| Institution: | 1.Department of Radiology,University of California, San Diego,La Jolla,USA;2.Department of Psychiatry,University of California, San Diego,La Jolla,USA;3.Department of Neurosciences,University of California, San Diego,La Jolla,USA;4.Neuroradiology Section, Department of Radiology and Biomedical Imaging,University of California,San Francisco,USA;5.Clinical Neurochemistry Laboratory,The Sahlgrenska Academy at G?teburg University,Gotheburg, M?lndal,Sweden;6.UCL Institute of Neurology,London,UK;7.Institute of Clinical Medicine, University of Oslo and Division of Mental Health and Addiction,Oslo University Hospital,Oslo,Norway;8.Department of Neurology,Massachusetts General Hospital,Boston,USA |
| 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. |
