Post mortem biochemistry differences between vitreous humor and cerebrospinal fluid

Pathology ◽  
2019 ◽  
Vol 51 ◽  
pp. S115
Author(s):  
Jack Garland ◽  
Winston Philcox ◽  
Sinead McCarthy ◽  
Kilak Kesha ◽  
Leo Lam ◽  
...  
2018 ◽  
Vol 289 ◽  
pp. 397-407 ◽  
Author(s):  
Konrad Sydow ◽  
Theresa Kueting ◽  
Frank Musshoff ◽  
Burkhard Madea ◽  
Cornelius Hess

Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 491
Author(s):  
Joaquín Fernández-Irigoyen ◽  
Paz Cartas-Cejudo ◽  
Marta Iruarrizaga-Lejarreta ◽  
Enrique Santamaría

Lipid metabolism is clearly associated to Parkinson’s disease (PD). Although lipid homeostasis has been widely studied in multiple animal and cellular models, as well as in blood derived from PD individuals, the cerebrospinal fluid (CSF) lipidomic profile in PD remains largely unexplored. In this study, we characterized the post-mortem CSF lipidomic imbalance between neurologically intact controls (n = 10) and PD subjects (n = 20). The combination of dual extraction with ultra-performance liquid chromatography-electrospray ionization quadrupole-time-of-flight mass spectrometry (UPLC-ESI-qToF-MS/MS) allowed for the monitoring of 257 lipid species across all samples. Complementary multivariate and univariate data analysis identified that glycerolipids (mono-, di-, and triacylglycerides), saturated and mono/polyunsaturated fatty acids, primary fatty amides, glycerophospholipids (phosphatidylcholines, phosphatidylethanolamines), sphingolipids (ceramides, sphingomyelins), N-acylethanolamines and sterol lipids (cholesteryl esters, steroids) were significantly increased in the CSF of PD compared to the control group. Interestingly, CSF lipid dyshomeostasis differed depending on neuropathological staging and disease duration. These results, despite the limitation of being obtained in a small population, suggest extensive CSF lipid remodeling in PD, shedding new light on the deployment of CSF lipidomics as a promising tool to identify potential lipid markers as well as discriminatory lipid species between PD and other atypical parkinsonisms.


2021 ◽  
Author(s):  
Alba Cervantes-González ◽  
David J Irwin ◽  
Daniel Alcolea ◽  
Corey T McMillan ◽  
Alice Chen-Plotkin ◽  
...  

Abstract Background. Frontotemporal dementia (FTD) clinical diagnosis is challenged by the variable correspondence between the clinical syndrome and underlying neuropathological changes, the phenotypic overlap with Alzheimer's disease (AD) and the lack of pathophysiologic diagnostic biomarkers. As synapse degeneration is an early event in pathological frontotemporal lobar degeneration (FTLD), a surrogate marker of synapse loss could be used to monitor early pathologic changes. The aim of this study was to evaluate the relationship of antemortem cerebrospinal fluid (CSF) levels of 9 synaptic proteins with postmortem global tau and TDP-43 burden in a neuropathological FTLD cohort. Methods. We included patients with a neuropathological confirmation of FTLD-Tau (n=24, mean age-at-CSF 67 years+/-11), FTLD-TDP (n=25, 66 years+/-9) or AD (n=25, 73 years+/-6) as well as cognitively normal controls (n=35, 69 years+/-7) from the Penn FTD Center and ADRC. A subset of 39 FTLD patients presented without AD comorbidity (neurofibrillary tangle score of B0/B1 according to the NIA-AA classification) and 18 AD patients presented without TDP-43 comorbidity. We quantified the synaptic panel in antemortem CSF by targeted mass spectrometry using isotopically-labeled peptides as internal standards. We used a semi-quantitative measure of tau and TDP-43 inclusions to quantify pathological burden across 16 brain regions. Statistical methods included Spearman rank correlations, one-way analysis of covariance (controlling for sex and age-at-CSF), linear regression (controlling for age-at-death) and receiver-operating characteristic curves. Result. CSF calsyntenin-1 and neurexin-2a were correlated in all patient groups (rs=.55 to .88). In FTLD-TDP, we observed low antemortem CSF levels of calsyntenin-1 and neurexin-2a compared to AD (.72-fold, p=.001, .77-fold, p=.04, respectively) and controls (.80-fold, p=.02, .78-fold, p=.02, respectively), which were inversely associated with post-mortem global TDP-43 burden (regression r2=.36, p=.04 and r2=.35, p=.04, respectively). Neurexin-2a showed 75.0% (95% CI 60-88) accuracy to discriminate FTLD-TDP from controls. Calsyntenin-1 showed 75.1% (95% CI 62-87) accuracy to discriminate FTLD-TDP from AD. None of the synaptic proteins were altered in FTLD-Tau compared to controls (0.79 to 1.12-fold, p>.12) or associated with post-mortem global tau burden (r2=.12, p=.36). Comorbidity had a limited effect on these findings. Conclusion. CSF calsyntenin-1 and neurexin-2a have potential as objective measures of TDP-43-mediated degeneration in FTLD.


2018 ◽  
Vol 76 (3) ◽  
pp. 245-250
Author(s):  
Guillaume Rousseau ◽  
Nicolas Bergerat ◽  
Guillaume Drevin ◽  
Pascal Reynier ◽  
Nathalie Jousset

2018 ◽  
Vol 12 ◽  
Author(s):  
Simin Mahinrad ◽  
Marjolein Bulk ◽  
Isabelle van der Velpen ◽  
Ahmed Mahfouz ◽  
Willeke van Roon-Mom ◽  
...  

1998 ◽  
Vol 14 (5) ◽  
pp. 459-471 ◽  
Author(s):  
UMAR K. MIAN ◽  
MARTIN MAYERS ◽  
YOGENDER GARG ◽  
QING-FENG LIU ◽  
GIRARD NEWCOMER ◽  
...  

2016 ◽  
Vol 12 (3) ◽  
pp. 248-256 ◽  
Author(s):  
Desirée H. J. L. M. Koopmanschap ◽  
Alireza R. Bayat ◽  
Bela Kubat ◽  
Henri M. de Bakker ◽  
Mathias W. M. Prokop ◽  
...  

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