ArticleJournal of molecular neuroscience : MN2026
Higher Serum Levels of Propionylcarnitine and Methionine are Associated with Reduced Cortical Amyloid Burden in Alzheimer's Disease.
Article in Journal of molecular neuroscience : MN, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Altered systemic metabolism contributes to Alzheimer’s disease (AD) pathology, yet the links between specific metabolites, cortical amyloid deposition, and cognition remain unclear. This study conducted targeted profiling of over 600 serum metabolites across 26 biochemical classes in 746 ADNI participants (CN = 248, MCI = 403, AD = 95), identifying propionylcarnitine and methionine as significantly associated metabolites. Relationships among these metabolites, cortical Aβ accumulation, and cognitive performance were examined using regression and mediation analyses, adjusting for age, sex, education, and APOE ε4 status. The results showed that serum propionylcarnitine and methionine levels did not differ across diagnostic groups. In AD participants, higher propionylcarnitine (β = − 0.24, FDR p = 0.019) and methionine (β = − 0.33, FDR p = 0.005) levels were associated with lower cerebellum-referenced cortical amyloid burden, whereas no significant associations were observed in CN or MCI individuals. Mediation analyses indicated that serum propionylcarnitine did not show significant indirect effects on cognitive performance via cortical amyloid burden in any group. For methionine, nominally significant indirect effects on cognition were observed in AD participants before FDR correction (ADAS-Cog 11: β = − 0.11, p = 0.040; ADAS-Cog 13: β = − 0.13, p = 0.044), but these did not remain significant after FDR adjustment (FDR p > 0.19), suggesting modest, non-significant associations of methionine with cognitive performance via cortical amyloid burden, although these findings were observational and did not imply causation. In short, higher propionylcarnitine and methionine were linked to lower cortical Aβ accumulation in AD, highlighting future research directions to explore their mechanistic roles in AD pathology.
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