scholarly journals Serum Heart-Type Fatty Acid-Binding Protein and Cerebrospinal Fluid Tau: Marker Candidates for Dementia with Lewy Bodies

2007 ◽  
Vol 4 (5) ◽  
pp. 366-375 ◽  
Author(s):  
Brit Mollenhauer ◽  
Petra Steinacker ◽  
Erik Bahn ◽  
Mirko Bibl ◽  
Peter Brechlin ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Fatty Acid ◽  
Dementia With Lewy Bodies ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Lewy Bodies ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

scholarly journals Fatty Acid Binding Protein 3 Enhances the Spreading and Toxicity of α-Synuclein in Mouse Brain

2020 ◽  
Vol 21 (6) ◽  
pp. 2230 ◽  
Author(s):  
Yasushi Yabuki ◽  
Kazuya Matsuo ◽  
Ichiro Kawahata ◽  
Naoya Fukui ◽  
Tomohiro Mizobata ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Mouse Brain ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Lewy Bodies ◽  
Substantia Nigra Pars Compacta ◽  
Fatty Acid Binding ◽  
Knock Out ◽  
Acid Binding Protein ◽  
The Brain

Oligomerization and/or aggregation of α-synuclein (α-Syn) triggers α-synucleinopathies such as Parkinson’s disease and dementia with Lewy bodies. It is known that α-Syn can spread in the brain like prions; however, the mechanism remains unclear. We demonstrated that fatty acid binding protein 3 (FABP3) promotes propagation of α-Syn in mouse brain. Animals were injected with mouse or human α-Syn pre-formed fibrils (PFF) into the bilateral substantia nigra pars compacta (SNpc). Two weeks after injection of mouse α-Syn PFF, wild-type (WT) mice exhibited motor and cognitive deficits, whereas FABP3 knock-out (Fabp3−/−) mice did not. The number of phosphorylated α-Syn (Ser-129)-positive cells was significantly decreased in Fabp3−/− mouse brain compared to that in WT mice. The SNpc was unilaterally infected with AAV-GFP/FABP3 in Fabp3−/− mice to confirm the involvement of FABP3 in the development of α-Syn PFF toxicity. The number of tyrosine hydroxylase (TH)- and phosphorylated α-Syn (Ser-129)-positive cells following α-Syn PFF injection significantly decreased in Fabp3−/− mice and markedly increased by AAV-GFP/FABP3 infection. Finally, we confirmed that the novel FABP3 inhibitor MF1 significantly antagonized motor and cognitive impairments by preventing α-Syn spreading following α-Syn PFF injection. Overall, FABP3 enhances α-Syn spreading in the brain following α-Syn PFF injection, and the FABP3 ligand MF1 represents an attractive therapeutic candidate for α-synucleinopathy.

scholarly journals Fatty Acid-Binding Protein 3 in Cerebrospinal Fluid of Hip Fracture Patients with Delirium

2020 ◽  
Vol 77 (1) ◽  
pp. 183-190
Author(s):  
Bjørn Erik Neerland ◽  
Nathalie Bodd Halaas ◽  
Ane Victoria Idland ◽  
Kristi Henjum ◽  
Kaj Blennow ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Fatty Acid ◽  
Hip Fracture ◽  
Fatty Acid Binding Protein ◽  
Neuronal Damage ◽  
Binding Protein ◽  
Fatty Acid Binding ◽  
Cognitively Normal ◽  
Acid Binding Protein ◽  
Normal Controls

Background: Delirium is associated with dementia and thus biomarkers reflecting neurodegeneration are of interest. Fatty acid-binding protein 3 (FABP3) is a cytoplasmic neuronal protein that has been isolated from the brain. It is released following brain injury and concentrations in cerebrospinal fluid (CSF) are also higher in neurodegenerative disorders such as Alzheimer’s disease (AD). Objective: To examine the relationship between CSF FABP3 concentration and delirium in hip fracture patients compared to a group of cognitively normal controls. Methods: CFS FABP3 concentration was measured in 128 hip fracture patients with (n = 71) and without (n = 57) delirium, and in cognitively unimpaired adults ≥64 years (n = 124) undergoing elective surgery. Results: CSF FABP3 (pg/ml) concentration (median (IQR)) was higher in hip-fracture patients compared to cognitively normal controls (5.7 (4.2–7.7) versus 4.5 (3.4–6.1), p < 0.001). There was a significant weak correlation between age and CSF FABP3 (ρ= 0.3, p < 0.001). After adjustment for age, the association between CSF FABP3 and hip-fracture was no longer statistically significant (β= 0.05, p = 0.5). There were no significant differences in CSF FABP3 concentration between hip fracture patients with (5.4 (4.1–8.2)) and without (5.8 (4.2–7.2)) delirium. CSF FABP3 concentration correlated positively with CSF AD biomarkers p-tau (ρ= 0.7, p < 0.01) and t-tau (ρ= 0.7, p < 0.01). Conclusion: CSF FABP3 concentrations were higher in hip fracture patients compared with cognitively normal older adults, indicating ongoing age-related neurodegeneration in these patients. There were no differences of CSF FABP3 concentrations across delirium groups, suggesting that neuronal damage or degeneration reflected by FABP3 may not be directly linked to delirium pathophysiology.

scholarly journals Cerebrospinal fluid heart fatty acid‐binding protein as a predictive biomarker of neurodegeneration in Alzheimer’s disease

2021 ◽  
Vol 7 (1) ◽  
pp. 44-55
Author(s):  
Lu Pan ◽  
Ya-Nan Ou ◽  
Lin Tan ◽  
Lan Tan ◽  
Jin-Tai Yu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Fatty Acid ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Predictive Biomarker ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
T Tau

Objective This study aims to investigate whether the heart fatty acid‐binding protein (HFABP) in the cerebrospinal fluid (CSF) was a potential predictive biomarker for Alzheimer’s disease (AD). Methods We evaluated the associations of CSF HFABP levels with core biomarkers, cognition, and brain structure in a sample population ( n = 302) from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. Multiple linear regression and mixed‐effects models were employed in the analyses. AD progression was assessed using the Kaplan–Meier survival analysis. Results CSF HFABP was higher in patients with mild cognitive impairment and AD than the normal controls ( p < 0.001) and was particularly higher in those with amyloid‐β (Aβ) pathologic features. CSF HFABP was associated with higher baseline CSF t‐tau ( p < 0.001), CSF p‐tau ( p < 0.001), and CSF t‐tau/Aβ42 and CSF p‐tau/Aβ42 ( p < 0.01). Moreover, CSF HFABP was found to play predictive roles in hippocampal atrophy ( p < 0.01), cognitive decline ( p < 0.05), and the risk of AD ( p < 0.001). Conclusion Our findings suggest that CSF HFABP can be a predictive biomarker of AD.

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