Growing Points in the Neurobiology of Alzheimer’s Disease

Conference paper
Part of the NATO ASI Series book series (volume 9)


The last 15 years have seen rapid expansion in scientific enquiry into the neurobiological basis of Alzheimer’s Disease (AD). The new findings exhibit a promising cohesion and convergence of the evidence that has emerged from studies of different aspects of the disease and from observations during life and post mortem. It is also significant that structural lesions and the neurochemical deficits which have come into view during the past decade have proved highly selective, consistently affecting certain systems while leaving others intact. This suggests that there may be a unitary aetiological basis for the disease, of which the diverse neurobiological lesions are different expressions.


Neurofibrillary Tangle Brodmann Area Paired Helical Filament ChAT Activity Paired Helical Filament 
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  1. Arai, H., Kosaka, K. and Iizuka T. (1984). Change of biogenic amines and their metabolites in postmortem brains from patients with Alzheimer-type dementia. J. Neurochem. 43: 388–393.PubMedCrossRefGoogle Scholar
  2. Blessed, G., Tomlinson, B. E., Roth, M. (1968). The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects. Br. J. Psychiatry 114: 797–811.PubMedCrossRefGoogle Scholar
  3. Blocq, P. and Marinesco G. (1892). Sur les lesions et la pathogenie de l’epilepsie dite essentielle. Sem. Med. ( Paris ) 12: 445.Google Scholar
  4. Bondareff, W., Mountjoy, C. Q., Roth, M. (1982). Loss of neurons of origin of the adrenergic projection to cerebral cortex (nucleus locus coeruleus) in senile dementia. Neurol. 32: 164–168.Google Scholar
  5. Bondareff, W. (1983). Age and Alzheimer’s disease. Lancet 1:1447. Bondareff, W., Personal Communication.Google Scholar
  6. Chase, T. N. et al. (1984). Regional cortical dysfunction in Alzheimer’s disease as determined by positron emission tomography. Ann. Neurol. 15 (Suppl.): S170–S174.PubMedCrossRefGoogle Scholar
  7. Cross, A. J., (1981). Reduced dopamine-beta-hydroxylase activity in Alzheimer’s disease. Br. Med. J. 282: 93–94.Google Scholar
  8. Crowther, R. A., (1985). Analysis of the structure of paired helical filaments. Proc. EMSA 43: 734–737.Google Scholar
  9. Curcio, C. A., Kemper, T. (1984). Nucleus raphe dorsalis in dementia of the Alzheimer type: neurofibrillary changes and neuronal packing density. J. Neuropath. Exp. Neurol. 43: 359–368.PubMedCrossRefGoogle Scholar
  10. De Leon, M. J., (1983). Positron emission tomographic studies of aging and Alzheimer’s disease. Am. J. Neurocardiol. 4: 568–571.Google Scholar
  11. Glenner, G. G., Wong, C. W. (1984). Alzheimer’s disease: initial report of the purification and characterization of a novel amyloid protein. Biochem. Biophys. Res. Comm. 120: 885–890.Google Scholar
  12. Lauter, H. and Meyer, J. E. (1968). Clinical and nosological concepts of senile dementia. In: Senile Dementia: Clinical and Therapeutic Aspects. Muller, C. H. and Ciompi, L. Huber, Bern.Google Scholar
  13. Mann, D. N., Yates, P. O., Hawkes, J. (1982). The noradrenergic system in Alzheimer and multi-infarct dementias. J. Neurol Neurosurg Psychiatry 45: 113–119.PubMedCrossRefGoogle Scholar
  14. Masters, C. L., Multhaup, G., Sims, G., Poltgeisser, J. (1985). Neuronal origin of a cerebral amyloid: neurofibrillary tangles of Alzheimer’s disease contain the same protein as the amyloid plaque cores and blood vessels. Proc. Natl. Acad. Sci. USA, in press.Google Scholar
  15. Metuzals, J. et al. (1981). Organization of the neurofilamentous network. Cel. Tiss. Res. 214: 455–482.Google Scholar
