Version 1
: Received: 14 February 2020 / Approved: 15 February 2020 / Online: 15 February 2020 (15:06:18 CET)
How to cite:
Zhou, B.; Fukushima, M. Clinical Utility of the Pathogenesis-related Proteins in Alzheimer’s Disease. Preprints2020, 2020020203. https://doi.org/10.20944/preprints202002.0203.v1
Zhou, B.; Fukushima, M. Clinical Utility of the Pathogenesis-related Proteins in Alzheimer’s Disease. Preprints 2020, 2020020203. https://doi.org/10.20944/preprints202002.0203.v1
Zhou, B.; Fukushima, M. Clinical Utility of the Pathogenesis-related Proteins in Alzheimer’s Disease. Preprints2020, 2020020203. https://doi.org/10.20944/preprints202002.0203.v1
APA Style
Zhou, B., & Fukushima, M. (2020). Clinical Utility of the Pathogenesis-related Proteins in Alzheimer’s Disease. Preprints. https://doi.org/10.20944/preprints202002.0203.v1
Chicago/Turabian Style
Zhou, B. and Masanori Fukushima. 2020 "Clinical Utility of the Pathogenesis-related Proteins in Alzheimer’s Disease" Preprints. https://doi.org/10.20944/preprints202002.0203.v1
Abstract
The Aβ cascade and alternations of biomarkers in neuro-inflammation, synaptic dysfunction and neuronal injury followed by Aβ have progressed. But the question is how to use the biomarkers. Here, we examine the evidence and pathogenic implications of protein interactions and the time order of alternation. After the deposition of Aβ, the change of tau, NfL and NG is the main alternation and connection to others. The neuro-inflammation, synaptic dysfunction and neuronal injury function is exhibited prior the structural and metabolic changes in the brain following Aβ deposition. The time order of such biomarkers compared to the tau protein is not clear. Despite the close relationship between biomarkers and plaque Aβ deposition, several factors favor one or the other. There is an interaction between the proteins that CSF SNAP-25, VILIP-1 and YKL-40 can predict the brain amyloid burden. The Aβ cascade hypothesis could be the pathway, but not all subjects are converted to AD, even with very high elevated Aβ. The interaction of biomarkers and the time order of change require further research to identify the right subjects and right molecular target for precision medicine therapies.
Keywords
Alzheimer’s disease; biomarkers dynamics; interaction; time order
Subject
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
