Skip to main content
SpringerLink
Log in

Relationships Between Aging and Neurodegenerative Disease

  • Chapter
Sense and Senility: The Neuropathology of the Aged Human Brain

  • 91 Accesses

Abstract

Simple comparisons between the catalogues of damage that occur in the ‘normal’ elderly and in patients with the common neurodegenerative disorders of old age (AD and PD) show much overlap. For example, in AD the larger pyramidal cells of the cerebral cortex (especially those of the frontal, temporal and cingulate gyri) and the hippocampus (CA1 and subiculum), amygdala (cortical and medial nuclei), suprachiasmatic nucleus, nucleus basalis complex, locus caeruleus and ventral tegmentum are all seriously decimated, yet these same cell types are affected, though to a lesser extent, in normally aged individuals. In PD the gross loss of the pigmented cells of the substantia nigra and, again, cells of the locus caeruleus and nucleus basalis contrasts similarly with the lesser involvement in ‘normal’ aging. However, this is not always the rule with, for example, Purkinje cells in the cerebellum1 and neurones of the sexually dimorphic nucleus2 being nerve cell types that are clearly affected with aging but do not apparently suffer additional damage in either AD or PD. Some regions, such as the cranial nerve nuclei, the mammillary bodies, the olivary and pontine nuclei, the dentate nucleus, paraventricular and supraoptic nuclei3 seem to resist equally the effects of aging and both of these forms of neurodegeneration. Many of the regressive changes taking place within surviving cells in areas of cell loss (i.e. dendritic reduction, perikaryal shrinkage, loss of nucleic acid) also seem magnified in AD and PD.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 129.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 169.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Hall TC, Miller AKH, Corsellis JAN. Variations in the human Purkinje cell population according to age and sex. Neuropath Appl Neurobiol 1975; 1: 267–292.

    Article  Google Scholar 

  2. Swaab DF, Fliers E, Partiman TS. The suprachiasmatic nucleus of the human brain in relation to sex, age and senile dementia. Brain Res 1985; 342: 37–44.

    Article  PubMed  CAS  Google Scholar 

  3. Goudsmit E, Hopman MA, Fliers E et al. The supraoptic and paraventricular nuclei of the human hypothalamus in relation to sex, age and Alzheimer’s disease. Neurobiol Aging 1990; 11: 529–536.

    Article  PubMed  CAS  Google Scholar 

  4. Tomlinson BE, Blessed G, Roth M. Observations on the brains of non-demented old people. J Neurol Sci 1968; 7: 331–356.

    Article  PubMed  CAS  Google Scholar 

  5. Ball MJ. Neuronal loss, neurofibrillary tangles and granulovacuolar degeneration in the hippocampus with aging and dementia. A quantitative study. Acta Neuropathol 1977; 37: 111–118.

    Article  CAS  Google Scholar 

  6. Mann DMA, Yates PO, Marcyniuk B. Some morphometric observations on the cerebral cortex and hippocampus in presenile Alzheimer’s disease, senile dementia of Alzheimer type and Down’s syndrome in middle age. J Neurol Sci 1985; 69: 139–159.

    Article  PubMed  CAS  Google Scholar 

  7. Mann DMA, Tucker CM, Yates PO. The topographic distribution of senile plaques and neurofibrillary tangles in the brains of non-demented persons of different ages. Neuropath Appl Neurobiol 1987; 13: 123–139.

    Article  CAS  Google Scholar 

  8. Mann DMA, Esiri MM. The site of the earliest lesions of Alzheimer’s disease. N Engl J Med 1988; 318: 789–790.

    Article  PubMed  CAS  Google Scholar 

  9. Mann DMA, Esiri MM. Regional acquisition of plaques and tangles in Down’s syndrome patients under 50 years of age. J Neurol Sci 1989; 89: 169–179.

    Article  PubMed  CAS  Google Scholar 

  10. Mann DMA, Brown AMT, Prinja D et al. An analysis of the morphology of senile plaques in Down’s syndrome patients of different ages using immunocytochemical and lectin histochemical methods. Neuropath Appl Neurobiol 1989; 15: 317–329.

