Reference: Annals of the ICRP. — Oxford: Pergamon Press, 1986. — 43 p.
URL: http://www.icrp.org/publication.asp?id=ICRP%20Publication%2049
Author: Hunt W.A.
Reference: Military radiobiology / J.J. Conklin, R.I. Walker (Eds.). — San Diego: Academic Press, Inc., 1987. — P. 321–330.
Author: S. Mizumatsu, M.L. Monje, D.R. Morhardt et al.
Reference: Cancer Res. ― 2003. ― Vol. 63, № 14. ― P. 4021–4027.
Keywords: cognitive impairment, subgranular zone, hippocampal dentate gyrus, X-ray
Abstract: Therapeutic irradiation of the brain is associated with a number of adverse effects, including cognitive impairment. Although the pathogenesis of radiation-induced cognitive injury is unknown, it may involve loss of neural precursor cells from the subgranular zone (SGZ) of the hippocampal dentate gyrus and alterations in new cell production (neurogenesis). Young adult male C57BL mice received whole brain irradiation, and 6-48 h later, hippocampal tissue was assessed using immunohistochemistry for detection of apoptosis and numbers of proliferating cells and immature neurons. Apoptosis peaked 12 h after irradiation, and its extent was dose dependent. Forty-eight h after irradiation, proliferating SGZ cells were reduced by 93-96%; immature neurons were decreased from 40 to 60% in a dose-dependent fashion. To determine whether acute cell sensitivity translated into long-term changes, we quantified neurogenesis 2 months after irradiation with 0, 2, 5, or 10 Gy. Multiple injections of BrdUrd were given to label proliferating cells, and 3 weeks later, confocal microscopy was used to determine the percentage of BrdUrd-labeled cells that showed mature cell phenotypes. The production of new neurons was significantly reduced by X-rays; that change was dose dependent. In contrast, there were no apparent effects on the production of new astrocytes or oligodendrocytes. Measures of activated microglia indicated that changes in neurogenesis were associated with a significant inflammatory response. Given the known effects of radiation on cognitive function and the relationship between hippocampal neurogenesis and associated memory formation, our data suggest that precursor cell radiation response and altered neurogenesis may play a contributory if not causative role in radiation-induced cognitive impairment.
Author: P. Hall, H.O. Adami, D. Trichopoulos et al.
Reference: BMJ. ― 2004. ― Vol. 328, № 7430. ― P. 19–24.
Keywords: cognitive function, Sweden, learning ability, spatial recognition, infancy
Abstract:
OBJECTIVE:To determine whether exposure to low doses of ionising radiation in infancy affects cognitive function in adulthood.
DESIGN: Population based cohort study.
SETTING: Sweden.
PARTICIPANTS: 3094 men who had received radiation for cutaneous haemangioma before age 18 months during 1930-59.
MAIN OUTCOME MEASURES: Radiation dose to frontal and posterior parts of the brain, and association between dose and intellectual capacity at age 18 or 19 years based on cognitive tests (learning ability, logical reasoning, spatial recognition) and high school attendance.
RESULTS: The proportion of boys who attended high school decreased with increasing doses of radiation to both the frontal and the posterior parts of the brain from about 32% among those not exposed to around 17% in those who received > 250 mGy. For the frontal dose, the multivariate odds ratio was 0.47 (95% confidence interval 0.26 to 0.85, P for trend 0.0003) and for the posterior dose it was 0.59 (0.23 to 1.47, 0.0005). A negative dose-response relation was also evident for the three cognitive tests for learning ability and logical reasoning but not for the test of spatial recognition.
CONCLUSIONS: Low doses of ionising radiation to the brain in infancy influence cognitive abilities in adulthood.
Author: M. Yamada, F. Kasagi, H. Sasaki et al.
Reference: J. Am. Geriatr. Soc. — 2003. — Vol. 51, № 3. — P. 410–414.
Keywords: vascular dementia, Alzheimer’s disease, Hiroshima
Abstract: OBJECTIVES: To investigate the association between midlife risk factors and the development of vascular dementia (VaD) or Alzheimer’s disease (AD) 25 to 30 years later.
DESIGN: A prevalence study within a longitudinal cohort study.
SETTING: Subjects in the Adult Health Study (a prospective cohort study begun in 1958) have been followed through biennial medical examinations in Hiroshima, Japan.
PARTICIPANTS: One thousand seven hundred seventy-four subjects in Hiroshima, Japan born before September 1932 (1,660 with no dementia, 114 with dementia (51 with AD, and 38 with VaD) diagnosed from 1992 to 1997 according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria).
MEASUREMENTS: The subjects were examined for effect on dementia of sex, age, education, atomic bomb radiation dose, and midlife factors associated with risk (smoking, alcohol intake, physical activity, dietary habits, systolic blood pressure (SBP), body mass index, and history of diabetes mellitus) that had been evaluated in 1965-1970.
