https://transhumanist.ru/index.php?action=history&feed=atom&title=SYNJ2SYNJ2 - История изменений2026-06-22T18:06:42ZИстория изменений этой страницы в викиMediaWiki 1.43.6https://transhumanist.ru/index.php?title=SYNJ2&diff=4628&oldid=prevOdysseusBot: Новая страница: «Synaptojanin-2 (EC 3.1.3.36) (Synaptic inositol 1,4,5-trisphosphate 5-phosphatase 2) [KIAA0348] ==Publications== {{medline-entry |title=DNA methylation analysis...»2021-04-29T19:27:10Z<p>Новая страница: «Synaptojanin-2 (EC 3.1.3.36) (Synaptic inositol 1,4,5-trisphosphate 5-phosphatase 2) [KIAA0348] ==Publications== {{medline-entry |title=DNA methylation analysis...»</p>
<p><b>Новая страница</b></p><div>Synaptojanin-2 (EC 3.1.3.36) (Synaptic inositol 1,4,5-trisphosphate 5-phosphatase 2) [KIAA0348]<br />
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==Publications==<br />
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{{medline-entry<br />
|title=DNA methylation analysis on purified neurons and glia dissects age and Alzheimer's disease-specific changes in the human cortex.<br />
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30045751<br />
|abstract=Epigenome-wide association studies (EWAS) based on human brain samples allow a deep and direct understanding of epigenetic dysregulation in Alzheimer's disease (AD). However, strong variation of cell-type proportions across brain tissue samples represents a significant source of data noise. Here, we report the first EWAS based on sorted neuronal and non-neuronal (mostly glia) nuclei from postmortem human brain tissues. We show that cell sorting strongly enhances the robust detection of disease-related DNA methylation changes even in a relatively small cohort. We identify numerous genes with cell-type-specific methylation signatures and document differential methylation dynamics associated with aging specifically in neurons such as [[CLU]], [[SYNJ2]] and [[NCOR2]] or in glia [[RAI1]],CXXC5 and [[INPP5A]]. Further, we found neuron or glia-specific associations with AD Braak stage progression at genes such as [[MCF2L]], [[ANK1]], [[MAP2]], [[LRRC8B]], [[STK32C]] and [[S100B]]. A comparison of our study with previous tissue-based EWAS validates multiple AD-associated DNA methylation signals and additionally specifies their origin to neuron, e.g., [[HOXA3]] or glia ([[ANK1]]). In a meta-analysis, we reveal two novel previously unrecognized methylation changes at the key AD risk genes [[APP]] and [[ADAM17]]. Our data highlight the complex interplay between disease, age and cell-type-specific methylation changes in AD risk genes thus offering new perspectives for the validation and interpretation of large EWAS results.<br />
|mesh-terms=* ADAM17 Protein<br />
* Aging<br />
* Alzheimer Disease<br />
* Amyloid beta-Protein Precursor<br />
* Autopsy<br />
* Cell Separation<br />
* DNA Methylation<br />
* Epigenesis, Genetic<br />
* Epigenomics<br />
* Genetic Predisposition to Disease<br />
* Genome-Wide Association Study<br />
* Humans<br />
* Neuroglia<br />
* Neurons<br />
* Organ Specificity<br />
* Transcriptome<br />
|keywords=* Aging<br />
* Alzheimer’s disease<br />
* Brain<br />
* Cell sorting<br />
* DNA methylation<br />
* EWAS<br />
* Epigenetics<br />
* Glia<br />
* Neurodegeneration<br />
* Neuron<br />
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058387<br />
}}</div>OdysseusBot