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Vascular dementia in Spatz-Lindenberg's disease (SLD): cortical synaptophysin immunoreactivity as compared with dementia of Alzheimer type and non-demented controls

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Summary

The generalized form of von Winiwarter-Buerger's disease (WBD) occasionally involves the brain. However, pure cerebral forms of the disease were also described by Spatz and Lindenberg (“Spatz-Lindenberg's disease”, SLD). Both, the type I, which involves the large basal arteries, and the type II, which results in a sickle-shaped granular atrophy of the cerebral cortex, are often accompanied by (“vascular”) dementia, which Lindenberg and Spatz mainly attributed to the bilateral involvement of the second frontal gyrus by granular atrophy. Recently, synaptic deprivation of the cortical gray matter has been shown to occur in the dementia of Alzheimer type (DAT) and other neurodegenerative disorders. In DAT, the synaptic loss highly correlated with the degree of the mental impairment. We wanted to examine whether similar changes also occurred in dementia of vascular origin, for which SLD, although infrequent, is a typical example. In fact, we found that in three cases of typical SLD type II the synaptophysin immunoreactivity of the cortical neuropil in areas without overt infarcts or scar formation was as much reduced as in Alzheimer's disease. Although it must be taken into account that in the present cases the synapse loss might, at least in part, be due to secondary (Wallerian) degeneration as a result of the neuronal loss in the “watershed” regions of the arterial blood supply, it cannot be excluded that a decline of cortical synaptic contacts in areas without necroses or scars may occur as a primary event, contributing to the pathogenesis of the dementia. Final conclusions can only be expected from investigations into further cases of cerebro-vascular disorders with and without dementia.

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References

  1. Berlit P, Kessler C, Krause K-H (1984) New aspects of thromboangiitis obliterans (von Winiwarter-Buerger disease). Eur Neurol 23:394–399

    Google Scholar 

  2. Bruetsch WL (1971) Cerebral thromboangiitis obliterans. In: Minckler J (ed) Pathology of the nervous system, vol 2. McGraw-Hill, New York, pp 1449–1456

    Google Scholar 

  3. Buerger L (1924) The circulatory disturbances of the extremities. WB Saunders, Philadelphia

    Google Scholar 

  4. Doerr W (1970) Entzündliche Erkrankungen der Gefäßwände. In: Altmann HW, Büchner F, Cottier H et al (eds) Handbuch der allgemeinen Pathologie, vol 3/4. Springer, Berlin, pp 620–658

    Google Scholar 

  5. Eicke WJ (1957) Die Endangiitis obliterans der Hirngefäße. In: Lubarsch O, Henke F, Rössle R (eds) Handbuch der speziellen pathologischen Anatomie und Histologie, vol 13/1B. Springer Verlag, Berlin Göttingen Heidelberg, pp 1536–1562

    Google Scholar 

  6. Engelmann U, Scheppelmann D, Mainzer HP (1989) DIPSY-Bildverarbeitung auf dem PC. MBI Technical Report, no. 21. German Cancer Research Center, Heidelberg

    Google Scholar 

  7. Fahey JM, Hedayat B, Cook JR, Isaacson RL, van Buskirk RG (1989) Nimodipine's ability to inhibit neuronal death due to oxygen deprivation or exposure to methylmercury and its effects on differentiation. In: Traber J, Gispen WH (eds) Nimodipine and central nervous system function. New vistas. Schattauer, Stuttgart, pp 117–140

    Google Scholar 

  8. Fisher CM (1957) Cerebral thromboangiitis. Medicine (Baltimore) 36:169–209

    Google Scholar 

  9. Hermann WM, Stephan K (1991) Wirksamkeit und therapeutische Relevanz von Nimodopine bei primär-degenerativer Demenz und Multiinfarkt-Demenz. In: Möller H-J (ed) Hirnleistungsstörungen im Alter. Springer Verlag, Berlin Heidelberg New York Tokyo, pp 81–93

    Google Scholar 

  10. Jellinger K (1968) Morphologische Aspekte der zerebrovaskulären Insuffizienz. Wien Med Wochenschr 40:829–837

    Google Scholar 

  11. Jellinger K (1971) Die sogenannte cerebrale Form der Endangiitis obliterans. Nervenarzt 42:397–401

    Google Scholar 

  12. Kitagawa K, Matsumoto M, Sobue K, Tagaya M, Okabe T, Niinobe M, Ohtsuki T, Nanda N, Kimura K, Mikoshiba K, Kamada T (1992) The synapsin I brain distribution in ischemia. Neuroscience 46:287–299

    Google Scholar 

  13. Kriegelstein J, Karkoutly Ch, Seifel Nasr M, Nuglisch J (1989) Ischemic brain damage and the role of calcium. In: Traber J, Gispen WH (eds) Nimodipine and central nervous system function. New Vistas. Schattauer, Stuttgart, pp 101–108

    Google Scholar 

  14. Lassmann H, Weiler R, Fischer R, Bancher C, Jellinger K, Floor E, Danielczyk W, Seitelberger F, Winkler H (1992) Synaptic pathology in Alzheimer's disease: immunological data for markers of synaptic and large dense-core vesicles. Neuroscience 46:1–8

