Histochemical and Biochemical Effects of the Injection of AF64A into The Nucleus Basalis of Meynert:Relevance to Animal Models of Senile Dementia of the Alzheimer Type

  • M. R. Kozlowski
  • R. E. Arbogast
Part of the Advances in Behavioral Biology book series (ABBI, volume 30)


The fourth largest cause of death in the United States is senile dementia of the Alzheimer type (SDAT; 9). The initial symptom of this disorder is loss of short term memory. This is followed over a period of years by progressive dementia, complete loss of ability to care for oneself and finally, death (16). The most universal neuropathological change seen in victims of SDAT is a loss of acetylcholine in the cerebral cortex (3, 13). This loss appears due to the death of neurons in the nucleus basalis of Meynert (nbM), an area which supplies the cortex with a substantial proportion of its cholinergic innervation (8, 17). Thus animals with selective lesions of the nbM may be useful models of SDAT in humans.


AChE Activity Senile Dementia Lesion Hemisphere ChAT Activity Choline Acetyl 
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  1. 1.
    Asante, J.W., Cross, A.J., Deakin, J.F.W., Johnson, J.A. and Slater, H.R. (1983): Br. J. Pharmacol. 80: 573 P.Google Scholar
  2. 2.
    Caulfield, M.P., May, P.J., Peddler, E.K. and Prince, A.K. (1983): Br. J. Pharmacol. 79: 287 P.Google Scholar
  3. 3.
    Davies, P. (1979): Brain Res. 171: 319–327.CrossRefGoogle Scholar
  4. 4.
    Fisher, A. and Hanin, I. (1980): Life Sci. 27: 1615–1634.CrossRefGoogle Scholar
  5. 5.
    Fisher, A., Mantione, C.R., Abraham, D.J. and Hanin, I. (1982): J. Pharmacol. Exp. Ther. 222: 140–145.Google Scholar
  6. 6.
    Hardy, H., Heimer, L., Switzer, R. and Watkins, D. (1976): Neurosci. Lett. 3: 1–5.CrossRefGoogle Scholar
  7. 7.
    Houser, C.R., Crawford, G.D., Barber, R.P., Salvaterra, P.M. and Vaughn, J.E. (1983): Brain Res. 266: 97–119.CrossRefGoogle Scholar
  8. 8.
    Johnston, M.V., McKinney, M. and Coyle, J.T. (1979): Proc. Natl. Acad. Sci. 76: 5392–5396.CrossRefGoogle Scholar
  9. 9.
    Katzman, R. (1976): Arch. Neurol. 33: 217–218.CrossRefGoogle Scholar
  10. 10.
    Mantione, C.R., Zigmond, M.J., Fisher, A. and Hanin, I. (1983): J. Neurochem. 41: 251–255.CrossRefGoogle Scholar
  11. 11.
    Marshall, J.F., Van Oordt, K. and Kozlowski, M.R. (1983): Brain Res. 274: 283–289.CrossRefGoogle Scholar
  12. 12.
    Mesulam, M.-M., Mufson, E.J., Levey, A.I. and Wainer, B.H. (1983): J. Comp. Neurol. 214: 170–197.CrossRefGoogle Scholar
  13. 13.
    Perry, E.K., Gibson, P.H., Blessed, G., Perry, R.H. and Tomlinson, B.E. (1977): J. Neurol. Sci. 34: 274–265.CrossRefGoogle Scholar
  14. 14.
    Sandberg, K., Sanberg, P.R., Hanin, I., Fisher, A. and Coyle, J.T. (1984): Behay. Neurosci. 98: 162–165.CrossRefGoogle Scholar
  15. 15.
    Schrier, B.K. and Shuster, L. (1967): J. Neurochem. 14: 977–985.CrossRefGoogle Scholar
  16. 16.
    Sinex, F.M. and Myers, R.H. (1982): In: Alzheimer’s. Disease, Down’s Syndrome and Aging (eds) F.M. Sinex and C.R. Merril, The New York Academy of Sciences, New York, pp. 3–13.Google Scholar
  17. 17.
    Whitehouse, P.J., Price, D.L., Struble, R.G., Clark, A.W., Coyle, J.T. and DeLong, M.R. (1982): Science 215: 1237–1239.CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • M. R. Kozlowski
    • 1
  • R. E. Arbogast
    • 1
  1. 1.Department of Medicinal SciencesPfizer Central ResearchGrotonUSA

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