    Article  CAS  Google Scholar 

  11. Mann DMA, Prinja D, Davies CA et al. Immunocytochemical profile of neurofibrillary tangles in Down’s syndrome patients of different ages. J Neurol Sci 1989; 92: 247–260.

    Article  PubMed  CAS  Google Scholar 

  12. Mann DMA. The pathological association between Down syndrome and Alzheimer disease. Mech Aging Dev 1988; 43: 99–136.

    Article  PubMed  CAS  Google Scholar 

  13. Mann DMA. Alzheimer’s disease and Down’s syndrome. Histopath 1988; 13: 125–138.

    Article  CAS  Google Scholar 

  14. Whalley A. The dementia of Down’s syndrome and its relevance to aetiological studies of Alzheimer’s disease. Ann NY Acad Sci 1982; 396: 39–53.

    Article  PubMed  CAS  Google Scholar 

  15. Oliver C, Holland AJ. Down’s syndrome and Alzheimer’s disease: a review. Psychol Med 1986; 16: 307–322.

    Article  PubMed  CAS  Google Scholar 

  16. Wisniewski HM, Rabe A. Discrepancy between Alzheimer type neuropathology and dementia in persons with Down’s syndrome. Ann NY Acad Sci 1986; 477: 247–259.

    Article  PubMed  CAS  Google Scholar 

  17. Ikeda S-I, Allsop D, Glenner GG. The morphology and distribution of plaque and related deposits in the brains of Alzheimer’s disease and control cases: an immunohistochemical study using amyloid β protein antibody. Lab Invest 1989; 60: 113–122.

    PubMed  CAS  Google Scholar 

  18. Ogomori K, Kitamoto T, Tateishi J et al. β amyloid protein is widely distributed in the central nervous system of patients with Alzheimer’s disease. Am J Pathol 1989; 134: 243–251.

    PubMed  CAS  Google Scholar 

  19. Bugiani O, Giaccone G, Frangione B et al. Alzheimer patients: preamyloid deposits are more widely distributed than senile plaques throughout the central nervous system. Neurosci Lett 1989; 103: 262–268.

    Google Scholar 

  20. Iwatsubo T, Odaka N, Suzuki N et al. Visualization of Aβ42(43)-positive and Aβ40-positive senile plaques with end-specific Aβmonclonal antibodies: Evidence that an initially deposited species is Aβ1–42(43). Neuron 1994; 13: 45–53.

    Article  PubMed  CAS  Google Scholar 

  21. Mann DMA, Brown AMT, Prinja D et al. A morphological analysis of senile plaques in the brains of non-demented persons of different ages using silver, immunocytochemical and lectin histochemical staining techniques. Neuropath Appl Neurobiol 1990; 16: 17–25.

    Article  CAS  Google Scholar 

  22. Davies L, Wolska B, Hilbich C et al. β4 amyloid protein deposition and the diagnosis of Alzheimer’s disease: prevalence in aged brains determined by immunocytochemistry compared with conventional neuropathologic techniques. Neurology 1988; 38: 1688–1693.

    Article  PubMed  CAS  Google Scholar 

  23. Price JL, Davis PB, Morris JC et al. The distribution of plaques, tangles and related immunohistochemical markers in healthy aging and Alzheimer’s disease. Neurobiol Aging 1991; 12: 295–312.

    Article  PubMed  CAS  Google Scholar 

  24. Ohgami T, Kitamoto T, Shin R-W et al. Increased senile plaques without microglia in Alzheimer’s disease. Acta Neuropathol 1991; 81: 242–247.

    Article  PubMed  CAS  Google Scholar 

  25. Fukumoto H, Asami-Odaka A, Suzuki N et al. Amyloid β protein (Aβ) deposition in normal aging has the same characteristics as that in Alzheimer’s disease: predominance of Aβ42(43) and association of Aβ40 with cored plaques. Am J Pathol 1996; 148: 259–265.