RESULTS: VaD prevalence increased significantly with age, higher SBP, and lower milk intake. The odds ratios of VaD for age (in 5-year increments), SBP (10 mmHg increments), and milk intake (almost daily/less than four times a week) were 1.29, 1.33, and 0.35, respectively. The risk factors for VaD were compatible with the risk factors for stroke in this study population. AD prevalence increased significantly with age and lower education. Other midlife factors and radiation dose did not show any significant association with VaD or AD.
CONCLUSION: Increased SBP and low milk intake in midlife were associated with VaD detected 25 to 30 years later. Early behavioral control of the risk factors for vascular disease might reduce the risk of dementia.
URL: http://hnb.tokushukai.jp/contents/risk-factors-for-dementia/abstract/93
Author: Anderson N.E.
Reference: Curr. Opin. Neurol. — 2003. — Vol. 16, № 6. — P. 677–683.
Keywords: childhood brain tumour, Cognitive complication, endocrine dysfunction
Abstract:
PURPOSE OF REVIEW: As the treatment of childhood brain tumours has improved, long-term survival has become more common. Cognitive, physical and psychological complications of the tumour and its treatment have been recognized more frequently in long-term survivors. This review highlights new studies on the cognitive and endocrine complications in survivors. Less-common late effects of treatment are also discussed.
RECENT FINDINGS: Cognitive abnormalities and endocrine dysfunction are the most common complications in long-term survivors. Radiotherapy is the main cause of cognitive dysfunction, but intrathecal methotrexate and surgery are contributory factors. New studies have provided information on the frequency of endocrine complications and risk factors for the development of endocrine disorders. Endocrine complications are uncommon when the tumour has been treated with surgery alone. The risk of developing endocrine dysfunction is increased by radiotherapy, and some studies suggest that chemotherapy has an additional deleterious effect. Primary hypothyroidism may be caused by scattered irradiation from spinal and cranial radiotherapy. Direct involvement of the hypothalamus by the tumour, and hypothalamic damage secondary to surgery or radiotherapy, may cause obesity. Hypothalamic tumours also may be associated with hypersomnolence and other features consistent with narcolepsy. The pathogenesis of hypersomnolence in these patients has not been resolved. Long-term childhood brain-tumour survivors are 40 times more likely to develop a stroke than sibling controls. Superficial siderosis of the central nervous system can develop many years after curative treatment of a cerebellar tumour, but effective treatment for this disorder is not yet available.
SUMMARY: An attempt to understand the factors that contribute to the long-term morbidity of childhood brain tumours can lead to changes in treatment that improve the quality of life in survivors. Prevention, early recognition and treatment of these complications are attainable goals.
M.K. Schindler, L. Wang, L.D. Selemon et al.
Author: F.S. Torubarov, V.V. Blagoveschenskaya, P.V. Chesalin, M.K. Nikolaev
Reference: Журн. невропатол. и психиатр. им. С.С. Корсакова (Journal of neuropathology and psychiatry named after S.S. Korsakov), 1989
Abstract: One of the very first reports on the subject. For details contact the publisher. Homepage of the publisher: http://www.mediasphera.ru/contacts/
Author: Zhavoronkova L. A., Lavrova T. P., Belostocky A. V., Kholodova N. B., Skoryatina I. G., Voronov V. P.
Reference: ЖУРНАЛ ВЫСШЕЙ НЕРВНОЙ ДЕЯТЕЛЬНОСТИ ИМ. И.П. ПАВЛОВА (Journal of higher nerbous activities named after I.P.Pavlov), 2006
Keywords: EEG, space-frequency parameter, cognitive performance
Abstract: Changes in frequency and space parameters of the EEG coherence evoked by cognitive performance were analyzed in 13 healthy subjects and participants of the Chernobyl clean-up. In healthy subjects, the EEG coherences in the alpha and beta frequency bands were significantly increased during arithmetic count and during visuospatial performance. Each test was characterized by regionally-specific features. Chernobyl patients demonstrated a global decrease in the EEG coherence predominantly in the alpha and beta frequency bands, especially in the frontal cortical areas. Patients with various pathological EEG patterns demonstrated specific impairment of EEG parameters. In patients with a “flat” EEG pattern, the EEG coherence predominantly decreased in the frontal associative areas, especially during arithmetic calculation. In patients with a “hypersynchronous” EEG pattern, the decrease in the EEG coherence was most pronounced in the parietal associative areas, especially during the visuospatial performance. The revealed impairments of the EEG coherence reactivity may be a reflection of disorders of the intracortical and corti-cosubcortical interaction and can result from the remote postradiation brain atrophy, especially, of cortical structures.
Author: A.I. Nyagu, K.N. Loganovsky, N.Yu. Chuprovskaya et al.
Reference: Український медичний часопис (Ukrainian Medical Magazine), 1997
Abstract: For detail contact the publisher:
Publisher: «МОРИОН»
address: 02140, Kiev, prosp. Bazhana 10A
tel: 380(44)585-97-10