102.
  14. Koopman MB, Rüdiger SGD. Alzheimer cells on their way to derailment show selective changes in protein quality control network. Front Mol Biosci. 2020;20(7):214.
  15. Ito N, Kamiguchi K, Nakanishi K, et al. A novel nuclear DnaJ protein, DNAJC8, can suppress the formation of spinocerebellar ataxia 3 polyglutamine aggregation in a J-domain independent manner. Biochem Biophys Res Commun. 2016;474(4):626–633.
  16. Lyon MS, Milligan C. Extracellular heat shock proteins in neurodegenerative diseases: New perspectives. Neurosci Lett. 2019;711:134462.
  17. Fontaine SN, Zheng D, Sabbagh JJ, et al. DnaJ/Hsc70 chaperone complexes control the extracellular release of neurodegenerative-associated proteins. EMBO J. 2016;35(14):1537–1549.
  18. Sogorb-Esteve A, Swift IJ, Woollacott IOC, Warren JD, Zetterberg H, Rohrer JD. Differential chemokine alteration in the variants of primary progressive aphasia-a role for neuroinflammation. J Neuroinflam. 2021;18(1):224.
  19. Alt C, Laschinger M, Engelhardt B. Functional expression of the lymphoid chemokines CCL19 (ELC) and CCL 21 (SLC) at the blood-brain barrier suggests their involvement in G-protein-dependent lymphocyte recruitment into the central nervous system during experimental autoimmune encephalomyelitis. Eur J Immunol. 2002;32(8):2133–44.
  20. Su M-L, Chang T-M, Chiang C-H, et al. Inhibition of chemokine (C-C motif) receptor 7 sialylation suppresses CCL19-stimulated proliferation, invasion and anti-anoikis. PLoS One. 2014;9(6):e98823.
  21. Williams JL, Holman DW, Klein RS. Chemokines in the balance: maintenance of homeostasis and protection at CNS barriers. Front Cell Neurosci. 2014;8:154.

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