Cerebrospinal fluid phosphorylated tau protein at serine 199 is a useful diagnostic biomarker in Alzheimer’s disease and mild cognitive impairment

Author(s):  
K Urakami ◽  
H Arai ◽  
N Itoh ◽  
K Ishiguro ◽  
H Oono ◽  
...  
2017 ◽  
Vol 30 (5) ◽  
pp. 477-485 ◽  
Author(s):  
Ana GB Rabelo ◽  
Camila VL Teixeira ◽  
Thamires NC Magalhães ◽  
Ana Flávia MK Carletti-Cassani ◽  
Augusto CS Amato Filho ◽  
...  

Introduction The search for a reliable neuroimaging biomarker in Alzheimer’s disease is a matter of intense research. The presence of cerebral microbleeds seems to be a potential biomarker. However, it is not clear if the presence of microbleeds has clinical usefulness to differentiate mild Alzheimer’s disease and amnestic mild cognitive impairment from normal aging. We aimed to verify if microbleed prevalence differs among three groups: mild Alzheimer’s disease, amnestic mild cognitive impairment due to Alzheimer’s disease, and normal controls. Moreover, we studied whether microbleeds were associated with apolipoprotein E allele ɛ4 status, cerebrospinal fluid amyloid-beta, total and phosphorylated tau protein levels, vascular factors, and cognition. Methods Twenty-eight mild Alzheimer’s disease patients, 34 with amnestic mild cognitive impairment and 36 cognitively normal elderly subjects underwent: magnetic resonance imaging with a susceptibility-weighted imaging sequence on a 3T scanner, apolipoprotein E genotyping and a full neuropsychological evaluation. Only amnestic mild cognitive impairment and mild Alzheimer’s disease underwent cerebrospinal fluid analysis. We compared the groups and verified if microbleeds were predicted by all other variables. Results Mild Alzheimer’s disease presented a higher prevalence of apolipoprotein E allele ɛ4 in relation to amnestic mild cognitive impairment and control group. No significant differences were found between groups when considering microbleed presence. Logistic regression tests failed to find any relationship between microbleeds and the variables. We performed three different regression models using different independent variables: Model 1 - amyloid-beta, phosphorylated tau protein, total tau, apolipoprotein E allele ɛ4 status, age, and sex; Model 2 - vascular risk factors, age, and sex; Model 3 - cognitive scores sex, age, and education. Conclusion Although microbleeds might be related to the Alzheimer’s disease process, their presence is not a good candidate for a neuroimaging biomarker of the disease, especially in its early phases.


2015 ◽  
Vol 11 (7S_Part_7) ◽  
pp. P324-P324 ◽  
Author(s):  
Laura D. Baker ◽  
Jeannine S. Skinner ◽  
Suzanne Craft ◽  
Kaycee M. Sink ◽  
Thomas Montine ◽  
...  

2000 ◽  
Vol 21 ◽  
pp. 155
Author(s):  
Katsuya Urakami ◽  
Hiroyuki Arai ◽  
Koichi Ishiguro ◽  
Hideto Ohno ◽  
Hideki Kohno ◽  
...  

2019 ◽  
Author(s):  
Daniel A. Llano ◽  
Priya Devanarayan ◽  
Viswanath Devanarayan ◽  

AbstractSensitive and accurate biomarkers for the prediction of conversion from mild cognitive impairment (MCI) to Alzheimer’s Disease (AD) are needed to both support clinical care and enhance clinical trial design. Here, we examined the potential of cerebrospinal fluid (CSF) levels of a peptide derived from a neural protein involved in synaptic transmission, VGF (a non-initialism), to enhance accuracy of prediction of conversion from MCI to AD. The performance of conventional biomarkers (CSF Aβ1-42 and phosphorylated tau +/− hippocampal volume) was compared to the same biomarkers with CSF VGF peptide levels. It was observed that VGF peptides are lowered in patients with AD compared to controls and that combinations of CSF Aβ1-42 and phosphorylated tau, hippocampal volume and VGF peptide levels outperformed conventional biomarkers alone (hazard ratio = 2.2 vs. 3.9). VGF peptide levels were correlated most strongly with total tau levels, but not hippocampal volume, suggesting that they serve as a marker for neuronal degradation, but not necessarily in the hippocampus. The latter point suggests that VGF may serve as a more general marker of neurodegeneration. Future work will be needed to determine the specificity of VGF for AD vs. other neurodegenerative diseases.


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