  16. Morrison, J. H. et al. (1985). Somatostatin immunoreactivity in neuritic plaques of Alzheimer’s patients. Nature 314: 90–92.PubMedCrossRefGoogle Scholar
  17. Mountjoy, C. Q. et al. (1984). Correlation of cortical cholinergic and GABA deficits with quantitative neuropathological findings in senile dementia. Brain 107: 507–518.PubMedCrossRefGoogle Scholar
  18. Mountjoy, C. Q., (1983). Cortical neuronal counts in normal elderly controls and demented patients. Neurobiol. Ageing 4: 1–11.Google Scholar
  19. Mountjoy, C. Q., (1986). Biochemical and neuropathological changes in the brain and their correlation to the severity of dementia in Alzheimer’s disease. In: Biological Psychiatry 1985; Shagass, C., Elsevier Science Publishing Co. Inc., 1415–1417.Google Scholar
  20. Perry, E. K., Perry, R. H. (1985). A review of neuropathological and neurochemical correlates of Alzheimer’s disease. In: Dan Med. Bull. Gerontology, Special Suppl. Series no. 1, 32: 27–34.Google Scholar
  21. Perry, G., (1985). Paired helical filaments from Alzheimer’s disease patients contain cytoskeletal components. Proc. Natl. Acad. Sci. USA 82: 3916–3920.Google Scholar
  22. Pilleri, G. (1966). Kluver-Bucy syndrome in man. A clinicoanatomical contribution to the function of the medial temporal lobe structures. Psychiatrie Neurol. 152: 65–103.Google Scholar
  23. Price, D. L., Basal forebrain cholinergic neurons and neuritic plaques in primate brain. In: Katzman, R., op. cit. 65–77.Google Scholar
  24. Probst, A. (1984). Neuritic changes in Alzheimer’s disease and established in neuritic plaques as shown by Golgi impregnation and method. A review. In: Pilleri, G., Tagliavini F. eds., Brain Path. vol. 1.Google Scholar
  25. Rossor, M. N., (1984). Neurochemical characteristics of early and late onset types of Alzheimer’s disease. Br. Med. J. 288: 361–364.Google Scholar
  26. Roth, M. (1971). Classification and aetiology in mental disorders of old age; some recent developments. In: Recent Developments in Psychogeriatrics, Kay, D. W. K., Walk, A. eds, Ashford: Headley Bros., 1–18.Google Scholar
  27. Roth, M. and Wischik, C. M. (1985). The heterogeneity of Alzheimer’s disease and its implications for scientific investigations of the disorder. In: Recent advences in Psychogeriatrics, Arie, T. ed., Churchill Livingstone, 71–92.Google Scholar
  28. Roth, M. (1986). The association of clinical and neurological findings and its bearing on the classification and aetiology of Alzheimer’s disease. Br. Med. Bull. 42: 42–50.Google Scholar
  29. Simchowicz, T. (1910). Histologische Studien über die senile demenz. Hist. Histopath. Arb. 4: 267.Google Scholar
  30. Terry, R. D., (1981). Some morphometric aspects of the brain in senile dementia of the Alzheimer type. Ann. Neurol. 10: 184–192.Google Scholar
  31. Whitehouse, P. J. et al. (1982). Alzheimer’s disease and senile dementia: loss of neurons in the basal forebrain. Science 215: 1237–1239.PubMedCrossRefGoogle Scholar
  32. Whitehouse, P. J., (1982). Alzheimer’s disease and senile dementia: loss of neurons in the basal forebrain. Science 215: 1237–1239.Google Scholar
  33. Wischik, C. M., (1985). Subunit structure of paired helical filaments in Alzheimer’s disease. J. Cell. Biol. 100: 1905–1912.Google Scholar
  34. Wischik, C. M., Crowther, R. A. (1986). Subunit structure of the Alzheimer tangle. Br. Med. Bull. 42: 51–56.Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1987

Authors and Affiliations

  • M. Roth
    • 1
  1. 1.Department of PsychiatryUniversity of CambridgeCambridgeUK

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