Plasma neurofilament light chain levels and cognitive testing as predictors of fast progression in Alzheimer’s disease

Author(s):  
Roberto Santangelo ◽  
Federica Agosta ◽  
Francesco Masi ◽  
Edoardo Gioele Spinelli ◽  
Giordano Cecchetti ◽  
...  

2006 ◽  
Vol 14 (7S_Part_19) ◽  
pp. P1038-P1039
Author(s):  
Holly Soares ◽  
Sheng Feng ◽  
Hana Florian ◽  
Michael Gold ◽  
Hoi-Kei Lon ◽  
...  


2017 ◽  
Vol 108 ◽  
pp. 355-360 ◽  
Author(s):  
Simone Lista ◽  
Nicola Toschi ◽  
Filippo Baldacci ◽  
Henrik Zetterberg ◽  
Kaj Blennow ◽  
...  


2020 ◽  
Vol 16 (S5) ◽  
Author(s):  
Ignacio Illán‐Gala ◽  
Alberto Lleó ◽  
Anna M. Karydas ◽  
Adam M. Staffaroni ◽  
Henrik Zetterberg ◽  
...  


2017 ◽  
Vol 13 (7S_Part_7) ◽  
pp. P361-P361
Author(s):  
Simone Lista ◽  
Nicola Toschi ◽  
Filippo Baldacci ◽  
Kaj Blennow ◽  
Henrik Zetterberg ◽  
...  




2020 ◽  
Vol 142 ◽  
pp. 104960 ◽  
Author(s):  
Stephanie A. Schultz ◽  
Jeremy F. Strain ◽  
Adedamola Adedokun ◽  
Qing Wang ◽  
Oliver Preische ◽  
...  


Brain ◽  
2020 ◽  
Author(s):  
Joana B Pereira ◽  
Shorena Janelidze ◽  
Rik Ossenkoppele ◽  
Hlin Kvartsberg ◽  
Ann Brinkmalm ◽  
...  

Abstract It is currently unclear how amyloid-β and tau deposition are linked to changes in synaptic function and axonal structure over the course of Alzheimer’s disease. Here, we assessed these relationships by measuring presynaptic (synaptosomal-associated protein 25, SNAP25; growth-associated protein 43, GAP43), postsynaptic (neurogranin, NRGN) and axonal (neurofilament light chain) markers in the CSF of individuals with varying levels of amyloid-β and tau pathology based on 18F-flutemetamol PET and 18F-flortaucipir PET. In addition, we explored the relationships between synaptic and axonal markers with cognition as well as functional and anatomical brain connectivity markers derived from resting-state functional MRI and diffusion tensor imaging. We found that the presynaptic and postsynaptic markers SNAP25, GAP43 and NRGN are elevated in early Alzheimer’s disease i.e. in amyloid-β-positive individuals without evidence of tau pathology. These markers were associated with greater amyloid-β pathology, worse memory and functional changes in the default mode network. In contrast, neurofilament light chain was abnormal in later disease stages, i.e. in individuals with both amyloid-β and tau pathology, and correlated with more tau and worse global cognition. Altogether, these findings support the hypothesis that amyloid-β and tau might have differential downstream effects on synaptic and axonal function in a stage-dependent manner, with amyloid-related synaptic changes occurring first, followed by tau-related axonal degeneration.



Author(s):  
Min Su Kang ◽  
◽  
Arturo Aliaga Aliaga ◽  
Monica Shin ◽  
Sulantha Mathotaarachchi ◽  
...  


2019 ◽  
Vol 7 (S3) ◽  
pp. S133-S133 ◽  
Author(s):  
Federico Massa ◽  
Riccardo Meli ◽  
Silvia Morbelli ◽  
Flavio Nobili ◽  
Matteo Pardini


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