The minus of a plus is a minus. Mass death of selected neuron populations in sporadic late-onset neurodegenerative disease may be due to a combination of subtly decreased capacity to repair oxidative DNA damage and increased propensity for damage-related apoptosis

Petkova, Rumena; Chelenkova, Pavlina; Tournev, Ivaylo; Chakarov, Stoyan

doi:10.1080/13102818.2016.1179593

Cited by 2 publications

(2 citation statements)

References 136 publications

(111 reference statements)

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“…Indeed, cells that are not expected to divide may not be subjected to the genome integrity checks that are routinely carried out in dividing cells and are, therefore, not likely to be assessed as too damaged to keep [14,15]. This mechanism seems to ensure neuronal lifespan roughly comparable to the lifespan of the organism, although some authors speculate that increased attrition of adult neurons secondary to oxidative damage and poor supply of replacement neurons from the neuronal stem cell niche may constitute an important component of the pathogenetic mechanism of late-onset neurodegenerative disease [16][17][18]. In any case, assessment of IR-inflicted damage may show very different results when carried out in radiosensitive and radioresistant types of cells and tissues.…”

Section: Individual Capacity For Dna Repairmentioning

confidence: 99%

Some problems and errors in cytogenetic biodosimetry

Mosse

Kilchevsky

Nikolova

et al. 2016

Biotechnology & Biotechnological Equipment

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Human radiosensitivity is a quantitative trait that is generally subject to binomial distribution. Individual radiosensitivity, however, may deviate significantly from the mean (by 2-3 standard deviations). Thus, the same dose of radiation may result in different levels of genotoxic damage (commonly measured as chromosome aberration rates) in different individuals. There is significant genetic component in individual radiosensitivity. It is related to carriership of variant alleles of various single-nucleotide polymorphisms (most of these in genes coding for proteins functioning in DNA damage identification and repair); carriership of a different number of alleles producing cumulative effects; amplification of gene copies coding for proteins responsible for radioresistance, mobile genetic elements and others. Among the other factors influencing individual radioresistance are: the radioadaptive response; the bystander effect; the levels of endogenous substances with radioprotective and antimutagenic properties and environmental factors such as lifestyle and diet, physical activity, psychoemotional state, hormonal state, certain drugs, infections and others. These factors may have radioprotective or sensibilizing effects. Apparently, there are too many factors that may significantly modulate the biological effects of ionizing radiation. Thus, conventional methodologies for biodosimetry (specifically, cytogenetic methods) may produce significant errors if personal traits that may affect radioresistance are not accounted for.

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Section: Individual Capacity For Dna Repairmentioning

confidence: 99%

Some problems and errors in cytogenetic biodosimetry

Mosse

Kilchevsky

Nikolova

et al. 2016

Biotechnology & Biotechnological Equipment

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“…Thus, individual variance in IRC may become more pronounced and/or may determine the susceptibility to common diseases and conditions in later age [35,36], the outcomes of therapies (especially those based on genotoxic effects such as anticancer and immunosuppressive therapies) and the risk for development of therapy-associated adverse effects [36,37]. IRC is a key determinant of the capacity for cell and tissue renewal and plays a major role in the risk for development of cancer and degenerative disease [37][38][39][40]. Studies of individual repair capacity are currently part of the rapidly expanding field of individualised (personalised) medicine, dedicated to tailoring of therapies to meet the needs of a particular patient, assessment of eligibility for specific types of therapy, prognostication of outcomes from different therapies and anticipation of potential adverse effects.…”

mentioning

confidence: 99%

Reproductive outcomes in pregnant women aged 35 or older: the role of individual repair capacity

Petkova¹,

Dimitrova²,

Zhelev³

et al. 2015

Biodiscovery

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Abbreviations: 8-OH-dG -8-hydroxydeoxyguanosine, AMA -advanced maternal age, AR -assisted reproduction, BER -base excision repair, CDC -US Centre for disease prevention and control, DIC -disseminated intravascular coagulation, DS -Down syndrome, HELLP -haemolysis/elevated liver enzymes/low platelets, ICSI -intracytoplasmic sperm injection, IRC -individual repair capacity, IUGR -intrauterine growth restriction, IUI -intrauterine insemination, IVF -in vitro fertilisation, LIF -leukaemia inhibitory factor, NER -nucleotide excision repair, PCOS -polycystic ovary syndrome, PIH -pregnancy-induced hypertension, ROS -reactive oxygen species, TTD -trichothiodystrophy, w.g. -weeks of gestation, WHO -World Health Organisation, XP -xeroderma pigmentosum. AbstractAt present, childbirth is being progressively postponed until later age. Women aged 35 or older may have to wait longer to conceive than younger women and are more likely to be referred to fertility evaluations, but in a significant proportion a spontaneous conception would be achieved in the timeframe typical of younger women. Pregnancies where mothers are ≥ 35 are associated with more risks for pregnancy loss, chromosomal disease, pregnancy-associated complications, prematurity and low birthweight. These concerns, however, are not uncommon in younger women as well. This puts forward the question whether advanced age per se is the underlying cause for the increased risk for adverse outcomes in older pregnant women, or whether there might be other factors that account for it but do not radically worsen the prospects for favourable outcomes. The individual risks associated with childbirth late in life may stem from maternal genetic background rather than being a simple function of age. There is plenty of preliminary evidence that individual capacity for identification and repair of DNA damage may constitute a major factor in female fertility and fecundity. Subtle deficiencies in the repair capacity may have little to no importance in younger pregnant women but may make a significant difference in older women. The outcomes of pregnancies in women >35 are largely dependent on the prepregnancy health status and the quality of antenatal care, and may not be dramatically different from outcomes in younger women.

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The minus of a plus is a minus. Mass death of selected neuron populations in sporadic late-onset neurodegenerative disease may be due to a combination of subtly decreased capacity to repair oxidative DNA damage and increased propensity for damage-related apoptosis

Cited by 2 publications

References 136 publications

Some problems and errors in cytogenetic biodosimetry

Some problems and errors in cytogenetic biodosimetry

Reproductive outcomes in pregnant women aged 35 or older: the role of individual repair capacity

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