Cerebrospinal Fluid Biomarker for Alzheimer Disease Predicts Postoperative Cognitive Dysfunction

2016 ◽  
Vol 60 (5) ◽  
pp. 195-196 ◽  
Author(s):  
Lisbeth Evered ◽  
Brendan Silbert ◽  
David A. Scott ◽  
David Ames ◽  
Paul Maruff ◽  
...  
2016 ◽  
Vol 124 (2) ◽  
pp. 353-361 ◽  
Author(s):  
Lisbeth Evered ◽  
Brendan Silbert ◽  
David A. Scott ◽  
David Ames ◽  
Paul Maruff ◽  
...  

Abstract Background Postoperative cognitive dysfunction (POCD) affects 16 to 21% of the elderly 3 months after anesthesia and surgery and is associated with adverse outcomes. The exact cause of POCD remains unknown. The authors hypothesized that elderly individuals with Alzheimer disease (AD) neuropathology, identified by cerebrospinal fluid (CSF) analysis, would have increased the risk for POCD. Methods CSF samples were collected from 59 patients 60 yr or older who received combined spinal and general anesthesia for elective total hip replacement. Patients underwent neuropsychological testing preoperatively and at 7 days, 3 months, and 12 months postoperatively. POCD at 3 months and cognitive decline at 12 months were calculated by using the reliable change index. CSF amyloid β1–42 (Aβ1–42), total-tau, phosphorylated-tau, and neurofilament light were assayed with enzyme-linked immunosorbent assay methods. Results POCD was identified in 5 of 57 patients (8.8%) at 3 months. For Aβ1–42, 11 patients were below the cut-point for AD neuropathology of whom 3 were classified with POCD (27.3%; 95% CI, 6.0 to 61%), whereas of the 46 patients above the cut-point, 2 were classified with POCD (4.3%; 95% CI, 0.5 to 14.8%) (P = 0.01). There was no significant difference in the incidence of POCD in relation to the cut-points for any of the other analytes. Conclusions Low CSF Aβ1–42 may be a significant predictor of POCD at 3 months. This indicates that patients with AD neuropathology even in the absence of clinically detectable AD symptoms may be susceptible to POCD.


2019 ◽  
Vol 129 (5) ◽  
pp. e150-e154 ◽  
Author(s):  
Miles Berger ◽  
David M. Murdoch ◽  
Janet S. Staats ◽  
Cliburn Chan ◽  
Jake P. Thomas ◽  
...  

PLoS Medicine ◽  
2020 ◽  
Vol 17 (8) ◽  
pp. e1003289 ◽  
Author(s):  
Hana Saddiki ◽  
Aurore Fayosse ◽  
Emmanuel Cognat ◽  
Séverine Sabia ◽  
Sebastiaan Engelborghs ◽  
...  

2017 ◽  
Vol 42 (6) ◽  
pp. 366-377 ◽  
Author(s):  
Marina Weiler ◽  
Brunno Machado de Campos ◽  
Camila Vieira de Ligo Teixeira ◽  
Raphael Fernandes Casseb ◽  
Ana Flávia Mac Knight Carletti-Cassani ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ying Zhang ◽  
Yong Lin ◽  
Qing Liu ◽  
Xuemei Yuan ◽  
Anqiong Mao ◽  
...  

Postoperative cognitive dysfunction (POCD) is a kind of serious neurologic complications and dexmedetomidine has a certain effect on POCD. However, functional mechanism of dexmedetomidine on POCD still remains unclear, so the research mainly studied the effect of dexmedetomidine on cognitive function and protein expression in hippocampus and prefrontal cortex cerebrospinal fluid after extracorporeal circulation operation in aged rats. We Found that, compared with POCD group, the cognitive function was improved in POCD + Dex group. We speculate that dexmedetomidine could improve the cognitive function after extracorporeal circulation operation in aged rats and Aβ, p-Tau, and PSD95 protein might have contributed to this favorable outcome.


2021 ◽  
Vol 80 (3) ◽  
pp. 1281-1297
Author(s):  
Keith W. VanDusen ◽  
Yi-Ju Li ◽  
Victor Cai ◽  
Ashley Hall ◽  
Sarah Hiles ◽  
...  

Background: Postoperative cognitive dysfunction (POCD), a syndrome of cognitive deficits occurring 1–12 months after surgery primarily in older patients, is associated with poor postoperative outcomes. POCD is hypothesized to result from neuroinflammation; however, the pathways involved remain unclear. Unbiased proteomic analyses have been used to identify neuroinflammatory pathways in multiple neurologic diseases and syndromes but have not yet been applied to POCD. Objective: To utilize unbiased mass spectrometry-based proteomics to identify potential neuroinflammatory pathways underlying POCD. Methods: Unbiased LC-MS/MS proteomics was performed on immunodepleted cerebrospinal fluid (CSF) samples obtained before, 24 hours after, and 6 weeks after major non-cardiac surgery in older adults who did (n = 8) or did not develop POCD (n = 6). Linear mixed models were used to select peptides and proteins with intensity differences for pathway analysis. Results: Mass spectrometry quantified 8,258 peptides from 1,222 proteins in > 50%of patient samples at all three time points. Twelve peptides from 11 proteins showed differences in expression over time between patients with versus without POCD (q < 0.05), including proteins previously implicated in neurodegenerative disease pathophysiology. Additionally, 283 peptides from 182 proteins were identified with trend-level differences (q < 0.25) in expression over time between these groups. Among these, pathway analysis revealed that 50 were from 17 proteins mapping to complement and coagulation pathways (q = 2.44*10–13). Conclusion: These data demonstrate the feasibility of performing unbiased mass spectrometry on perioperative CSF samples to identify pathways associated with POCD. Additionally, they provide hypothesis-generating evidence for CSF complement and coagulation pathway changes in patients with POCD.


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