Low dose of carbon ion irradiation induces early delayed cognitive impairments in mice

Сорокина, С. С.; Malkov, Anton; Shubina, Liubov; Заичкина, С. И.; Pikalov, V. A.

doi:10.1007/s00411-020-00889-0

Cited by 4 publications

(5 citation statements)

References 57 publications

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“…Fractionated LDR induced sustained inflammatory responses, marked by heightened activity of microglia and astrocytes, especially in the juvenile hippocampus in the initial months after LDR [83]. SHK mice showed emotional and cognitive impairments, along with neuronal damage, 2 months after LDR exposure [64]. Mice with a mutation in the excision repair cross-complementing rodent repair deficiency, complementation group 2 (ERCC2) DNA repair gene and exposed to X-ray exhibited behavioral and molecular changes at various intervals, including 4, 12, and 18 months post-exposure [53].…”

Section: Long-term Toxicity Of Ldrmentioning

confidence: 97%

“…Previous research involving rodents has demonstrated that low-dose exposure to charged particles below 1 Gy can lead to behavioral impairments associated with disruptions in brain regions, especially the hippocampus [64,[66][67][68][69]76,78,79,82]. Specifically, proton irradiation at doses of 0.1 and 1 Gy [82] results in dose-dependent reductions in dendritic complexity and spines in the dentate gyrus.…”

Section: Long-term Toxicity Of Ldrmentioning

confidence: 99%

“…Other observations include spatial memory deficits following 48 Ti-particle irradiation (5 cGy) [68], impaired attentional set-shifting due to 28 Si-particle exposure (5 cGy) [69], and hippocampal anomalies, disrupted fear memory, anxiety, and diminished new neuron survival in males as a result of 28 Si-particle irradiation (0.2 and 1 Gy) [79]. Additionally, accelerated carbon ion exposure (0.7 Gy) induces anxiety, impaired memory retention, and a reduction in dorsal hippocampal cells two months postirradiation [64]. Considering that ion beams in radiotherapy possess an increased relative biological effectiveness (RBE), which is influenced by ion type, energy level, and Abbreviations: AD, Alzheimer's disease; Aβ, amyloid β; APBB1, amyloid beta precursor protein binding family B member 1; APP, amyloid precursor protein; CREB, cAMP Response Element-Binding Protein; CCR2, CC motif chemokine receptor 2; ED, embryonic day; ERCC2, excision repair cross-complementing rodent repair deficiency, complementation group 2; fEPSP, field excitatory postsynaptic potential; IR, irradiation; KO, knockout; LDR, low-dose radiation; LTP, long-term potentiation; LRP1, LDL receptor-related protein 1; NMRI, Naval Medical Research Institute; PND, postnatal day; PSD95, postsynaptic density 95; Rac1, Rac Family Small GTPase 1; Rac2, Rac Family Small GTPase 2; Tg, transgenic.…”

Section: Long-term Toxicity Of Ldrmentioning

confidence: 99%

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Low-Dose Radiation Therapy for Neurological Disorders: A Double-Edged Sword

Weerasinghe-Mudiyanselage,

Kim,

Kang

et al. 2024

Discovery Medicine

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Radiation therapy targeting the central nervous system is widely utilized for the management of various brain tumors, significantly prolonging patient survival. Presently, investigations are assessing both clinical and preclinical applications of low-dose radiation (LDR) for the treatment of neuropathological conditions beyond tumor therapy. Special focus is given to refractory neurodegenerative diseases linked to neuroinflammation, such as Alzheimer's and Parkinson's diseases, where LDR has shown promising results. This comprehensive review examines the existing experimental data regarding the utilization of LDR in neurological disorders. It covers potential advantages in reducing neurodegenerative alterations and inflammation, as well as possible adverse effects, including neurological impairments. The review underscores the importance of the exposure protocol and the age at which LDR is administered in the context of the nervous system's pathological and physiological states, as these elements are crucial in determining LDR's therapeutic and toxic outcomes. The article concludes with a discussion on the future directions and challenges in optimizing LDR use, aiming to reduce toxicity while effectively managing neurological disorders.

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Section: Long-term Toxicity Of Ldrmentioning

confidence: 97%

Section: Long-term Toxicity Of Ldrmentioning

confidence: 99%

Section: Long-term Toxicity Of Ldrmentioning

confidence: 99%

See 1 more Smart Citation

Low-Dose Radiation Therapy for Neurological Disorders: A Double-Edged Sword

Weerasinghe-Mudiyanselage,

Kim,

Kang

et al. 2024

Discovery Medicine

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“…To assess general activity and anxiety levels, spatial learning, and short-and long-term hippocampus-dependent memory 2 months after exposure, an open eld test, a Barnes maze, and a novel object recognition test were used, which were accompanied by automatic video-tracking of mice using custom software. The procedure for conducting behavioral tests was previously described in detail in our paper (Sorokina et al 2021).…”

Section: Behavioral Testsmentioning

confidence: 99%

“…No pathological cells were found in the irradiated and control groups. Thus, total irradiation with a low dose of carbon ions at this stage may result in a cognitive de cit in mice with no signs of pathological neurodegenerative changes (Sorokina et al 2021). Literature data on the effect of proton irradiation in a therapeutic dose range on cognitive abilities of laboratory animals and their relation to morphological changes in the brain, particularly to the response of microglia to irradiation, are rather contradictory as far as the studies differ in the characteristics of the irradiation used, doses, duration, methods of observation, and animal models (Kiffer et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Behavioral performance and microglial status in mice after moderate dose of proton irradiation

Sorokina,

Malkov,

Rozanova

et al. 2023

Radiat Environ Biophys

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The cognitive impairment is a remote effect of gamma radiation treatment of malignancies. The major part of the studies on the effect of proton irradiation (a promising alternative in the treatment of radioresistant tumors and tumors located close to critical organs) on the cognitive abilities of laboratory animals and their relation to morphological changes in the brain is rather contradictory. The aim of this study was to investigate cognitive functions and the dynamics of changes in morphological parameters of hippocampal microglial cells after proton irradiation. Two months after the cranial irradiation, 8-9-week-old male SHK mice were tested for total activity, spatial learning, as well as long-and short-term hippocampusdependent memory. To estimate the morphological parameters of microglia, the brain slices of control and irradiated animals each with different time after proton irradiation (24 h, 7 days, 1 month) were stained for microglial marker Iba-1. No changes in behavior or de cits in short-term and long-term hippocampus-dependent memory were found, but the impairment of episodic memory was observed. A change in the morphology of hippocampal microglial cells, which is characteristic of the transition of cells to an activated state, was detected. Radiation-induced oxidative stress into the brain tissue of mice one day after exposure resulted in a slight decrease in cell density, which was restored to the control level by 30 days after exposure, probably due to the activation of proliferation. The results obtained may be promising with regard to the future use of using high doses of protons per fraction in the irradiation of tumors.

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