ReviewPhysiological research2023
Mitochondria in human reproduction: novel paradigm in the onset of neurodegenerative disorders.
Review in Physiological research, 2023. 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, 2 citations in OpenAlex.
- Abundance of Maternal Mitochondrial Genome Is Dispensable up to the Mitochondrial Genome Activation in Post-Implantation Embryos.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Age, Race, and Ethnicity of Maternal Grandparents in Autism Spectrum Disorder, a California Multigenerational Study.Autism research : official journal of the International Society for Autism Research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The disease progression of neurodegenerative disorders (NDD), including Alzheimer's, Parkinson's and Huntington's disease, is inextricably tied to mitochondrial dysfunction. However, although the contribution by nuclear gene mutations is recognised for familial onset of NDD, the degree to which cytoplasmic inheritance serves as a predetermining factor for the predisposition and onset of NDD is not yet fully understood. We review the reproductive mechanisms responsible for ensuring a healthy mitochondrial population within each new generation and elucidate how advanced maternal age can constitute an increased risk for the onset of NDD in the offspring, through the increased heteroplasmic burden. On the one hand, this review draws attention to how assisted reproductive technologies (ART) can impair mitochondrial fitness in offspring. On the other hand, we consider qualified ART approaches as a significant tool for the prevention of NDD pathogenesis.
Indexed as
Identifiers
37159849PMC10226399W4367853545What 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.