September 21, 2024

World Alzheimer's Day: Raising Awareness

On September 21, our focus turns to Alzheimer's Disease, extending our support to individuals living with dementia, their dedicated caregivers, and healthcare professionals.

Origins of World Alzheimer's Day: In 1994, Alzheimer's Disease International (ADI) initiated World Alzheimer's Day, uniting a global community to shed light on dementia's impact. This annual event emphasizes the imperative of collective action in addressing this pressing issue.

WANT TO KNOW MORE? For a better understanding of Alzheimer's Disease, patient stories, and how you can contribute to our mission of raising awareness about this disease while celebrating World Alzheimer's Day, please visit Alzheimer's Disease International: https://www.alzint.org/

September 21, 2024

World Alzheimer's Day: Raising Awareness

On September 21, our focus turns to Alzheimer's Disease, extending our support to individuals living with dementia, their dedicated caregivers, and healthcare professionals.

Origins of World Alzheimer's Day: In 1994, Alzheimer's Disease International (ADI) initiated World Alzheimer's Day, uniting a global community to shed light on dementia's impact. This annual event emphasizes the imperative of collective action in addressing this pressing issue.

WANT TO KNOW MORE? For a better understanding of Alzheimer's Disease, patient stories, and how you can contribute to our mission of raising awareness about this disease while celebrating World Alzheimer's Day, please visit Alzheimer's Disease International: https://www.alzint.org/

WHAT IS ALZHEIMER'S DISEASE?

Alzheimer's Disease (AD) is a progressive neurological disease. AD is generally characterized by widespread deposition of amyloid beta (amyloid-β) plaques outside neurons and aggregation of abnormally phosphorylated tau proteins (p-tau) within neurons. There is also decreased production of neurotransmitters. These changes are associated with damage and loss of neurons in various parts of the brain. The biological mechanisms that lead to the neuronal damage develop years before the onset of clinical symptoms.

SYMPTOMS & TREATMENTS

Initial signs often manifest as short-term memory difficulties, progressing to confusion, disorientation, memory loss, language problems, and behavioral changes. In advanced stages, daily assistance becomes necessary, with profound short- and long-term memory challenges.

While there's currently no cure for AD, approved treatments focus on elevating neurotransmitter levels in the brain. Ongoing research is focused on therapies preventing the pathogenic mechanisms in early stages.

THE VITAL ROLE OF DIAGNOSIS

Appropriate and timely diagnosis is crucial in supporting and treating individuals with AD, but also for adequate care and the possibility of participating in clinical trials.

   

>55M

People are living with dementia
in the world

139M
is the estimated number of people
living with dementia in 20501.
 
 
Underdiagnosed
AD is often underdiagnosed2.
Missed or delayed diagnosis is more common among ethnic and racial underrepresented groups3,4,5.
 

HOW IS AD DIAGNOSED?

Diagnosis entails a comprehensive examination including medical history, cognitive assessments, physical examination, and neurological evaluation.

Accurate diagnosis, prognosis, and disease monitoring are notoriously difficult when relying on clinical information only. Therefore, biomarkers underlying pathologic mechanisms, such as amyloid-β deposition and phosphorylated tau (p-tau), play an important role; research has shown that they correlate with pathological features of the disease7.

These biomarkers can be detected in the brain using positron emission tomography (PET) scans or measured in cerebrospinal fluid (CSF). Technological breakthroughs have made measuring these markers in a simple blood sample possible. Although brain scans are precise, their high cost, invasive nature, and low availability prevent their widespread use in clinical practice. Biomarkers in CSF or blood are relevant because they show elevation at the early stages of the disease5.

 

WHY p-Tau181 IS A PROMISING BIOMARKER

p-Tau181 is a promising biomarker for AD. The p-Tau181 biomarker strongly corresponds to the density of amyloid- β plaques and tau tangles measured by PET scanning8,9.

In addition, p-Tau181 is highly accurate for the differential diagnosis of Alzheimer's disease from other neurodegenerative disorders, including non-AD dementia9.

p-Tau181 is also effective at detecting early pathological changes in AD since the levels in plasma increase in early disease stages9,10,11,12. The p-Tau181 biomarker can identify patients at risk of developing Alzheimer’s disease in individuals with subjective cognitive decline and mild cognitive impairment combined with cognitive testing and additional genotyping11.

The use of p-Tau181 as a biomarker for AD has also been positively demonstrated in an ethnically diverse population13.

The amount of p-Tau181 increases with symptom progression and severity, allowing disease progression and therapeutic response monitoring. response14,15.

NON-INVASIVE, COST-EFFECTIVE,  AND SCALABLE TESTING 

Blood-based tests offer advantages over CSF tests by allowing for more comfortable patient sampling and less time required by healthcare professionals. Blood collection can be performed in conjunction with routine blood sampling; samples can be collected more often, which is advantageous when closer monitoring is needed.

The advent of ultra-sensitive technology is enabling the possibility of moving toward widespread blood-sampled testing in clinical practice and trials.

 

Wieslab offers pTau-181 testing

As a piece of the puzzle in the early diagnosis, Wieslab offers the p-Tau181 biomarker test for Alzheimer's Disease suspicion,  using a blood sample and single molecule array digital ELISA (SIMOA®) technology.

