Cerebrospinal fluid levels of tau phosphorylated at threonine 181 in patients with Alzheimer’s disease and vascular dementia

• Published in: Neurological sciences Vol. 29; no. 6; pp. 417 - 423
• Main Authors: Ravaglia, Sabrina, Bini, Paola, Sinforiani, Elena, Franciotta, Diego, Zardini, Elisabetta, Tosca, Pietro, Moglia, Arrigo, Costa, Alfredo
• Format: Journal Article
• Language: English
• Published: Milan Springer Milan 01.12.2008; Springer Nature B.V
• Subjects: Aged; Aged, 80 and over; Alzheimer Disease - cerebrospinal fluid; Alzheimer Disease - diagnosis; Alzheimer Disease - physiopathology; Biomarkers - analysis; Biomarkers - cerebrospinal fluid; Brain - metabolism; Brain - pathology; Brain - physiopathology; Catalytic Domain - physiology; Cognition Disorders - cerebrospinal fluid; Cognition Disorders - diagnosis; Cognition Disorders - physiopathology; Dementia; Dementia, Vascular - cerebrospinal fluid; Dementia, Vascular - diagnosis; Dementia, Vascular - physiopathology; Disease Progression; Female; Humans; Male; Medicine; Medicine & Public Health; Middle Aged; Neurology; Neurons - metabolism; Neurons - pathology; Neuropsychological Tests; Neuroradiology; Neurosciences; Neurosurgery; Original Article; Phosphorylation; Psychiatry; tau Proteins - analysis; tau Proteins - cerebrospinal fluid; tau Proteins - chemistry; Threonine - metabolism; Vascular dementia; Cerebrospinal fluid; Alzheimer’s disease; Tau protein; Biological markers
• ISSN: 1590-1874; 1590-3478
• DOI: 10.1007/s10072-008-1023-1

In 31 patients with probable Alzheimer’s disease (AD), 19 with probable vascular dementia (VaD) and 20 with Possible AD and Possible VaD, cerebrospinal fluid (CSF) tau levels hyperphosphorylated at threonine 181 (Ptau) were measured by ELISA. Thirty-six age-matched subjects were used as controls. The severity of the cognitive decline was assessed at the time of CSF analysis and after a 12-month follow-up. The groups had comparable age, degree of cognitive impairment and disease duration; these parameters were not related to P-tau levels. P-tau discriminated between demented patients and controls, but no significant difference emerged between AD and the other groups. By contrast, higher P-tau values were found to predict, independently of the clinical diagnosis, a more rapid evolution of cognitive decline. Whether these findings are due to a lack of CSF P-tau specificity or to the low reliability of clinical and radiological criteria remains unclear. P-tau may be useful in the evaluation of disease evolution, by predicting the rate of cognitive decline.