Amino acid concentrations in cerebrospinal fluid and serum in Alzheimer's disease and vascular dementia

1993 ◽  
Vol 6 (1) ◽  
pp. 1-9 ◽  
Author(s):  
M. Martinez ◽  
A. Frank ◽  
E. Diez-Tejedor ◽  
A. Hernanz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Amino Acid ◽  
Vascular Dementia ◽  
Amino Acid Concentrations

O5-05-04: Large scale proteomics exploration of human cerebrospinal fluid (CSF) in Alzheimer's disease patients using stable isotope labeling amino acid in vivo (SILAV)

2015 ◽  
Vol 11 (7S_Part_7) ◽  
pp. P326-P326
Author(s):  
Sylvain Lehmann ◽  
Guillaume Gras-Combe ◽  
Jérôme Vialaret ◽  
Luc Bauchet ◽  
Mamadou Lamine Tall ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Amino Acid ◽  
Stable Isotope ◽  
Large Scale ◽  
Isotope Labeling ◽  
Stable Isotope Labeling ◽  
Human Cerebrospinal Fluid

scholarly journals Brevican and Neurocan Peptides as Potential Cerebrospinal Fluid Biomarkers for Differentiation Between Vascular Dementia and Alzheimer’s Disease

2020 ◽  
pp. 1-13
Author(s):  
Karolina Minta ◽  
Gunnar Brinkmalm ◽  
Erik Portelius ◽  
Per Johansson ◽  
Johan Svensson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Vascular Dementia ◽  
Extracellular Enzymes ◽  
Control Group ◽  
Healthy Controls ◽  
Clear Trend ◽  
Cerebrospinal Fluid Biomarkers

Background: Brevican and neurocan are central nervous system-specific extracellular matrix proteoglycans. They are degraded by extracellular enzymes, such as metalloproteinases. However, their degradation profile is largely unexplored in cerebrospinal fluid (CSF). Objective: The study aim was to quantify proteolytic peptides derived from brevican and neurocan in human CSF of patients with Alzheimer’s disease (AD) and vascular dementia (VaD) compared with controls. Methods: The first cohort consisted of 75 individuals including 25 patients with AD, 7 with mild cognitive impairment (MCI) diagnosed with AD upon follow-up, 10 patients with VaD or MCI diagnosed with VaD upon follow-up, and 33 healthy controls and cognitively stable MCI patients. In the second cohort, 31 individuals were included (5 AD patients, 14 VaD patients and 12 healthy controls). Twenty proteolytic peptides derived from brevican (n = 9) and neurocan (n = 11) were quantified using high-resolution parallel reaction monitoring mass spectrometry. Results: In the first cohort, the majority of CSF concentrations of brevican and neurocan peptides were significantly decreased inVaDas compared withADpatients (AUC = 0.83.0.93, p≤0.05) and as compared with the control group (AUC = 0.79.0.87, p ≤ 0.05). In the second cohort, CSF concentrations of two brevican peptides (B87, B156) were significantly decreased in VaD compared with AD (AUC = 0.86.0.91, p ≤ 0.05) and to controls (AUC = 0.80.0.82, p ≤ 0.05), while other brevican and neurocan peptides showed a clear trend to be decreased in VaD compared with AD (AUC = 0.64.80, p > 0.05). No peptides differed between AD and controls. Conclusion: Brevican and neurocan peptides are potential diagnostic biomarkers for VaD, with ability to separate VaD from AD.

scholarly journals Arylesterase Activity of Paraoxonase-1 in Serum and Cerebrospinal Fluid of Patients with Alzheimer’s Disease and Vascular Dementia

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 456 ◽  
Author(s):  
Arianna Romani ◽  
Alessandro Trentini ◽  
Wiesje M. van der Flier ◽  
Tiziana Bellini ◽  
Giovanni Zuliani ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Vascular Dementia ◽  
Apolipoprotein A1 ◽  
Paraoxonase 1 ◽  
Imaging Biomarkers ◽  
Composite Parameter ◽  
Older Subjects ◽  
T Tau

Background: It has been suggested that circulating Paraoxonase-1 (PON1) and apolipoprotein A1 (APOA1), which closely interacts with the antioxidant enzyme, could be implicated in Alzheimer’s disease (AD) and vascular dementia (VaD) development. This study aimed to evaluate PON1 changes in serum and cerebrospinal fluid (CSF) as evidence for its association with AD or VaD. Methods: Serum PON-arylesterase activity was measured in patients with AD, VaD, and CONTROLS distributed in two cohorts: Ferrara cohort (FC: n = 503, age = 74 years) and Amsterdam Dementia cohort (ADC: n = 71, age = 65 years). In the last cohort, CSF PON-arylesterase, CSF β-amyloid1-42, p-tau and t-tau, and imaging biomarkers were also measured. Results: AD and VaD patients of FC showed significantly lower levels of serum PON-arylesterase compared to CONTROLS, but this outcome was driven by older subjects (>71 years, p < 0.0001). In the younger ADC, a similar decreasing (but not significant) trend was observed in serum and CSF. Intriguingly, PON-arylesterase per APOA1 correlated with t-tau in AD group (r = −0.485, p = 0.002). Conclusion: These results suggest that decreased peripheral PON-arylesterase might be a specific feature of older AD/VaD patients. Moreover, we showed that PON-arylesterase/APOA1 is inversely related to neurodegeneration in AD patients, suggesting a prognostic usefulness of this composite parameter.

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