Редактирование: COX5A

Cytochrome c oxidase subunit 5A, mitochondrial precursor (Cytochrome c oxidase polypeptide Va)

==Publications==

{{medline-entry
|title=[[COX5A]] Plays a Vital Role in Memory Impairment Associated With Brain Aging [i]via[/i] the [[BDNF]]/ERK1/2 Signaling Pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32754029
|abstract=Cytochrome c oxidase subunit Va ([[COX5A]]) is involved in maintaining normal mitochondrial function. However, little is known on the role of [[COX5A]] in the development and progress of Alzheimer's disease (Martinez-Losa et al., 2018). In this study, we established and characterized the genomic profiles of genes expressed in the hippocampus of Senescence-Accelerated Mouse-prone 8 (SAMP8) mice, and revealed differential expression of [[COX5A]] among 12-month-aged SAMP8 mice and 2-month-aged SAMP8 mice. Newly established transgenic mice with systemic [[COX5A]] overexpression (51% increase) resulted in the improvement of spatial recognition memory and hippocampal synaptic plasticity, recovery of hippocampal [[CA1]] dendrites, and activation of the [[BDNF]]/ERK1/2 signaling pathway [i]in vivo[/i]. Moreover, mice with both [[COX5A]] overexpression and [[BDNF]] knockdown showed a poor recovery in spatial recognition memory as well as a decrease in spine density and branching of dendrites in [[CA1]], when compared to mice that only overexpressed [[COX5A]]. [i]In vitro[/i] studies supported that [[COX5A]] affected neuronal growth [i]via[/i] [[BDNF]]. In summary, this study was the first to show that [[COX5A]] in the hippocampus plays a vital role in aging-related cognitive deterioration [i]via[/i] [[BDNF]]/ERK1/2 regulation, and suggested that [[COX5A]] may be a potential target for anti-senescence drugs.

|keywords=* BDNF
* COX5A
* ERK1/2
* brain senescence
* memory impairment
* mitochondria
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7365906
}}