Cerebrospinal fluid tau and beta-amyloid 42 proteins identify Alzheimer disease in subjects with mild cognitive impairment - PubMed (original) (raw)
Comparative Study
. 2002 Nov;59(11):1729-34.
doi: 10.1001/archneur.59.11.1729.
Affiliations
- PMID: 12433260
- DOI: 10.1001/archneur.59.11.1729
Comparative Study
Cerebrospinal fluid tau and beta-amyloid 42 proteins identify Alzheimer disease in subjects with mild cognitive impairment
M Riemenschneider et al. Arch Neurol. 2002 Nov.
Abstract
Context: Cerebrospinal fluid tau protein and beta-amyloid 42 (Abeta42) protein are altered even in very mild Alzheimer disease (AD). So far, few data exist for subjects with mild cognitive impairment (MCI).
Objective: To investigate the potential of cerebrospinal fluid tau and Abeta42 for predicting progression from MCI to AD in a longitudinal study of 28 patients with MCI who received follow-up for 18 months.
Design: An 18-month prospective study.
Setting: Clinical follow-up study of community-residing subjects with MCI.
Main outcome measures: Cerebrospinal fluid tau and Abeta42 concentrations were measured using enzyme-linked immunosorbent assay at baseline. The potential of both biomarkers was evaluated to predict the progression to dementia, the end point of this study, using multiple logistic regression analysis.
Results: Of 28 subjects with MCI, 12 progressed to dementia (2 to frontotemporal dementia; 10 to AD). Six subjects had progressive MCI, and 10 subjects showed stable MCI. Cerebrospinal fluid tau levels were significantly elevated in patients who progressed to probable AD (P =.002) and subjects with progressive MCI (P =.003) compared with subjects who had stable MCI. Cerebrospinal fluid Abeta42 levels were significantly lower in patients who progressed to probable AD (P =.007) and those with progressive MCI (P =.04) than in subjects with stable MCI. Logistic regression analysis identified elevated tau protein level as a predictor of cognitive deterioration (P =.02), whereas a delayed verbal recall score at baseline was significantly associated with the development of probable AD (P =.03).
Conclusion: Our results indicate that altered tau and Abeta42 concentrations may be detectable in subjects who are clinically diagnosed as having MCI but demonstrate the pathological changes of AD.
Comment in
- Time and memory.
Rosenberg RN. Rosenberg RN. Arch Neurol. 2002 Nov;59(11):1699-700. doi: 10.1001/archneur.59.11.1699. Arch Neurol. 2002. PMID: 12433252 No abstract available. - The diagnosis of Alzheimer disease before it is Alzheimer dementia.
Frisoni GB, Padovani A, Wahlund LO. Frisoni GB, et al. Arch Neurol. 2003 Jul;60(7):1023; author reply 1023-4. doi: 10.1001/archneur.60.7.1023-a. Arch Neurol. 2003. PMID: 12873864 No abstract available. - Evolutionary time and human memory.
Rosenberg RN. Rosenberg RN. JAMA. 2002 Dec 18;288(23):3045-7. doi: 10.1001/jama.288.23.3045. JAMA. 2002. PMID: 14619910 No abstract available.
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