ReviewBiogerontology2025
Analyzing different aging theories in the context of the brain: DNA damage, inflammation, redox imbalance, and neurodevelopment intertwine.
Review in Biogerontology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Aging is not a disease: an evolutionary and comparative biological reappraisal.Biogerontology · 2026Review
- Selective resilience in brain aging: challenging the scope of the disposable soma theory.Biogerontology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
The neuronal tissue is notable for its unique regulation of the immune system, response to DNA damage, endurance against reactive oxygen and nitrogen species, and control of inflammatory pathways. Here, I discuss some uniqueness of the brain's aging process in light of the free radical theory of aging, DNA-damage accumulation, inflammaging, and aging as a consequence of a programmed developmental process. Key points include (i) the resilience of the neuronal tissue to oxidative stress; (ii) the neuron's efficiency in repairing learning-induced DNA damage, even with fewer repair pathways than other cell types; (iii) TLR9 and NFκB at the intersection of memory and inflammation; (iv) RELA linking the skin-brain axis during development, DNA damage response, and pro-inflammatory control; (v) PARP1 at the crossroad of all discussed aging theories. Data points to a "burden threshold" where the beneficial regulations of distinct pathways shift toward neurotoxic activities.
Indexed as
Identifiers
40323483What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.