    Google Scholar 

  15. Lindenberg R, Spatz H (1940) Über die Thromboendarteriitis obliterans der Hirngefäße (cerebrale Form der v. Winiwarter-Buerger'schen Krankheit). Virchows Arch [A] 305:531–557

    Google Scholar 

  16. Masliah E, Tetry RD (1993) The role of synaptic proteins in the pathogenesis of disorders of the central nervous system. Brain Pathol 3:77–86

    Google Scholar 

  17. Masliah E, Terry RD, DeTeresa RM, Hansen LA (1989) Immunohistochemical quantification of the synapse-related protein synaptophysin in Alzheimer's disease. Neurosci Lett 103:234–239

    Google Scholar 

  18. Masliah E, Terry RD, Alford M, DeTheresa RM (1990) Quantitative immunohistochemistry of synaptophysin in human neocortex: an alternative method to estimate density of presynaptic terminals in paraffin sections. J Histochem Cytochem 38:837–844

    Google Scholar 

  19. Noetzel H, Theodossiou A (1957) Beitrag zur Morphologie und Pathogenese der generalisierten Endarteriitis obliterans. Beitr Pathol Anat Allg Pathol 117:109–132

    Google Scholar 

  20. Nyakas C, Markel E, Kramers RJK, Gáspár E, Bohus B, Luiten PGM (1989) Effects of nimodipine on hypoxia-induced learning and memory deficits. In: Traber J, Gispen WH (eds) Nimodipine and central nervous system function. New vistas. Schattauer, Stuttgart, pp 175–194

    Google Scholar 

  21. Perdahl E, Adolfsson R, Alafuzoff I, Albert KA, Nestler EJ, Greengard P, Winblad B (1984) Synapsin I (protein I) in different brain regions in senile dementia of Alzheimer type and in multiinfarct dementia. J Neural Transm 60:133–141

    Google Scholar 

  22. Quandt J, Sommer H (1969) Die zerebrale Form der Endangiitis obliterans. In: Quandt J (ed) Die zerebrale Durchblutungsstörungen des Erwachsenenalters, 2nd edn. Schattauer, Stuttgart, pp 735–752

    Google Scholar 

  23. Simpson GG, Roe A, Lewontin RC (1960) Quantitative Zoology. Harcourt Brace & World, New York, p 273

    Google Scholar 

  24. Spatz H (1935) Über die Beteiligung des Gehirns bei der v. Winiwarter-Buerger'schen Krankheit (Thromboendangiitis obliterans). Dtsch Z Nervenheilkd 136:86–132

    Google Scholar 

  25. Spector PC, Goodnight JH, Sall JP, Sarl WS (1985) The GLM procedure. In: SASR User's Guide: statistics, 5th edn. SAS Institute Inc, Cary, N.C. pp 433–506

    Google Scholar 

  26. Sporel-Özakat E, Edwards PM, Gerritsen van der Hoop R, Gispen WH (1989) Nimodipine and neural plasticity. In: Traber J, Gispen WH (eds) Nimodipine in central nervous system function. New Vistas. Schattauer, Stuttgart, pp 71–85

    Google Scholar 

  27. Terry RD, Masliah E, Salmon DP, Butters N, DeTheresa R, Hill R, Hansen LA, Katzman R (1991) Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol 30:572–580

    Google Scholar 

  28. Torvik A, Jörgensen L (1966) Thrombotic and embolic occlusions of the carotid arteries in an autopsy Series. 2. Cerebral lesions and clinical course. J Neurol Sci 3:410–432

    Google Scholar 

  29. Ule G, Kolkmann FW (1972) Generalisierende und nekrotisierende Arteriitiden. Die Endarteriitis obliterans von Winiwarter-Bürger. In: Gänshirt H (ed) Der Hirnkreislauf. Thieme, Stuttgart, pp 109–113

    Google Scholar 

  30. Walton JN (1977), Buerger's disease. In: Walton JN (ed) Brain's diseases of the nervous system, 8th edn. Oxford University Press, Oxford, p376

    Google Scholar 

  31. Weibel ER (1979) Stereological methods. Practical methods for biological morphometry, vol 1. Academic Press, New York

    Google Scholar 

  32. Zhan SS, Beyreuther K, Schmitt HP (1993) Quantitative assessment of the synaptophysin immuno-reactivity of the corticalneuropil in various neurodegenerative disorders with dementia. Dementia 4:66–74

    Google Scholar 

  33. Zülch KJ (1969) Cerebral form of von Winiwarter-Buerger's disease: does it exist? Angiology 20:61–69

    Google Scholar 

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Zhan, S.S., Beyreuther, K. & Schmitt, H.P. Vascular dementia in Spatz-Lindenberg's disease (SLD): cortical synaptophysin immunoreactivity as compared with dementia of Alzheimer type and non-demented controls. Acta Neuropathol 86, 259–264 (1993). https://doi.org/10.1007/BF00304140

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