Radiosensitivity in Alzheimer Disease and Parkinson Disease

Robbins, Jay H.; Otsuka, Fujio; Re, Tarone; Polinsky, R. J.; Brumback, R. A.; Moshell, A N; Nee, L. E.; Ganges, MaryB.; Cayeux, SophieJ.

doi:10.1016/s0140-6736(83)91461-7

Cited by 55 publications

(14 citation statements)

References 13 publications

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“…It is probable that excessive ODLs are present in most of the nuclear genes after FCIR despite of a functioning repair mechanism in normal animals. The conditions resemble the presence of excessive ODLs, due to disease conditions [29], or repair deficit in humans [31,[34][35][36][37]. Therefore, transcription of immediately early genes with ODLs immediately during cerebral oxidative stress gives rise to aberrant or variant mRNA.…”

Section: Resultsmentioning

confidence: 99%

Neuronal NOS inhibitor that reduces oxidative DNA lesions and neuronal sensitivity increases the expression of intact c-fos transcripts after brain injury

Cui

Liu

2001

J Biomed Sci

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In response to oxidative stress, the ischemic brain induces immediate early genes when its nuclear genes contain gene damage. Antioxidant that reduces gene damage also reduces cell death. To study the mechanism of neuronal sensitivity, we investigated the transcription of the c-fos gene after brain injury of the ischemia-reperfusion type using focal cerebral ischemia-reperfusion in Long-Evans hooded rats. We observed a significant (p < 0.01) increase in c-fos mRNA in the ischemic cortex immediately after brain injury. However, the c-fos transcript was sensitive to RNase A protection assay (RPA) upon reperfusion. The transcript became significantly resistant to RPA (42%, p < 0.03) when 3-bromo-7-nitroindazole (25 mg/kg, i.p.), known to abolish nitric oxide, gene damage and neuronal sensitivity, was injected. Our data suggest that neuronal nitric oxide synthase and aberrant mRNA from genes with oxidative damage could be associated with neuronal sensitivity.

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Section: Resultsmentioning

confidence: 99%

Neuronal NOS inhibitor that reduces oxidative DNA lesions and neuronal sensitivity increases the expression of intact c-fos transcripts after brain injury

Cui

Liu

2001

J Biomed Sci

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“…Indeed, while ELF-MF exposure does not affect the repair system of DNA in mammalian cells which have suffered from gamma ray irradiation (Cossarizza et al 1989), exposure at 5 Gy to 60Co radiation (Frazier et al 1990) or oxidative injury (Cantoni et al 1995), other in vitro and in vivo studies have given both contradictory and inconclusive results (for a review, see Vijayalaxmi and Obe 2005). Possible negative effects on the quality of DNA repair are of great interest because a miss-repair of DNA breakage could be another of the multiple molecular events which accumulate sequentially and may result in cancer promotion and/or copromotion (Wertheimer and Leeper 1979, Juutilainen et al 1990, Wrensch et al 1993, Loomis et al 1994, Hardell et al 1995, Kheifets et al 2005, Klaeboe et al 2005, Savitz and Loomis 1995, Forssen et al 2006, in Alzheimer's (Jones et al 1989, Mullaart et al 1990, Robbins et al 1983), Huntington's (Bridges 1981, Scudiero et al 1981, and Parkinson's disease (Robbins et al 1983).…”

Section: Discussionmentioning

confidence: 99%

Brain DNA damage and 70-kDa heat shock protein expression in CD1 mice exposed to extremely low frequency magnetic fields

Mariucci¹,

Villarini²,

Moretti³

et al. 2010

International Journal of Radiation Biology

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“…(2) Increased tendency of patients with sporadic neurodegenerative diseases to somatic mutations in general A generalized tendency to develop somatic mutations might be detectable in other tissues, perhaps even blood. Studies of DNA damage in response to UV radiation in lymphoblasts showed that PD and AD-derived lines, but not ALS, were more sensitive than controls [94,95]. Micronuclei, nuclear structures where chromothripsis may occur [96], were found more often in peripheral blood leucocytes (PBL) from PD and AD than controls [97].…”

Section: Rationale For a Role Of Somatic Mutations In Neurodegenerationmentioning

confidence: 99%

Review: Somatic mutations in neurodegeneration

Leija‐Salazar

Piette

Proukakis

2018

Neuropathology Appl Neurobio

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Somatic mutations are postzygotic mutations which may lead to mosaicism, the presence of cells with genetic differences in an organism. Their role in cancer is well established, but detailed investigation in health and other diseases has only been recently possible. This has been empowered by the improvements of sequencing techniques, including single‐cell sequencing, which can still be error‐prone but is rapidly improving. Mosaicism appears relatively common in the human body, including the normal brain, probably arising in early development, but also potentially during ageing. In this review, we first discuss theoretical considerations and current evidence relevant to somatic mutations in the brain. We present a framework to explain how they may be integrated with current views on neurodegeneration, focusing mainly on sporadic late‐onset neurodegenerative diseases (Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis). We review the relevant studies so far, with the first evidence emerging in Alzheimer's in particular. We also discuss the role of mosaicism in inherited neurodegenerative disorders, particularly somatic instability of tandem repeats. We summarize existing views and data to present a model whereby the time of origin and spatial distribution of relevant somatic mutations, combined with any additional risk factors, may partly determine the development and onset age of sporadic neurodegenerative diseases.

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Radiosensitivity in Alzheimer Disease and Parkinson Disease

Cited by 55 publications

References 13 publications

Neuronal NOS inhibitor that reduces oxidative DNA lesions and neuronal sensitivity increases the expression of intact c-fos transcripts after brain injury

Neuronal NOS inhibitor that reduces oxidative DNA lesions and neuronal sensitivity increases the expression of intact c-fos transcripts after brain injury

Brain DNA damage and 70-kDa heat shock protein expression in CD1 mice exposed to extremely low frequency magnetic fields

Review: Somatic mutations in neurodegeneration

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