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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=COX5A</id>
	<title>COX5A - История изменений</title>
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	<updated>2026-06-06T23:47:10Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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		<id>https://transhumanist.ru/index.php?title=COX5A&amp;diff=6243&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Cytochrome c oxidase subunit 5A, mitochondrial precursor (Cytochrome c oxidase polypeptide Va)  ==Publications==  {{medline-entry |title=COX5A Plays a Vital R...»</title>
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		<updated>2021-05-12T15:19:04Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Cytochrome c oxidase subunit 5A, mitochondrial precursor (Cytochrome c oxidase polypeptide Va)  ==Publications==  {{medline-entry |title=&lt;a href=&quot;/COX5A&quot; title=&quot;COX5A&quot;&gt;COX5A&lt;/a&gt; Plays a Vital R...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Cytochrome c oxidase subunit 5A, mitochondrial precursor (Cytochrome c oxidase polypeptide Va)&lt;br /&gt;
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==Publications==&lt;br /&gt;
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{{medline-entry&lt;br /&gt;
|title=[[COX5A]] Plays a Vital Role in Memory Impairment Associated With Brain Aging [i]via[/i] the [[BDNF]]/ERK1/2 Signaling Pathway.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32754029&lt;br /&gt;
|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&amp;#039;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.&lt;br /&gt;
&lt;br /&gt;
|keywords=* BDNF&lt;br /&gt;
* COX5A&lt;br /&gt;
* ERK1/2&lt;br /&gt;
* brain senescence&lt;br /&gt;
* memory impairment&lt;br /&gt;
* mitochondria&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7365906&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
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