{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T01:01:20Z","timestamp":1792717280694,"version":"4.5.0"},"reference-count":45,"publisher":"Society for Neuroscience","issue":"10","license":[{"start":{"date-parts":[[2013,9,6]],"date-time":"2013-09-06T00:00:00Z","timestamp":1378425600000},"content-version":"vor","delay-in-days":184,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2013,3,6]]},"abstract":"<jats:p>ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and has been detected in macrophages, microglia, and neurons. ABCA7 promotes efflux of lipids from cells to apolipoproteins and can also regulate phagocytosis and modulate processing of amyloid precursor protein (APP) to generate the Alzheimer's disease (AD) amyloid-\u03b2 (A\u03b2) peptide. Genome-wide association studies have indicated that<jats:italic>ABCA7<\/jats:italic>single nucleotide polymorphisms confer increased risk for late-onset AD; however, the role that ABCA7 plays in the brain in the AD context is unknown. In the present study, we crossed ABCA7-deficient (A7<jats:sup>\u2212\/\u2212<\/jats:sup>) mice with J20 amyloidogenic mice to address this issue. We show that ABCA7 loss doubled insoluble A\u03b2 levels and thioflavine-S\u2013positive plaques in the brain. This was not related to changes in APP processing (assessed by analysis of full-length APP and the APP \u03b2 C-terminal fragment). Apolipoprotein E regulates cerebral A\u03b2 homeostasis and plaque load; however, the apolipoprotein E concentration was not altered by ABCA7 loss. Spatial reference memory was significantly impaired in both J20 and J20\/A7<jats:sup>\u2212\/\u2212<\/jats:sup>mice compared with wild-type mice; however, there were no cognitive differences between J20 and J20\/A7<jats:sup>\u2212\/\u2212<\/jats:sup>mice. There were also no major differences detected in hippocampal or plaque-associated microglial\/macrophage markers between J20 and J20\/A7<jats:sup>\u2212\/\u2212<\/jats:sup>mice, whereas the capacity for bone marrow-derived macrophages derived from A7<jats:sup>\u2212\/\u2212<\/jats:sup>mice to take up oligomeric A\u03b2 was reduced by 51% compared with wild-type mice. Our results suggest that ABCA7 plays a role in the regulation of A\u03b2 homeostasis in the brain and that this may be related to altered phagocyte function.<\/jats:p>","DOI":"10.1523\/jneurosci.4165-12.2013","type":"journal-article","created":{"date-parts":[[2013,3,6]],"date-time":"2013-03-06T17:55:06Z","timestamp":1362592506000},"page":"4387-4394","source":"Crossref","is-referenced-by-count":199,"title":["Deletion of<i>Abca7<\/i>Increases Cerebral Amyloid-\u03b2 Accumulation in the J20 Mouse Model of Alzheimer's Disease"],"prefix":"10.1523","volume":"33","author":[{"given":"Woojin 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