Abstract
BackgroundEpidemiological and molecular findings suggest a relationship between Alzheimer’s disease (AD) and dyslipidemia, although the nature of this association is not well understood.ResultsUsing linear mixed effects models, we investigated the relationship between CSF levels of heart fatty acid binding protein (HFABP), a lipid binding protein involved with fatty acid metabolism and lipid transport, amyloid-β (Aβ), phospho-tau, and longitudinal MRI-based measures of brain atrophy among 295 non-demented and demented older individuals. Across all participants, we found a significant association of CSF HFABP with longitudinal atrophy of the entorhinal cortex and other AD-vulnerable neuroanatomic regions. However, we found that the relationship between CSF HABP and brain atrophy was significant only among those with low CSF Aβ1–42 and occurred irrespective of phospho-tau181p status.ConclusionsOur findings indicate that Aβ-associated volume loss occurs in the presence of elevated HFABP irrespective of phospho-tau. This implicates a potentially important role for fatty acid binding proteins in Alzheimer’s disease neurodegeneration.
Highlights
Epidemiological and molecular findings suggest a relationship between Alzheimer’s disease (AD) and dyslipidemia, the nature of this association is not well understood
Recent work suggests that CSF levels of heart fatty acid binding protein (HFABP or FABP3), a lipid binding protein involved with fatty acid metabolism and lipid transport [15] may have diagnostic and prognostic value in the earliest stages of AD [16,17,18,19,20]
Among non-demented older individuals at risk for AD and demented participants diagnosed with probable AD, we investigated whether CSF HFABP is associated with brain atrophy over time and whether interactions between high CSF HFABP and low CSF Aβ1–42 and high CSF HFABP and high CSF p-tau181p are associated with brain atrophy over time
Summary
Epidemiological and molecular findings suggest a relationship between Alzheimer’s disease (AD) and dyslipidemia, the nature of this association is not well understood. A growing number of epidemiological and experimental studies suggest an association between Alzheimer’s disease (AD) and dyslipidemia. Genetic linkage and genome-wide association studies have identified a number of genes involved with cholesterol metabolism and transport as AD susceptibility loci [3,4] and cellular and molecular biology research has indicated a critical role for neuronal membrane phospholipids (‘lipid rafts’) in modulating AD-associated pathogenesis [5]. In animal models, apolipoprotein E modulates the relationship between low-density lipoproteins and amyloid-β (Aβ) deposition [6,7] suggesting an indirect effect of intra-cranial cholesterol on Alzheimer’s pathology. We evaluated the relationship between CSF HFABP and other lipid binding proteins including Apolipoprotein (Apo) C III, Apo D, and Apo E
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