Assessment of Cerebrospinal Fluid (CSF) βββββ-Amyloid (1-42), Phosphorylated Tau (ptau-181) and Total Tau Protein in Patients with Alzheimer’s Disease (AD) and Other Dementia at Siriraj Hospital, Thailand
Jedsada Thaweepoksomboon MD*, Vorapun Senanarong MD, FRCP*, Niphon Poungvarin MD, FRCP*, Tipa Chakorn MD**, Nopwan Siwasariyanon MSc*, Lerdchai Washirutmangkur MSc*, Suthipol Udompunthuruk MSc***
Affiliation : * Division of Neurology, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand ** Division of Emergency Medicine, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand *** Institution of Research Development, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand
Background : The combination of decreased cerebrospinal fluid (CSF) levels of β-amyloid (1-42) and increased levels of
phosphorylated tau (ptau-181) or total tau protein are known to be biomarkers of Alzheimer’s disease (AD). These biomarkers
can also be used as predictors of disease progression in persons with mild cognitive impairment. Utilizing biomarkers to
differentiate Alzheimer’s disease (AD) against non-Alzheimer dementia (non-AD) needs to be explored.
Objective : To evaluate the clinical use of CSF biomarker: β-amyloid (1-42), phosphorylated tau (ptau-181) and total tau
protein for distinguishing Alzheimer’s disease (AD) from non-Alzheimer dementia (non-AD) in Thai patients.
Material and Method: Thirty patients diagnosed of dementia during 2005-2007 at Siriraj hospital were offered CSF analysis
for β-amyloid (1-42), phosphorylated tau (ptau-181) and total tau protein. Diagnosis of dementia was performed by a
concensus diagnostic group utilizing a standard criteria for diagnosis of AD and other dementia. All CSF testing was
performed by Enzyme-Linked Immunoassay (ELISA) technique of the INNOTESTTM to analyze these biomarkers.
Results : Thirty demented patients were recruited in the study. Fourteen had AD and 16 had non-AD including 5 vascular
dementia, 5 normal pressure hydrocephalus, 4 frontotemporal lobar degeneration and others. Mean age of the AD group was
67.79 (12.30) and that of non-AD group was 65.75 (15.04). Twelve AD had decreased levels of CSF β-amyloid (1-42) (less
than 487 pg/ml). Only one patient with AD had increased CSF phosphorylated tau (ptau-181) (more than 61 pg/ml). None of
the AD patient had increased CSF total tau (more than 425 pg/ml). Eight patients with non-AD had decreased levels of CSF
β-amyloid (1-42), one had increased CSF total tau protein, and none had increased CSF phosphorylated tau (ptau-181)
protein. The sensitivity of decreased level of CSF β-amyloid (1-42) in AD against non-AD dementia was 85.71%. Those of
increased CSF total tau and phosphorylated tau (ptau-181) protein in AD against non-AD dementia were 7.14% and 0%
consecutively. The specificity of decreased level of CSF β-amyloid (1-42) in AD against non-AD dementia was 50%. The
specificity of increased CSF total tau and phosphorylated tau (ptau-181) protein in AD against non-AD dementia were 100%
and 93.75% sequentially. The combination of 2 biomarkers would increase specificity but decrease sensitivity.
Conclusion : CSF biomarker analysis should be encouraged to use as diagnostic aid in memory clinic especially to help
diagnosis of atypical presentation of AD. The usefulness of longitudinal data needs to be explored.
Keywords : CSF β-amyloid (1-42), CSF phosphorylated tau (ptau-181), CSF total tau protein, Alzheimer’s disease, non- Alzheimer dementia
