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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=ANKS1B</id>
	<title>ANKS1B - История изменений</title>
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	<updated>2026-04-08T06:00:45Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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	<entry>
		<id>https://transhumanist.ru/index.php?title=ANKS1B&amp;diff=5885&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Ankyrin repeat and sterile alpha motif domain-containing protein 1B (Amyloid-beta protein intracellular domain-associated protein 1) (AIDA-1) (E2A-PBX1-associated...»</title>
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		<updated>2021-05-12T14:58:05Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Ankyrin repeat and sterile alpha motif domain-containing protein 1B (Amyloid-beta protein intracellular domain-associated protein 1) (AIDA-1) (E2A-PBX1-associated...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Ankyrin repeat and sterile alpha motif domain-containing protein 1B (Amyloid-beta protein intracellular domain-associated protein 1) (AIDA-1) (E2A-PBX1-associated protein) (EB-1)&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=Explorative results from multistep screening for potential genetic risk loci of Alzheimer&amp;#039;s disease in the longitudinal VITA study cohort.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29027019&lt;br /&gt;
|abstract=Alzheimer&amp;#039;s disease (AD) is a neurodegenerative disorder that preferentially affects individuals of advanced age. Heritability estimates for AD range between 60 and 80%, but only few genetic risk factors have been identified so far. In the present explorative study, we aimed at characterizing the genetic contribution to late-onset AD in participants of the Vienna Transdanube Aging (VITA) longitudinal birth cohort study in a two-step approach. First, we performed a genome-wide screen of pooled DNA samples (n = 588) to identify allele frequency differences between AD patients and non-AD individuals using life-time diagnoses made at the age of 80 (t = 60 months). This analysis suggested a high proportion of brain-expressed genes required for cell adhesion, cell signaling and cell morphogenesis, and also scored in known AD risk genes. In a second step, we confirmed associations using individual genotypes of top-ranked markers examining AD diagnoses as well as the dimensional scores: FULD and MMSE determined up to the age of 82.5 (t = 90 months). Taken together, our study proposes genes [[ANKS1B]], ENST00000414107, LOC100505811, [[SLC22A14]], [[QRFPR]], ZDHHC8P1, [[ADAMTS3]] and [[PPFIA1]] as possible new candidates involved in the etiology of late-onset AD, with further research being needed to clarify their exact roles.&lt;br /&gt;
|mesh-terms=* Aged&lt;br /&gt;
* Aged, 80 and over&lt;br /&gt;
* Aging&lt;br /&gt;
* Alzheimer Disease&lt;br /&gt;
* Austria&lt;br /&gt;
* Cohort Studies&lt;br /&gt;
* Female&lt;br /&gt;
* Genetic Loci&lt;br /&gt;
* Genetic Predisposition to Disease&lt;br /&gt;
* Genetic Testing&lt;br /&gt;
* Humans&lt;br /&gt;
* Longitudinal Studies&lt;br /&gt;
* Male&lt;br /&gt;
|keywords=* Alzheimer’s disease&lt;br /&gt;
* Candidate gene identification&lt;br /&gt;
* Cohort study&lt;br /&gt;
* Genotyping microarray&lt;br /&gt;
* Pooled DNA analysis&lt;br /&gt;
|full-text-url=https://sci-hub.do/10.1007/s00702-017-1796-6&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
	</entry>
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