Abstract
OBJECTIVE—To test the hypothesis that as there is growing evidence that corpora amylacea, or amyloid bodies, in the CNS are derived primarily from neurons, it might be expected that their numbers in the spinal cord would decline with loss of neurons in motor neuron degeneration as they do in the retina on destruction of ganglion cells by glaucoma. METHODS—The numbers of corpora amylacea were counted in PAS stained transverse sections of the lumbar cord from 27 patients with motor neuron disease and 21 control subjects of similar age and sex mix. The numbers and sizes of corpora amylacea were determined both in the anterior horn grey matter and in the submeningeal white matter regions in each case. RESULTS—In both groups the total numbers in the white matter and submeningeal regions ranged from 160 to more than 5000/section and there was minimal significant difference between the two groups. No relation with age was found in this narrow age range. The mean diameters of the corpora amylacea were significantly less in the grey matter of both groups than in the submeningeal regions. However, their densities in the grey matter of the anterior horn were significantly reduced in the spinal cord sections in the motor neuron disease group, but only where few motor neurons remained. CONCLUSIONS—These findings support the view that corpora amylacea may arise from neurons, and suggest that that there may be two compartments, one mobile and one static, the second most likely remaining in the periphery of the spinal cord for prolonged periods.
Full Text
The Full Text of this article is available as a PDF (110.3 KB).
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
- Anzil A. P., Herrlinger H., Blinzinger K., Kronski D. Intraneuritic corpora amylacea. Demonstration in orbital cortex of elderly subjects by means of early postmortem brain sampling and electron microscopy. Virchows Arch A Pathol Anat Histol. 1974;364(4):297–301. doi: 10.1007/BF00432727. [DOI] [PubMed] [Google Scholar]
- Averback P., Langevin H. Corpora amylacea of the lumbar spinal cord and peripheral nervous system. Arch Neurol. 1978 Feb;35(2):95–96. doi: 10.1001/archneur.1978.00500260033008. [DOI] [PubMed] [Google Scholar]
- Cavanagh J. B., Gysbers M. F. Ultrastructural changes in axons caused by acrylamide above a nerve ligature. Neuropathol Appl Neurobiol. 1981 Jul-Aug;7(4):315–326. doi: 10.1111/j.1365-2990.1981.tb00103.x. [DOI] [PubMed] [Google Scholar]
- Cavanagh J. B., Nolan C. C., Brown A. W. Glial cell intrusions actively remove detritus due to toxic chemicals from within nerve cells. Neurotoxicology. 1990 Spring;11(1):1–12. [PubMed] [Google Scholar]
- Cissé S., Perry G., Lacoste-Royal G., Cabana T., Gauvreau D. Immunochemical identification of ubiquitin and heat-shock proteins in corpora amylacea from normal aged and Alzheimer's disease brains. Acta Neuropathol. 1993;85(3):233–240. doi: 10.1007/BF00227716. [DOI] [PubMed] [Google Scholar]
- Cissé S., Schipper H. M. Experimental induction of corpora amylacea-like inclusions in rat astroglia. Neuropathol Appl Neurobiol. 1995 Oct;21(5):423–431. doi: 10.1111/j.1365-2990.1995.tb01079.x. [DOI] [PubMed] [Google Scholar]
- Gray E. G. The fine structure of nerve. Comp Biochem Physiol. 1970 Oct 1;36(3):419–448. doi: 10.1016/0010-406x(70)91021-2. [DOI] [PubMed] [Google Scholar]
- Iwaki T., Hamada Y., Tateishi J. Advanced glycosylation end-products and heat shock proteins accumulate in the basophilic degeneration of the myocardium and the corpora amylacea of the glia. Pathol Int. 1996 Oct;46(10):757–763. doi: 10.1111/j.1440-1827.1996.tb03545.x. [DOI] [PubMed] [Google Scholar]
- Jackson M. C., Scollard D. M., Mack R. J., Lenney J. F. Localization of a novel pathway for the liberation of GABA in the human CNS. Brain Res Bull. 1994;33(4):379–385. doi: 10.1016/0361-9230(94)90280-1. [DOI] [PubMed] [Google Scholar]
