Selenium Levels in Serum, Red Blood Cells, and Cerebrospinal Fluid of Alzheimer’s Disease Patients: A Report from the Australian Imaging, Biomarker & Lifestyle Flagship Study of Ageing (AIBL)

2017 ◽  
Vol 57 (1) ◽  
pp. 183-193 ◽  
Author(s):  
Bárbara R. Cardoso ◽  
Dominic J. Hare ◽  
Ashley I. Bush ◽  
Qiao-Xin Li ◽  
Christopher J. Fowler ◽  
...  
2014 ◽  
Vol 10 ◽  
pp. P858-P858
Author(s):  
Kiyotaka Nakagawa ◽  
Takehiro Kiko ◽  
Katsutoshi Furukawa ◽  
Hiroyuki Arai ◽  
Teruo Miyazawa

Author(s):  
György Várady ◽  
Edit Szabó ◽  
Ágnes Fehér ◽  
Adrienn Németh ◽  
Boglárka Zámbó ◽  
...  

2020 ◽  
Author(s):  
Hualin Fu ◽  
Jilong Li ◽  
Peng Du ◽  
Weilin Jin ◽  
Daxiang Cui

AbstractSenile plaque is one of the most prominent pathological hallmarks of Alzheimer’s disease (AD). However, the mechanism governing the generation of senile plaques remains a mystery. Many researchers believed that senile plaques are derived from neuronal cells, however, there is also strong evidence showing that senile plaques are linked with cerebral microhemorrhage. We analyzed the major neural markers, cerebral blood vessel and blood-related markers in AD brain sections with immunohistochemistry in conjunction with fluorescence imaging and TUNEL assay. We found few colocalizations between neural markers and senile plaque Aβ staining while abundant colocalizations between blood markers such as HBA and ApoE with senile plaque Aβ. Senile plaques also colocalized with a characteristic blue autofluorescence, which is prominently located in the blood stream and associated with red blood cells. Additionally, senile plaques did not colocalize with blood vessel marker Collagen IV. It appears that Aβ either directly leaks out of damaged blood vessel wall or is transported out of blood vessel through blood vessel microaneurysm. By staining of another marker of cerebral blood vessel LRP1, we could also observe that Aβ directly came out broken blood vessels at the center of dense-core plaques. In AD brain tissues, platelets were found along blood vessel walls and also in senile plaques, thus platelets likely also contribute to senile plaque formation. In summary, we concluded that senile plaques are primarily induced by cerebral vessel leakage of red blood cells and other blood contents.


2011 ◽  
Vol 7 ◽  
pp. S134-S134
Author(s):  
Jean de Barry ◽  
Corinne Liegeois ◽  
Jean-Marc Michel ◽  
Francois Sellal

2019 ◽  
Vol 15 ◽  
pp. P672-P673
Author(s):  
Filippo Baldacci ◽  
Simona Daniele ◽  
Rebecca Piccarducci ◽  
Linda Giampietri ◽  
Deborah Giampietri ◽  
...  

2020 ◽  
Author(s):  
Simona Daniele ◽  
Filippo Baldacci ◽  
Rebecca Piccarducci ◽  
Giovanni Palermo ◽  
Linda Giampietri ◽  
...  

Abstract Background Red blood cells (RBC) account for more than 99% of α-syn concentrations in blood representing an interesting in vivo model for studying peripheral pathological alterations proved in neurodegeneration. The aim of the current study was to investigate the diagnostic value of total α-syn, Aβ 1-42 , tau and their heteroaggregates in RBCs of Lewy Body Dementias (LBDs) and Alzheimer’s disease (AD) patients compared to and healthy controls (HCs). Methods With a “home-made” sandwich enzyme-linked immunosorbent assay (ELISA) system, RBCs levels of total α-syn, Aβ 1-42 , tau and their heteroaggregates (α-syn/Aβ 1-42 and α-syn/tau) were measured in 27 subjects with LBDs (PDD, n = 17; DLB, n = 10), 51 subjects with AD (AD dementia, n = 37, prodromal AD, n = 14), and HC (n = 60). Results Compared with HC, total α-syn and tau concentrations as well as α-syn/tau heterodimers were significantly lower in LBDs group (p = 0.009, p = 0.009, and p < 0.001, respectively) and in AD group (p = 0.011, p = 0.003, and p < 0.001, respectively), whereas the heteroaggregates α-syn/Aβ 1-42 were significantly lower in AD dementia group (p < 0.001) only. RBC α-syn/tau heterodimers had the higher diagnostic accuracy for differentiating patients with LBD vs controls (AUROC = 0.80). Conclusion RBC α-syn heteroaggregates may be useful for differentiating between neurodegenerative dementias (LBD and AD) and healthy control. In particular, RBC α-syn/tau heterodimers have demonstrated good diagnostic accuracy for differentiating LBDs from HC. However, they are not consistently different between LBD and AD. Our findings also go beyond the clinical setting, suggesting that α-syn, Aβ 1-42 , and tau interact in vivo to promote the aggregation and accumulation of each other presumably accelerating cognitive dysfunction.


2012 ◽  
Vol 28 (3) ◽  
pp. 593-600 ◽  
Author(s):  
Takehiro Kiko ◽  
Kiyotaka Nakagawa ◽  
Tsuyoshi Tsuduki ◽  
Toshihide Suzuki ◽  
Hiroyuki Arai ◽  
...  

1997 ◽  
Vol 52A (4) ◽  
pp. B217-B220 ◽  
Author(s):  
D. Sabolovic' ◽  
M. Roudier ◽  
M. Boynard ◽  
C. Pautou ◽  
C. Sestier ◽  
...  

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