Talk:DNA damage theory of aging

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Academic review style

This article has the tone and style of an academic review, not an encyclopedia article. For example "Descriptions of decrements in function, characteristic of aging, associated with accumulation of DNA damages, are given later in this article." Having a Conclusions section is also more in the style of a review article than an encyclopedia article.Trashbird1240 (talk) 18:58, 6 March 2013 (UTC)[reply]

Not to mention that citations as in here "Here, we mention only some recent studies involving rodents plus one human study. Rutten et al. (2007) showed that single-strand breaks accumulate in the mouse brain with age. Sen et al. (2007) showed that DNA damages which block the polymerase chain reaction in rat brain accumulate with age.", without any link to the corresponding journal article are useless. --174.115.226.233 (talk) 17:40, 14 May 2013 (UTC)[reply]

I have found that citations like that often are copypasted directly from articles - and constitute copyviolation... Lova Falk talk 11:11, 29 May 2013 (UTC)[reply]

Mutation Theory of Aging

Given its recent boost in support by "Somatic mutation rates scale with lifespan across mammals" (Nature), it seems that maybe a separate Wikipedia page on the mutation theory of aging might be in order. — Preceding unsigned comment added by Tedtoal (talk • contribs) 00:08, 24 April 2022 (UTC)[reply]

MEDRS

did a few edits however this is going to need considerable time, perhaps early next week and lots of [1]--Ozzie10aaaa (talk) 18:15, 7 July 2017 (UTC)[reply]

Yeah, there's a lot to be done here. I start by flagging the problem sources. Pubmed's "cited by", filtered by "review" offers a later look at the specific topics. Sometimes it turns up something usable. LeadSongDog come howl! 19:41, 11 July 2017 (UTC)[reply]

Thsnks for your recommendation. I have added 5 secondary and one tertiary source so far, and plan to work on this further.Bernstein0275 (talk) 02:20, 15 July 2017 (UTC)[reply]

transcriptional changes in aging

This edit request by an editor with a conflict of interest was declined.

Another form of transcriptional changes in aging tissues is the increased transcriptional noise, a potentially universal, stochastic hallmark of ageing driven by damage accumulation. Studies on ageing cells have proposed that age-related transcriptional dysregulation in the form of cell-to-cell variability may introduce phenotypic variation among cells that could generally become detrimental to normal tissue function. Such increased transcriptional variability was found first in a selected panel of genes in heart cells ^[1] and, more recently, in the whole transcriptomes of immune cells,^[2] human pancreas cells ^[3] and more. However, in some cell types this pattern is not found despite observations of genetic and epigenetic damage in ageing haematopoietic stem cells(HSCs) and another pattern of transcriptional dis-regulation appears,^[4] in terms of breakdown of gene to gene coordination, on the basis of the transcriptional interrelations between genes. As suggested by the authors, this finding may have translational relevance in the current explosion of new strategies for combating ageing. Practical ways to prevent or slow the relentless accumulation of stochastic damage in cells during ageing may be developed on the basis of measures such as GCL as biomarkers.^[5]

Reason for the change:

The science of aging and the effect of DNA damage on the transcription was a mystery for long time. For the first time a universal hallmark of aging in the transcription was found.

References supporting change:

^[6] Orrl (talk) 13:43, 20 September 2022 (UTC)[reply]

Not done for now: Please specify where and why you seek this change implemented. PK650 (talk) 10:05, 23 September 2022 (UTC)[reply]

References

^ Bahar, R. et al. Increased cell-to-cell variation in gene expression in ageing mouse heart. Nature 441, 1011–1014 (2006).
^ Martinez-Jimenez, C. P. et al. Aging increases cell-to-cell transcriptional variability upon immune stimulation. Science 355, 1433–1436 (2017).
^ Enge, M. et al. Single-cell analysis of human pancreas reveals transcriptional signature of aging and somatic mutation patterns. Cell 171, 321–330.e14 (2017).
^ Levy, Orr. "Age-related loss of gene-to-gene transcriptional coordination among single cells". Nature metabolism. Nature metabolism.
^ Vijg, Jan (2020). "Loss of gene coordination as a stochastic cause of ageing". Nature Metabolism. 2 (11): 1188–1189. doi:10.1038/s42255-020-00295-2. PMID 33139958. S2CID 226244292.
^ Vijg, Jan (2020). "Loss of gene coordination as a stochastic cause of ageing". Nature Metabolism. 2 (11): 1188–1189. doi:10.1038/s42255-020-00295-2. PMID 33139958. S2CID 226244292.

[Bahar,_R._et_al._Increased_cell-to-cell_variation_in_gene_expression_in_ageing_mouse_heart._Nature_441,_1011–1014_(2006).-1] Bahar, R. et al. Increased cell-to-cell variation in gene expression in ageing mouse heart. Nature 441, 1011–1014 (2006).

[Martinez-Jimenez,_C._P._et_al._Aging_increases_cell-to-cell_transcriptional_variability_upon_immune_stimulation._Science_355,_1433–1436_(2017).-2] Martinez-Jimenez, C. P. et al. Aging increases cell-to-cell transcriptional variability upon immune stimulation. Science 355, 1433–1436 (2017).

[Enge,_M._et_al._Single-cell_analysis_of_human_pancreas_reveals_transcriptional_signature_of_aging_and_somatic_mutation_patterns._Cell_171,_321–330.e14_(2017).-3] Enge, M. et al. Single-cell analysis of human pancreas reveals transcriptional signature of aging and somatic mutation patterns. Cell 171, 321–330.e14 (2017).

[4] Levy, Orr. "Age-related loss of gene-to-gene transcriptional coordination among single cells". Nature metabolism. Nature metabolism.

[5] Vijg, Jan (2020). "Loss of gene coordination as a stochastic cause of ageing". Nature Metabolism. 2 (11): 1188–1189. doi:10.1038/s42255-020-00295-2. PMID 33139958. S2CID 226244292.

[6] Vijg, Jan (2020). "Loss of gene coordination as a stochastic cause of ageing". Nature Metabolism. 2 (11): 1188–1189. doi:10.1038/s42255-020-00295-2. PMID 33139958. S2CID 226244292.

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