Mitochondrial regulation of adult hippocampal neurogenesis: Insights into neurological function and neurodevelopmental disorders

被引:1
作者
Bonzano, Sara [1 ,2 ]
Dallorto, Eleonora [1 ,2 ,3 ]
Bovetti, Serena [1 ,2 ]
Studer, Michele [3 ]
De Marchis, Silvia [1 ,2 ]
机构
[1] Univ Turin, Dept Life Sci & Syst Biol, DBIOS, Via Acad Albertina 13, I-10123 Turin, Italy
[2] Neurosci Inst Cavalieri Ottolenghi NICO, Reg Gonzole 10, I-10043 Orbassano, Italy
[3] Univ Cote dAzur UCA, Inserm 1091, CNRS 7277, Inst Biol Valrose iBV, Ave Valrose 28, F-06108 Nice, France
关键词
Mitochondria; Nr2f1; BBSOAS; Adult neural stem cells; Dentate gyrus; NEURAL STEM-CELLS; NEWLY GENERATED NEURONS; DENTATE GRANULE CELLS; TS65DN MOUSE MODEL; COUP-TFI; CRITICAL PERIOD; STEM/PROGENITOR CELLS; GENE-EXPRESSION; OPTIC ATROPHY; DYNAMICS;
D O I
10.1016/j.nbd.2024.106604
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Mitochondria are essential regulators of cellular energy metabolism and play a crucial role in the maintenance and function of neuronal cells. Studies in the last decade have highlighted the importance of mitochondrial dynamics and bioenergetics in adult neurogenesis, a process that significantly influences cognitive function and brain plasticity. In this review, we examine the mechanisms by which mitochondria regulate adult neurogenesis, focusing on the impact of mitochondrial function on the behavior of neural stem/progenitor cells and the maturation and plasticity of newborn neurons in the adult mouse hippocampus. In addition, we explore the link between mitochondrial dysfunction, adult hippocampal neurogenesis and genes associated with cognitive deficits in neurodevelopmental disorders. In particular, we provide insights into how alterations in the transcriptional regulator NR2F1 affect mitochondrial dynamics and may contribute to the pathophysiology of the emerging neurodevelopmental disorder Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS). Understanding how genes involved in embryonic and adult neurogenesis affect mitochondrial function in neurological diseases might open new directions for therapeutic interventions aimed at boosting mitochondrial function during postnatal life.
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页数:15
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