Conclusions
It is clear that there is much to be learned from the investigation of brain aging in the great apes. Given the close genetic relationships of humans and great apes and the apes’ ability, especially in captivity, to survive to ages that begin to approach that of humans, the parallels and opportunities for research are numerous. To date only aspects of the pathology of Alzheimer’s disease have been demonstrated in the brains of great apes of advanced age, but the number of well-studied animals is quite small. If the great apes fail to develop lesions comparable to that of Alzheimer’s disease and Parkinson’s disease, then considering the 2–3% differences in genetic material, this would argue for a search for differences in genetic loci of importance to the etiopathogenesis of these two important human diseases. Furthermore, this then represents an important opportunity for the study of neuronal loss and other aspects of normal brain aging in the absence of superimposed lesions associated with these two age-related human diseases. The study of the aging process in the great ape species will provide data of importance to understanding the aging process in these animals themselves. As increasing numbers of great apes survive to advanced age in protected environments, the problems associated with aging will assume increasing importance. All such studies have been hampered by the lack of significant numbers of well prepared specimens from appropriately aged animals. The availability of the collection of specimens being prepared by the Great Ape Aging Project represents an important contribution to those interested in these problems.
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References
Coggeshall, R.E. and Lekan, H.A., 1996, Methods for determining numbers of cells and synapses: A case for more uniform standards of review, J. Comp. Neural. 364: 6–15.
Crystal, H., Dickson, D., Fuld, P., Masur, D., Scott, R., and Mehler, M., 1988, Clinico-pathologic studies in dementia: Non-demented subjects with pathologically confirmed Alzheimer’s disease, Neurology 38: 1682–1689.
Erwin, J., Bloomsmith, M., Boysen, S.T., Hof, P.R., Holloway, R., Lowenstine, L., McManamon, R., Perl, D.P., Young, W., Zihlman, A., this volume.
Gearing, M., Tigges, J., Mori, H., and Mirra, S.S., 1996, Aβ40 is a major form of β-amyloid in nonhuman primates, Neurobiol. Aging 17: 903–908.
Gearing, M., Tigges, J., Mori, H., and Mirra, S.S., 1997, beta-Amyloid (A beta) deposition in the brains of aged orangutans, Neurobiol. Aging 18: 139–146.
Gearing, M., Rebeck, G., Hyman, B., Tigges, J., and Mirra, S.S., 1994, Neuropathology and apolipoprotein E profile of aged chimpanzees: Implications for Alzheimer’s disease, Proc. Natl. Acad. Sci. USA 91: 9382–9386.
Gundersen, H.J., Bendtsen, T.F., Korbo, L., Marcussen, N., Moller, A., Nielsen, K., Nyengaard, J.R., and Pakkenberg, B., 1988a, Some new, simple and efficient stereology methods and their use in pathological research and diagnosis, APMIS 96: 379–394.
Gundersen, H.J., Bagger, P., Bendtsen, T.F., Evans, S.M., Korbo, L., Marcussen, N., Moller, A., Nielsen, K., and Pakkenberg, B., 1988b, The new stereology tools: Dissector, fractionator, nucleator and point sampling intercepts and their use in pathological research and diagnosis, APMIS 96: 857–881.
Herndon, J.G., Moss, M.B., Rosene, D.L., and Killiany, R.J., 1997, Patterns of cognitive decline in aged rhesus monkeys, Behav. Brain Res. 87: 25–34.
Kang, J., Lemaire, H.G., Unterbeck, A., Salbaum, J.M., Masters, C.L., Grzeschik, K.H., Multhaup, G., Beyreuther, K. and Muller Hill, B., 1987, The precursor of Alzheimer’s disease amyloid βA4 protein resembles a cell-surface receptor, Nature 325: 733–736.
Kidd, M., 1963, Paired helical filaments in electron microscopy of Alzheimer’s disease, Nature 197: 192–193.
Lee, V.M.Y., Balin, B.J., Otvos, L., Jr., and Trojanowski, J.Q., 1991, A major subunit of paired helical filaments and derivatized forms of normal tau, Science 251: 675–678.
Masters, C.L., Multhaup, G., Simms, G., Pottgiesser, J., Martins, R.N., and Beyreuther, K., 1985, Neuronal origin of a cerebral amyloid: Neurofibrillary tangles of Alzheimer disease contain the same protein as the amyloid of plaque cores and blood, EMBO J., 4(11): 2757–2763.
Morrison, J.H. and Hof, P.R., 1997, Life and death of neurons in the aging brain, Science 278: 412–419.
Moss, M.B., Killiany, R.J., Lai, Z.C., Rosene, D.L., and Herndon, J.G., 1997, Recognition memory span in rhesus monkeys of advanced age, Neurobiol. Aging 18: 13–19.
Nimchinsky, E.A., Vogt, B.A., Morrison, J.H., and Hof, P.R., 1995, Spindle neurons of the human cingulate cortex, J. Comp. Neurol. 355: 27–37.
Nimchinsky, E.A., Vogt, B.A., Morrison, J.H., and Hof, P.R., 1997, Neurofilament and calcium-binding proteins in the human cingulate cortex, J. Comp. Neurol. 384: 597–620.
Pakkenberg, B., Moller, A., Gundersen, H.J., Mouritzen Dam, A., and Pakkenberg, H., 1991, The absolute number of nerve cells in substantia nigra in normal subjects and in patients with Parkinson’s disease estimated with an unbiased stereological method, J. Neurol. Neurosurg. Psych. 54: 30–33.
Prelli, F., Castano, E., Glenner, G.G., and Frangione, B., 1988, Differences between vascular and plaque core amyloid in Alzheimer’s disease, J. Neurochem. 51: 648–651.
Price, D., Martin, L., Sisodia, S., Walker, L., Voytko, M., Wagster, M., Cork, L., and Koliatsos, V., 1994, The aged nonhuman primate: A model for the behavioral and brain abnormalities occurring in aged humans. Pp. 165–175 in: (Eds. R.D. Terry, R. Katzman, and K. Bick), Alzheimer’s Disease, New York: Raven Press.
Selkoe, D.J., 1994, Normal and abnormal biology of the β-amyIoid precursor protein, Ann. Rev. Neurosci. 17: 489–517.
Selkoe, D.J., Bell, D.S., Podlisny, M.B., Price, D.L., and Cork, L.C., 1987, Conservation of brain amyloid proteins in aged mammals and humans with Alzheimer’s disease, Science 235: 873–877.
West, M.J., Coleman, P.D., Flood, D.G., and Troncoso, J.C., 1994, Differences in the pattern of hippocampal neuronal loss in normal ageing and Alzheimer’s disease, Lancet 344: 769–772.
Wisniewski, H.M., Narang, H.K., and Terry, R.D., 1976, Neurofibrillary tangles of paired helical filaments, J. Neurol. Sci. 27: 173–181.
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Perl, D.P., Hof, P.R., Nimchinsky, E.A., Erwin, J.M. (2002). Studies of Age-Related Neuronal Pathology in Great Apes. In: Galdikas, B.M.F., Briggs, N.E., Sheeran, L.K., Shapiro, G.L., Goodall, J. (eds) All Apes Great and Small. Developments in Primatology: Progress and Prospects. Springer, Boston, MA. https://doi.org/10.1007/0-306-47461-1_20
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