Abnormalities of plasma cytokines and spleen in senile APP/PS1/Tau transgenic mouse model.
The blood-based diagnosis has a potential to provide an alternative approach for easy diagnosis of Alzheimer's disease (AD) with less invasiveness and low-cost. However, present blood-based AD diagnosis mainly focuses on measuring the plasma Aβ level because no other biomarkers are found to possess evident transport mechanisms to pass the blood-brain barrier. In order to avoid diagnosing non-demented individuals with Aβ abnormality, finding additional biomarkers to supplement plasma Aβ is essential. In this study, we introduce potential neurodegenerative biomarkers for blood-based diagnosis. We observed severe splenomegaly and structural destruction in the spleen with significantly decreased B lymphocytes in senile APPswe, PS1M146V and TauP301L transgenic mice. We also found that inflammatory cytokines associated with splenic dysfunction were altered in the plasma of these mice. These findings suggest potential involvement of the splenic dysfunction in AD and the importance of biomarker level alterations in the plasma as putative diagnostic targets for AD.
Center for Neuro-Medicine, Brain Science Institute, Korea Institute of Science and Technology, Hwarangno 14-gil 5, Seongbuk-gu, Seoul, Republic of Korea.
Seung-Hoon
SH
Yang
Center for Neuro-Medicine, Brain Science Institute, Korea Institute of Science and Technology, Hwarangno 14-gil 5, Seongbuk-gu, Seoul, Republic of Korea.|Biological Chemistry Program, Korea University of Science and Technology, 217 Gajungro, Yuseong-gu, Daejeon, Republic of Korea.
Jiyoon
J
Kim
Center for Neuro-Medicine, Brain Science Institute, Korea Institute of Science and Technology, Hwarangno 14-gil 5, Seongbuk-gu, Seoul, Republic of Korea.|Department of Medical Education, California Northstate University College of Medicine, 9700 W Taron Drive, Elk Grove, CA 95757, USA.
Michael Jisoo
MJ
Lee
Center for Neuro-Medicine, Brain Science Institute, Korea Institute of Science and Technology, Hwarangno 14-gil 5, Seongbuk-gu, Seoul, Republic of Korea.|Biological Chemistry Program, Korea University of Science and Technology, 217 Gajungro, Yuseong-gu, Daejeon, Republic of Korea.
YoungSoo
Y
Kim
D000544:Alzheimer Disease / Q000175:diagnosis / Q000235:genetics; D016229:Amyloid beta-Peptides / Q000097:blood / Q000134:cerebrospinal fluid / Q000235:genetics*; D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology; D015415:Biomarkers / Q000097:blood; D001812:Blood-Brain Barrier / Q000378:metabolism; D016207:Cytokines / Q000097:blood*; D004195:Disease Models, Animal; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010446:Peptide Fragments / Q000097:blood / Q000134:cerebrospinal fluid; D053764:Presenilin-1 / Q000235:genetics*; D013154:Spleen / Q000378:metabolism*; D013163:Splenomegaly / Q000473:pathology; D016875:tau Proteins / Q000235:genetics*
D016229:Amyloid beta-Peptides; D015415:Biomarkers; D016207:Cytokines; D010446:Peptide Fragments; D053764:Presenilin-1; C075222:amyloid beta-protein (1-42); D016875:tau Proteins