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Basic Science and Pathogenesis.

Georgia Malliou1,2, Lianne M Reus2,3,4, Yolande A L Pijnenburg1,2

  • 1Amsterdam Neuroscience, Neurodegeneration, Amsterdam, Netherlands.

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|December 23, 2025
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Summary
This summary is machine-generated.

Alzheimer's disease (AD) subtypes show distinct cerebrospinal fluid (CSF) metabolic profiles, revealing varied underlying disease mechanisms. This metabolic signature could guide the development of targeted therapies for specific AD patient groups.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Genomics

Background:

  • Alzheimer's disease (AD) is characterized by molecular heterogeneity, with five previously identified subtypes based on CSF proteomics.
  • These subtypes (S1-S5) involve distinct molecular pathways, including metabolic processes, suggesting metabolic differences.
  • Investigating CSF metabolic signatures associated with these AD subtypes is crucial for understanding disease heterogeneity.

Purpose of the Study:

  • To investigate the association between distinct molecular Alzheimer's disease (AD) subtypes and specific cerebrospinal fluid (CSF) metabolic signatures.
  • To identify unique and common metabolic alterations across different AD subtypes.
  • To explore the potential of metabolic profiling for guiding subtype-specific therapeutic strategies in AD.

Main Methods:

  • Untargeted metabolomics was performed on CSF samples from 601 individuals (416 AD patients, 185 controls) using HILIC-QTOF and GC-TOF platforms.
  • A total of 2,011 metabolites were detected, with 544 mapped to known classes.
  • Linear regression models compared metabolite levels between AD subtypes and controls, followed by pathway enrichment analysis.

Main Results:

  • 993 metabolites showed altered CSF levels across AD subtypes compared to controls, with the choroid plexus dysfunction subtype (S4) exhibiting the most changes.
  • Metabolites were primarily mapped to organic acids, carbohydrates, fatty acyls, and alkaloids, with distinct patterns of increase or decrease across subtypes.
  • Pathway analysis revealed enrichment in compound transport, amino acid metabolism, tRNA aminoacylation, and glucose homeostasis, varying by subtype.

Conclusions:

  • Distinct CSF metabolomic alterations are associated with different Alzheimer's disease (AD) proteomic subtypes, reflecting heterogeneous pathophysiological mechanisms.
  • Metabolic profiling of AD subtypes can inform the development of future subtype-specific therapies targeting metabolic pathways.
  • Therapies targeting glucose metabolism, for instance, might be most effective for patients within the RNA dysregulation subtype (S3).