Benefit from our expertise, flexible solutions, and exceptional customer service - talk to us about your testing needs today!
Contact us!

Explore our extensive testing range

Discover our comprehensive range of individual markers and test panels, accepting samples from customers worldwide. Remember to download our latest request forms!

 


References:

1. GBD 2019 Dementia Forecasting Collaborators. Estimating the global prevalence of dementia in 2019 and forecasted prevalence in 2050: an analysis for the Global Burden of Disease Study 2019. Lancet Public Health. 2022 Feb;7(2):e105-e125. doi: 10.1016/S2468-2667(21)00249-8. Epub 2022 Jan 6. PMID: 34998485
2. 2022 Alzheimer’s disease facts and figures. Alzheimers Dement 2022; doi.org/10.1002/alz.12638. PMID: 35289055
3. Gianasttasio KZ, Prather C, Glymour MM, Ciarleglio A, Power MC. Racial disparities and temporal trends in dementia misdiagnosis risk in the United States. Alzheimers Dement. 2019;5: 891-8 doi: 10.1016/j.trci.2019.11.008. PMID: 31890853; PMCID: PMC6926355.
4. Lin PJ, Daly AT, Olchanski N, Cohen JT, Neumann PJ, Faul JD, Fillit HM, Freund KM. Dementia diagnosis disparities by race and ethnicity. Med Care 2021;59(8):679-86 doi: 10.1097/MLR.0000000000001577. PMID: 34091580; PMCID: PMC8263486.
5. Babulal GM, Quiroz YT, Albensi BC, et al. Perspectives on ethnic and racial disparities in Alzheimer’s disease and related dementias: Update and areas of immediate need. Alzheimers Dement 2019;15:292–312. doi: 10.1016/j.jalz.2018.09.009. Epub 2018 Dec 13. PMID: 30555031; PMCID: PMC6368893.
6. 2020 Alzheimer's disease facts and figures. Alzheimer’s Dement 2020; doi:10.1002/alz.12068 . Epub ahead of print. PMID: 32157811.
7. Reviewed in Charlotte E Teunissen, Inge M W Verberk, Elisabeth H Thijssen, et al. Blood-based biomarkers for Alzheimer's disease: towards clinical implementation, Lancet Neurol 2022; 21: 66-77 doi: 10.1016/S1474-4422(21)00361-6. Epub 2021 Nov 24. PMID: 34838239.
8. Janelidze S, Mattsson N, Palmqvist S, et al. Plasma P-tau181 in Alzheimer's disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer's dementia. Nat Med 2020;26: 379-86 doi: 10.1038/s41591-020-0755-1. Epub 2020 Mar 2. PMID: 32123385.
9. Karikari TK, Pascoal TA, Ashton NJ, et al. Blood phosphorylated tau 181 as a biomarker for Alzheimer's disease: a diagnostic performance and prediction modeling study using data from four prospective cohorts. Lancet Neurol 2020; 19: 422-33 doi: 10.1016/S1474-4422(20)30071-5. PMID: 32333900.
10. Suarez-Calvet M, Karikari TK, Ashton NJ, et al. Novel tau biomarkers phosphorylated at T181, T217 or T231 rise in the initial stages of the preclinical Alzheimer's continuum when only subtle changes in Abeta pathology are detected. EMBO Mol Med. 2020 Dec 7;12(12):e12921. doi: 10.15252/emmm.202012921. Epub 2020 Nov 10. PMID: 33169916; PMCID: PMC7721364.
11. Palmqvist S, Tideman P, Cullen N, et al. Prediction of future Alzheimer's disease dementia using plasma phospho-tau combined with other accessible measures. Nat Med 2021; 27:1034.42 doi: 10.1038/s41591-021-01348-z. Epub 2021 May 24. PMID: 34031605.
12. Mattson-Carlgren N, Andersson E, Janelidze S, et al. Abeta deposition is associated with increases in soluble and phosphorylated tau that precede a positive Tau PET in Alzheimer's disease. Sci Adv. 2020 Apr 15;6(16):eaaz2387. doi: 10.1126/sciadv.aaz2387. PMID: 32426454; PMCID: PMC7159908.
13. Brickman AM, Manly JJ, Honig LS, et al. Plasma pTau181, p-tau217, and other blood-based Alzheimer’s disease biomarkers in a multi-ethnic, community study. Alzheimers Dement. 2021 Aug;17(8):1353-1364. doi: 10.1002/alz.12301. Epub 2021 Feb 13. PMID: 33580742; PMCID: PMC8451860.
14. O’Connor A, Karikari TK, Poole T, et al. Plasma phospho-tau181 in presymptomatic and symptomatic familial Alzheimer’s disease: a longitudinal cohort study. Mol Psychiatry 2021; 26: 5967–76 doi: 10.1038/s41380-020-0838-x. Epub 2020 Jul 14. PMID: 32665603; PMCID: PMC7612227.
15. Lleo A, Zetterberg H, Pegueroles JL, et al. Phosphorylated tau181 in plasma as a potential biomarker for Alzheimer's disease in adults with Down syndrome. Nat Commun 2021; 12:4304 doi: 10.1038/s41467-021-24319-x. PMID: 34262030; PMCID: PMC8280160.