Mitochondrial Function and Memory in Mice
Author Information
Author(s): Tanaka Daisuke, Nakada Kazuto, Takao Keizo, Ogasawara Emi, Kasahara Atsuko, Sato Akitsugu, Yonekawa Hiromichi, Miyakawa Tsuyoshi, Hayashi Jun-Ichi
Primary Institution: Graduate School of Life and Environmental Sciences, University of Tsukuba
Hypothesis
High loads of pathogenic mitochondrial DNA mutations impair spatial remote memory in mice.
Conclusion
Normal mitochondrial respiratory function is necessary for retention and consolidation of memory trace, and deficiencies in this function due to high loads of mutated mitochondrial DNA lead to impaired spatial remote memory.
Supporting Evidence
- High loads of mutated mitochondrial DNA were linked to severe memory impairments at long retention delays.
- Mitochondrial respiration deficiencies were observed in the high group of mito-mice.
- Normal mitochondrial function was associated with better retention of memory traces.
- α-CaMKII protein levels were reduced in high ΔmtDNA load mice, correlating with memory impairment.
- Behavioral tests showed no significant differences in spatial learning between low and high groups.
Takeaway
Mice with too much bad mitochondrial DNA have trouble remembering things that happened a long time ago because their energy factories (mitochondria) aren't working well.
Methodology
The study used trans-mitochondrial mice with varying loads of mutated mitochondrial DNA to assess their spatial learning and memory through behavioral tests.
Potential Biases
Potential bias due to the limited genetic variation in the mito-mice model.
Limitations
The study did not explore the effects of mitochondrial dysfunction on other cognitive functions beyond spatial memory.
Participant Demographics
Male mito-mice aged between 5 and 8 months.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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