4.5 Article

Mitochondrial Movement and Number Deficits in Embryonic Cortical Neurons from 3xTg-AD Mice

期刊

JOURNAL OF ALZHEIMERS DISEASE
卷 70, 期 1, 页码 139-151

出版社

IOS PRESS
DOI: 10.3233/JAD-190143

关键词

Alzheimer's disease; mitochondrial dynamics; mitochondrial size; sigma receptors

资金

  1. NIH [P20 GM109098, P01 AG027956, T32 AG052375, U54 GM104942, P20RR016440, P30RR032138/P30GM103488, P20GM103434]
  2. WVU Cancer Institute

向作者/读者索取更多资源

Mitochondrial dysfunction is often found in Alzheimer's disease (AD) patients and animal models. Clinical severity of AD is linked to early deficiencies in cognitive function and brain metabolism, indicating that pathological changes may begin early in life. Previous studies showed decreased mitochondrial function in primary hippocampal neurons from triple-transgenic Alzheimer's disease (3xTg-AD) mice and mitochondrial movement and structure deficits in primary neurons exposed to amyloid-beta oligomers. The present study characterized mitochondrial movement, number, and structure in 3xTg-AD primary cortical neurons and non-transgenic (nonTg) controls. We found a significant reduction in mitochondrial number and movement in 3xTg-AD primary cortical neurons with modest structural changes. Additionally, application of the sigma-1 receptor agonist, (+)SKF-10,047, markedly increased mitochondrial movement in both 3xTg-AD and nonTg primary cortical cultures after one hour of treatment. (+)SKF-10,047 also led to a trend of increased mitochondrial number in 3xTg-AD cultures. Embryonic mitochondrial movement and number deficits could be among the key steps in the early pathogenesis of AD that compromise cognitive or metabolic reserve, and amelioration of these deficits could be a promising area for further preclinical and clinical study.

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