- Jacobs J. M., Cavanagh J. B. Aggregations of filaments in Schwann cells of spinal roots of the normal rat. J Neurocytol. 1972 Sep;1(2):161–167. doi: 10.1007/BF01099182. [DOI] [PubMed] [Google Scholar]
- Kubota T., Holbach L. M., Naumann G. O. Corpora amylacea in glaucomatous and non-glaucomatous optic nerve and retina. Graefes Arch Clin Exp Ophthalmol. 1993;231(1):7–11. doi: 10.1007/BF01681693. [DOI] [PubMed] [Google Scholar]
- Loeffler K. U., Edward D. P., Tso M. O. Tau-2 immunoreactivity of corpora amylacea in the human retina and optic nerve. Invest Ophthalmol Vis Sci. 1993 Jul;34(8):2600–2603. [PubMed] [Google Scholar]
- Martin J. E., Mather K., Swash M., Garofalo O., Leigh P. N., Anderton B. H. Heat shock protein expression in corpora amylacea in the central nervous system: clues to their origin. Neuropathol Appl Neurobiol. 1991 Apr;17(2):113–119. doi: 10.1111/j.1365-2990.1991.tb00702.x. [DOI] [PubMed] [Google Scholar]
- Morris J. H., Hudson A. R., Weddell G. A study of degeneration and regeneration in the divided rat sciatic nerve based on electron microscopy. 3. Changes in the axons of the proximal stump. Z Zellforsch Mikrosk Anat. 1972;124(2):131–164. doi: 10.1007/BF00335677. [DOI] [PubMed] [Google Scholar]
- Nolan C. C., Brown A. W. Reversible neuronal damage in hippocampal pyramidal cells with triethyllead: the role of astrocytes. Neuropathol Appl Neurobiol. 1989 Sep-Oct;15(5):441–457. doi: 10.1111/j.1365-2990.1989.tb01245.x. [DOI] [PubMed] [Google Scholar]
- Nolan C. C., Brown A. W. Reversible neuronal damage in hippocampal pyramidal cells with triethyllead: the role of astrocytes. Neuropathol Appl Neurobiol. 1989 Sep-Oct;15(5):441–457. doi: 10.1111/j.1365-2990.1989.tb01245.x. [DOI] [PubMed] [Google Scholar]
- Probst A., Sandoz P., Vanoni C., Baumann J. U. Intraneuronal polyglucosan storage restricted to the lateral pallidum (Bielschowsky bodies). A golgi, light, and electron microscopic study. Acta Neuropathol. 1980;51(2):119–126. doi: 10.1007/BF00690453. [DOI] [PubMed] [Google Scholar]
- SCHWARZ G. A., YANOFF M. LAFORA'S DISEASE. DISTINCT CLINICO-PATHOLOGIC FORM OF UNVERRICHT'S SYNDROME. Arch Neurol. 1965 Feb;12:172–188. doi: 10.1001/archneur.1965.00460260062008. [DOI] [PubMed] [Google Scholar]
- Sbarbati A., Carner M., Colletti V., Osculati F. Extrusion of corpora amylacea from the marginal gila at the vestibular root entry zone. J Neuropathol Exp Neurol. 1996 Feb;55(2):196–201. doi: 10.1097/00005072-199602000-00008. [DOI] [PubMed] [Google Scholar]
- Singhrao S. K., Neal J. W., Piddlesden S. J., Newman G. R. New immunocytochemical evidence for a neuronal/oligodendroglial origin for corpora amylacea. Neuropathol Appl Neurobiol. 1994 Feb;20(1):66–73. doi: 10.1111/j.1365-2990.1994.tb00958.x. [DOI] [PubMed] [Google Scholar]
- Spencer P. S., Thomas P. K. Ultrastructural studies of the dying-back process. II. The sequestration and removal by Schwann cells and oligodendrocytes of organelles from normal and diseases axons. J Neurocytol. 1974 Dec;3(6):763–783. doi: 10.1007/BF01097197. [DOI] [PubMed] [Google Scholar]
- Takahashi K., Agari M., Nakamura H. Intra-axonal Corpora amylacea in ventral and lateral horns of the spinal cord. Acta Neuropathol. 1975;31(2):151–158. doi: 10.1007/BF00688149. [DOI] [PubMed] [Google Scholar]
- Tamura S., Takahashi M., Kawamura S., Ishihara T. Basophilic degeneration of the myocardium: histological, immunohistochemical and immuno-electronmicroscopic studies. Histopathology. 1995 Jun;26(6):501–508. doi: 10.1111/j.1365-2559.1995.tb00268.x. [DOI] [PubMed] [Google Scholar]
- Tate-Ostroff B., Majocha R. E., Marotta C. A. Identification of cellular and extracellular sites of amyloid precursor protein extracytoplasmic domain in normal and Alzheimer disease brains. Proc Natl Acad Sci U S A. 1989 Jan;86(2):745–749. doi: 10.1073/pnas.86.2.745. [DOI] [PMC free article] [PubMed] [Google Scholar]
