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Morris Water Maze Test: Optimization for Mouse Strain and Testing Environment

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Calorie restriction does not restore brain mitochondrial function in P301L tau mice, but it does decrease

Vedad Delic¹, Milene Brownlow², Aurelie Joly-Amado²

¹Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL 33620, United States.

Molecular and Cellular Neurosciences

|June 7, 2015

Summary

This summary is machine-generated.

Calorie restriction (CR) did not improve brain mitochondrial function in a mouse model of tauopathy. However, CR did decrease brain mitochondrial F0F1-ATPase activity, independent of genotype.

Keywords:

ATP synthase Alzheimer's Calorie restriction Complex I Mitochondria Tau

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Area of Science:

Neuroscience
Mitochondrial Biology
Aging Research

Background:

Calorie restriction (CR) extends lifespan and delays aging in various species.
CR may benefit Alzheimer's disease (AD) by reducing amyloid-beta and tau pathology.
Mutant tau expression impairs mitochondrial electron transport chain complex I activity.

Purpose of the Study:

To investigate the effects of 4-month CR on brain mitochondrial function in Tg4510 mice expressing human P301L tau.
To determine if CR can restore mitochondrial deficits caused by mutant tau expression.

Main Methods:

Utilized Tg4510 mice expressing human P301L tau.
Administered a 4-month calorie restriction (CR) diet.
Assessed brain mitochondrial function, including respiratory rates, membrane potential, complex I activity, and F0F1-ATPase activity.

Main Results:

Mutant tau expression decreased ADP-stimulated respiration and mitochondrial complex I activity.
CR did not restore these tau-induced mitochondrial deficits.
CR led to a genotype-independent decrease in brain mitochondrial F0F1-ATPase activity.

Conclusions:

CR does not ameliorate tau-induced mitochondrial dysfunction in the brain.
CR independently reduces brain mitochondrial F0F1-ATPase activity.
Further research is needed to understand the mechanisms behind CR's effect on F0F1-ATPase.