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Summary

Restoring mitochondrial function with CP2 reversed metabolic dysfunction in advanced Alzheimer's disease (AD). This approach coordinated mitochondrial and lipid metabolism, offering a potential disease-modifying therapy for AD.

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Area of Science:

Neuroscience
Metabolic research
Mitochondrial biology

Background:

Alzheimer's disease (AD) involves early mitochondrial dysfunction and lipid dysregulation.
The interplay between these factors and their therapeutic potential in AD are not well understood.

Purpose of the Study:

To investigate if restoring mitochondrial function can reverse metabolic dysfunction in advanced AD.
To explore the therapeutic potential of targeting mitochondrial complex I (mtCI) in AD models.

Main Methods:

Treatment of aged female APP/PS1 mice with a brain-penetrant mtCI modulator (CP2).
Development and utilization of iMiceBrain, a brain-specific genome-scale metabolic model.
Integration of transcriptomics, metabolomics, lipidomics, and metabolic network analyses.

Main Results:

CP2 treatment reprogrammed AD-associated molecular signatures and restored key metabolic pathways.
Metabolic modeling revealed enhanced mitochondrial substrate flexibility and normalized cholesterol metabolism.
Lipidomic analyses showed correction of disease-associated alterations in lipids like cholesteryl esters and phospholipids.

Conclusions:

Mild mtCI modulation restores metabolic resilience in advanced AD by coordinating mitochondrial and lipid metabolism.
Targeting mitochondrial function represents a promising disease-modifying therapeutic strategy for Alzheimer's disease.