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Drug Development.

Marta Turri1,2, Myriam Aubin3,4, Laura K Hamilton5

  • 1Université de Sherbrooke, Sherbrooke, QC, Canada.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease (AD) involves brain lipid changes. A stearoyl-CoA desaturase (SCD) inhibitor improved fatty acid alterations and synaptic density in the aggressive 5xFAD AD mouse model, suggesting a potential therapeutic strategy.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Alzheimer's disease (AD) is characterized by brain lipid alterations, yet effective therapies targeting lipid metabolism remain scarce.
  • Previous studies showed stearoyl-CoA desaturase (SCD) inhibition improved synaptic function in a slow-progressing AD mouse model.
  • This study investigates lipid metabolism in the rapidly progressing 5xFAD AD mouse model and the effects of an SCD inhibitor (SCDi).

Purpose of the Study:

  • To examine lipid metabolism disruptions in the 5xFAD AD mouse model.
  • To evaluate the therapeutic potential of an SCD inhibitor on fatty acid alterations and synapse loss in 5xFAD mice.

Main Methods:

  • Fatty acid (FA) profiling using gas chromatography-flame ion detection (GC-FID) in hippocampi of 5xFAD and control mice.
  • Immunohistochemistry (IHC) for amyloid plaques and glial markers (GFAP, Iba-1).
  • Intracerebroventricular infusion of SCDi or vehicle, followed by GC-FID and Golgi staining for dendritic spine quantification.

Main Results:

  • Significant FA alterations were observed in 5xFAD mice, with differences based on sex and age.
  • The C16:1/C16:0 desaturation index, indicative of SCD activity, increased in 5xFAD mice.
  • SCDi treatment normalized FA levels and improved dendritic spine density in female 5xFAD mice.

Conclusions:

  • SCD inhibition demonstrates beneficial effects on FA alterations and hippocampal dendritic spines in the aggressive 5xFAD AD model.
  • These findings reinforce the potential of SCD inhibition as a novel therapeutic target for Alzheimer's disease.