{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,24]],"date-time":"2026-07-24T01:07:53Z","timestamp":1784855273076,"version":"3.55.0"},"reference-count":75,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2024,10,29]],"date-time":"2024-10-29T00:00:00Z","timestamp":1730160000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2024,12]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Alzheimer's disease (AD) is classically characterized by alterations in memory consolidation. With the advent of diagnostic biomarkers, some patients clinically diagnosed with AD display biomarkers inconsistent with the diagnosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We aimed to explore differences in memory consolidation and neurodegeneration of the temporal and parietal lobes as a function of amyloid-\u03b2 status in amnestic mild cognitive impairment (aMCI).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We examined differences in memory consolidation and neurodegeneration between patients diagnosed with amyloid-\u03b2 positive aMCI (A\u03b2+ N\u2009=\u200978), amyloid-\u03b2 negative aMCI (A\u03b2\u2212 N\u2009=\u200948), and healthy participants (HP; N\u2009=\u200941), within a well-characterized clinical cohort.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A\u03b2+ exhibited more pronounced consolidation impairments compared to A\u03b2\u2212, while A\u03b2\u2212 faced more consolidation challenges than HP. Both A\u03b2+ and A\u03b2\u2212 were similar in hippocampal volume and entorhinal thickness, but A\u03b2+ had thinner inferior parietal cortex than A\u03b2\u2212. Using\n                      <jats:sup>18<\/jats:sup>\n                      F-fluoro-deoxyglucose-positron emission tomography, metabolism in both temporal and parietal regions was lower in A\u03b2+ relative to A\u03b2\u2212.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings suggest pathologies other than AD likely contribute to memory consolidation difficulties in aMCI, and neurodegeneration of the parietal cortex in combination with hypometabolism may contribute to more pronounced consolidation problems in A\u03b2+.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877241291223","type":"journal-article","created":{"date-parts":[[2024,11,25]],"date-time":"2024-11-25T01:55:01Z","timestamp":1732499701000},"page":"778-791","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":4,"title":["Memory consolidation, temporal and parietal atrophy, and metabolism in amyloid-\u03b2 positive and negative mild cognitive impairment"],"prefix":"10.1177","volume":"102","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6607-4000","authenticated-orcid":false,"given":"Cierra M","family":"Keith","sequence":"first","affiliation":[{"name":"Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, USA"},{"name":"Department of Behavioral Medicine and Psychiatry, West Virginia University, Morgantown, WV, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc W","family":"Haut","sequence":"additional","affiliation":[{"name":"Rockefeller 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