Comparison of Neuronal and Axonal Degeneration Markers Cystatin-C, Beta-Amyloid (1-42), Total and Phosphorylated Tau Protein Levels in Cerebrospinal Fluids of Patients with Multiple Sclerosis and Alzheimer’s Disease

Niche Journal ◽  
2013 ◽  
Vol 1 (2) ◽  
pp. 24-30
Author(s):  
Hulya Akdeniz ◽  
Zeynep Ginis ◽  
Selcuk Comoglu ◽  
Bilge Kocer ◽  
Ferda Pinarli ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cystatin C ◽  
Tau Protein ◽  
Axonal Degeneration ◽  
Beta Amyloid ◽  
Phosphorylated Tau ◽  
Protein Levels ◽  
Phosphorylated Tau Protein

Assay of Plasma Phosphorylated Tau Protein (Threonine 181) and Total Tau Protein in Early-Stage Alzheimer’s Disease

2018 ◽  
Vol 61 (4) ◽  
pp. 1323-1332 ◽  
Author(s):  
Che-Chuan Yang ◽  
Ming-Jang Chiu ◽  
Ta-Fu Chen ◽  
Hui-Ling Chang ◽  
Bing-Hsien Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Early Stage ◽  
Phosphorylated Tau ◽  
Total Tau ◽  
Phosphorylated Tau Protein

Phosphorylated tau protein in cerebrospinal fluid is elevated in Alzheimer's disease and other tauopathies

2000 ◽  
Vol 21 ◽  
pp. 155
Author(s):  
Katsuya Urakami ◽  
Hiroyuki Arai ◽  
Koichi Ishiguro ◽  
Hideto Ohno ◽  
Hideki Kohno ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Tau Protein ◽  
Phosphorylated Tau ◽  
Phosphorylated Tau Protein

scholarly journals Association of cellular and subcellular calcification with phosphorylated tau in the brains of Alzheimer’s disease patients

2020 ◽  
Author(s):  
Elena Tsolaki ◽  
Lajos Csincsik ◽  
Jing Xue ◽  
Imre Lengyel ◽  
Sergio Bertazzo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Detection Method ◽  
Phosphorylated Tau ◽  
Cell Nuclei ◽  
Middle Temporal ◽  
Early Marker ◽  
Phosphorylated Tau Protein

ABSTRACTDeposition of tau-tangles is an early marker for the development of Alzheimer’s disease (AD). Here we show that these aggregates of phosphorylated tau protein are associated with the calcification of cell nuclei and cell projections, especially in the middle temporal, superior temporal and parahippocampal gyri. This calcification is related to the aetiology of the disease, shedding new light on the mechanisms involved in AD and potentially providing a new detection method for AD progression.

scholarly journals Is cerebral microbleed prevalence relevant as a biomarker in amnestic mild cognitive impairment and mild Alzheimer’s disease?

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 ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Apolipoprotein E ◽  
Tau Protein ◽  
Amnestic Mild Cognitive Impairment ◽  
Phosphorylated Tau ◽  
Phosphorylated Tau Protein ◽  
Age And Sex

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.

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