期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 27, 期 2, 页码 299-305出版社
IOS PRESS
DOI: 10.3233/JAD-2011-110731
关键词
Alzheimer's disease; amyloid-beta; biomarkers; saliva; tau protein
资金
- National Institutes of Health [AG033398, ES004696-5897, ES007033-6364, ES016873, NS057567, NS062684-6221, AG005136]
- NINDS Institutional Center [Neuroproteomic P30 (NS055088)]
- Cheng-Mei Shaw Endowment
- Friends of Alzheimer's Research
- Alzheimer's Association of Western and Central Washington
- Department of Veterans Affairs
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P42ES004696, P30ES007033, R01ES016873] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P50NS062684, R01NS057567, P30NS055088] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG033398, P50AG005136] Funding Source: NIH RePORTER
Phosphorylation of tau protein is a critical event in the pathogenesis of Alzheimer's disease (AD). Increased phosphorylated tau and total tau levels, combined with reduced concentrations of amyloid-beta 1-42 (A beta(42)) in cerebrospinal fluid (CSF), but not in plasma or serum, have been generally accepted as sensitive AD diagnostic markers. However, obtaining CSF is a relatively invasive procedure that requires participation of specially trained medical professionals, i.e., CSF is not an ideal sample source for screening or early diagnosis of AD, which is essential to current and future neuroprotective treatments for the disease. Here, we identified tau, but not A beta species, with mass spectrometry in human saliva, a body fluid that is much more accessible compared to CSF or even blood. Quantitative assessment of salivary levels of total tau, phosphorylated tau, and A beta(42) using highly sensitive Luminex assays revealed that, while A beta(42) was not detectable, the phosphorylated tau/tau ratio significantly increased in patients with AD compared to healthy controls. These results suggest that salivary tau species could be ideal biomarkers for AD diagnosis, especially at early stages of the disease or even screening asymptomatic subjects, allowing for a much larger therapeutic window for AD patients.
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