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Brain glucose hypometabolism, an early feature of AD, reflects neuronal metabolic dysfunction before the onset of clinical symptoms. While A\u03b2 plaques are central to AD pathogenesis, the mechanisms by which different A\u03b2 species, such as plaques and soluble oligomers, drive cell-type-specific neurometabolic dysfunction during disease progression remain poorly understood. This study evaluated the roles of different A\u03b2 species in the neurometabolic trajectory across the presymptomatic, symptomatic, and advanced stages of AD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      5xFAD and wild-type (WT) mice were investigated for cognitive performance, quantitative A\u03b2 levels, and glial activation markers at 3, 6, and 12 months of age. Neuronal and astroglial metabolic activities were evaluated ex vivo using state-of-the-art\n                      <jats:sup>1<\/jats:sup>\n                      H-[\n                      <jats:sup>13<\/jats:sup>\n                      C]-NMR spectroscopy in conjunction with administration of [1,6-\n                      <jats:sup>13<\/jats:sup>\n                      C\n                      <jats:sub>2<\/jats:sub>\n                      ]glucose and [2-\n                      <jats:sup>13<\/jats:sup>\n                      C]acetate, respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The 5xFAD mice exhibited cognitive decline from 6 months that further deteriorated by 12 months. There was a marked increase in A\u03b2-plaque burden and soluble oligomers from 3 to 12 months of age. These mice showed a significant reduction in hippocampal glutamatergic (0.145\u2009\u00b1\u20090.031 vs. 0.172\u2009\u00b1\u20090.016 \u00b5mol\/g\/min,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.035) and GABAergic neuronal metabolic activity (0.027\u2009\u00b1\u20090.006 v\n                      <jats:italic>s<\/jats:italic>\n                      0.033\u2009\u00b1\u20090.003 \u00b5mol\/g\/min,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.028) as early as 3 months of age, with similar reductions observed in the cerebral cortex. The neurometabolic impairments further aggravated with age. Astrocytic metabolic activity was not significantly changed till 6 months but was increased at 12 months in 5xFAD mice in both the cerebral cortex (0.101\u2009\u00b1\u20090.014 vs. 0.084\u2009\u00b1\u20090.006 \u00b5mol\/g\/min,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.011) and hippocampus (0.103\u2009\u00b1\u20090.006 vs. 0.089\u2009\u00b1\u20090.012 \u00b5mol\/g\/min,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.011). The increase in astrocytic metabolic activity paralleled reactive gliosis, suggesting a shift from early neuronal metabolic impairment to heightened astroglial metabolic activity and inflammatory glial responses during the advanced AD stage. Notably, A\u03b2\n                      <jats:sub>40<\/jats:sub>\n                      oligomers exhibited a greater sensitivity to impairment in neuronal glucose oxidation and cognitive function than A\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      oligomers or fibrillar plaques.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      These findings delineate a sequential neurometabolic cascade during AD progression, characterized by early neuronal glucose hypometabolism, subsequent cognitive decline linked to soluble A\u03b2\n                      <jats:sub>40<\/jats:sub>\n                      oligomers, and late-stage astroglial metabolic activation. Collectively, these results suggest that soluble A\u03b2\n                      <jats:sub>40<\/jats:sub>\n                      oligomers exhibit the greatest sensitivity to neurometabolic and cognitive impairment during AD.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13195-026-02130-4","type":"journal-article","created":{"date-parts":[[2026,7,11]],"date-time":"2026-07-11T02:34:49Z","timestamp":1783737289000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["In vivo evidence for soluble A\u03b2 oligomer-driven neuronal metabolic dysfunction in 5xFAD mice"],"prefix":"10.1186","volume":"18","author":[{"given":"Chaynita","family":"Dashora","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anant Bahadur","family":"Patel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,7,11]]},"reference":[{"key":"2130_CR1","doi-asserted-by":"publisher","unstructured":"2023 Alzheimer\u2019s disease facts and figures. 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