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Alzheimer’s disease and normal aging: Neurophysiological and immunological aspects

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Abstract

We studied in humans the characteristics of brain visual evoked potentials (EP) elicited by presentation of a reverse chess-board patterns and also the following parameters of the immune status: the numbers of T- and B-lymphocytes, immunoglobulin levels in blood plasma, and level of sensibilization of lymphocytes to the brain antigen. Two groups were examined: aged persons (up to 65 years) with normal course of aging (the control group) and patients of the same age suffering from Alzheimer’s disease (AD). In the latter group, lower amplitudes of early and late EP components (P300, in particular) and longer peak latencies of late components were observed. The development of AD correlates with a drop in the number of lymphocytes, increased IgA level, and sensibilization of lymphocytes to brain antigen, which is indicative of an immunodeficit state and the development of an autoimmune process; the latter phenomena can be significant factors responsible for neuronal death.

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References

  1. N. F. Shakhmatov,Mental Aging: Happy vs Pathologica [in Russian], Meditsina, Moscow (1996).

    Google Scholar 

  2. V. N. Kazakov, B. B. Ivnev, P. Ya. Kravtsov, and A. G. Snegir’, “Alzheimer’s disease. The current state of the problem,”Arkh. Klin. Éksp. Med.,7, No. 1, 101–105 (1998).

    Google Scholar 

  3. V. V. Gnezditskii,Evoked Brain Potentials in Clinical Practice [in Russian], Publishing House of the Taganrog State Univ. of Radiotechniques, Taganrog (1997).

    Google Scholar 

  4. J. Thome, W. Gsell, M. Russler, et al., “Oxidative stress-associated parameters (lactoferrin, superoxide dismutases) in serum of patients with Alzheimer’s disease,”Life Sci.,60, No. 1, 9–13 (1997).

    Google Scholar 

  5. L. V. Androsova, T. V. Sekirina, N. D. Selezneva, et al., “Changes of the immulogical parameters in Alzheimer’s disease: connection with the gravity of disease,”Zh. Nevropatol. Psikhiat.,95, No. 1, 24–27 (1995).

    CAS  Google Scholar 

  6. L. Lahad, P. Poorkaj, K. Wang, et al., “Genomic structure and expression of STM2, the chromosome 1 familial Alzheimer disease gene,”Genomics,34, No. 2, 198–204 (1996).

    Article  Google Scholar 

  7. C. Gottfries, “Neurochemical aspects of dementia disorders,”Dementia,1, No. 1, 54–64 (1990).

    Google Scholar 

  8. P. Kravtsov, S. Sherbakov, A. Snegyr’, and B. Ivnev, “Some leatures of evoked brain potentials and neuropsychological characteristics of patients with various types of dementia,”Eur. J. Physiol.,430, No. 4, 32 (1995).

    Google Scholar 

  9. E. Pekkonen, V. Jousmaki, M. Kononen, et al., “Auditory sensory memory impairment in Alzheimer’s disease: an event-related potential study,”NeuroReport,5, No. 18, 2537–2540 (1994).

    Article  PubMed  CAS  Google Scholar 

  10. E. Sloan, G. Fenton, N. Kennedy, and J. Maclennan, “Neurophysiology and SPECT cerebral blood flow patterns in dementia,”Electroencephalogr. Clin. Neurophysiol.,93, No. 3, 163–170 (1991).

    Google Scholar 

  11. J. Bauer, M. Hull, and M. Berger, “Pathogenetic factors of Alzheimer’s disease,”Gerontol. Geriatr.,25, May, 155–159 (1995).

    Google Scholar 

  12. Clinical Immunology [in Russian], E. I. Sokolov (ed.), Meditsina, Moscow (1998).

    Google Scholar 

  13. N. V. Ponomareva, V. F. Fokin, L. V. Androsova, and Zh. I. Kolyaskina, “Neuroimmune interactions in normal aging and Alzheimer’s disease,”Vestn. Russ. Acad. Med. Sci.

  14. L. O. Badalyan, S. A. Groppa, L. V. Koval’chuk, et al., “Some peculiarities of the immune status of patients with Alzheimer’s disease,”Zh. Nevropatol. Psikhiat.,93, No. 2, 31–34 (1993).

    Google Scholar 

  15. M. Mattson, Q. Guo, K. Furukawa, and W. Pedersen, “Presenilins, the endoplasmic reticulum and neuronal apoptosis in Alzheimer’s disease,”J. Neurochem.,70, No. 1, 1–14 (1998).

    Article  PubMed  CAS  Google Scholar 

  16. C. Cotman and J. Su, “Mechanisms of neuronal death in Alzheimer’s disease,”Brain Pathol.,6, No. 4, 493–506 (1996).

    PubMed  CAS  Google Scholar 

  17. J. Kusiak, J. Izzo, and B. Zhao, “Neurodegeneration in Alzheimer’s disease. Is apoptosis involved?”,Mol. Chem. Neuropathol.,28, No. 1, 153–162 (1996).

    Article  PubMed  CAS  Google Scholar 

  18. S. Prusiner, “The prion disease,”Brain Pathol.,8, No. 3, 499–513 (1998).

    Article  PubMed  CAS  Google Scholar 

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Ivnev, B.B. Alzheimer’s disease and normal aging: Neurophysiological and immunological aspects. Neurophysiology 31, 23–25 (1999). https://doi.org/10.1007/BF02515005

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