    PubMed  CAS  Google Scholar 

  26. Rumble B, Retallack R, Hilbich C et al. Amyloid (A4) protein and its precursor in Down’s syndrome and Alzheimer’s disease. N Engl J Med 1989; 320: 1446–1452.

    Article  PubMed  CAS  Google Scholar 

  27. Iwatsubo T, Mann DMA, Odaka A et al. Amyloid β protein (Aβ) deposition: Aβ42(43) precedes Aβ40 in Down syndrome. Ann Neurol 1995; 37: 294–299.

    Article  PubMed  CAS  Google Scholar 

  28. Lemere CA, Blusztajn JK, Yamaguchi H et al. Sequence of deposition of heterogeneous amyloid β-peptides and APO E in Down syndrome: Implications for initial events in amyloid plaque formation. Neurobiol Dis 1996; 3: 16–32.

    Article  PubMed  CAS  Google Scholar 

  29. Kida E, Wisniewski KE, Wisniewski HM. Early amyloid-β deposits show different immunoreactivity to the amino-and carboxy-terminal regions of β-peptide in both Alzheimer’s disease and Down’s syndrome brain. Neurosci Lett 1995; 193: 1–4.

    Article  Google Scholar 

  30. Braak H, Braak E. Neurofibrillary changes confined to the entorhinal region and an abundance of cortical amyloid in cases of presenile and senile dementia. Acta Neuropathol 1990; 80: 479–486.

    Article  PubMed  CAS  Google Scholar 

  31. Bouras C, Hof PR, Morrison JH. Neurofibrillary tangle densities in the hippocampal formation in a non-demented population define subgroups of patients with differential early pathologic changes. Neurosci Lett 1993; 153: 131–135.

    Article  PubMed  CAS  Google Scholar 

  32. Gibb WRG. Idiopathic Parkinson’s disease and the Lewy body disorders. Neuropath Appl Neurobiol 1986; 12: 223–234.

    Article  CAS  Google Scholar 

  33. Gibb WRG, Lees AJ. The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson’s disease. J. Neurol Neurosurg Psychiat 1988; 51: 745–752.

    Article  PubMed  CAS  Google Scholar 

  34. Forno LS, Langston JW. Lewy bodies and aging: relation to Alzheimer’s and Parkinson’s diseases. Neurodegeneration 1993; 2: 19–24.

    Google Scholar 

  35. Forno LS. Concentric hyaline intraneuronal inclusions of Lewy type in the brains of elderly persons (50 incidental cases); relationship to Parkinsonism. J Amer Geriat Soc 1969; 17: 557–575.

    PubMed  CAS  Google Scholar 

  36. Katzman R. Alzheimer’s disease. N Engl J Med 1986; 314: 964–973.

    Article  PubMed  CAS  Google Scholar 

  37. Evans DA, Funkenstein H, Albert MS et al. Prevalence of Alzheimer’s disease in a community population of older persons. JAMA 1989; 262: 2551–2556.

    Article  PubMed  CAS  Google Scholar 

  38. Terry RD, De Teresa R, Hansen LA. Neocortical cell counts in normal human adult aging. Ann Neurol 1987; 21: 530–539.

    Article  PubMed  CAS  Google Scholar 

  39. Terry RD, Peck A, De Teresa R et al. Some morphometric aspects of the brain in senile dementia of the Alzheimer type. Ann Neurol 1981; 10: 184–192.

    Article  PubMed  CAS  Google Scholar 

  40. West MJ. Regionally specific loss of neurons in the aging human hippocampus. Neurobiol Aging 1993; 14: 287–293.

    Article  PubMed  CAS  Google Scholar 

  41. Duara R, Margolin RA, Robertson-Tschabo EA et al. Cerebral glucose utilization as measured with positron emission tomography in 21 resting healthy men between the ages of 21 and 83 years. Brain 1983; 106: 761–775.

    Article  Google Scholar 

  42. Sawle GV, Colebatch JG, Shah A et al. Striatal function in normal aging: implications for Parkinson’s disease. Ann Neurol 1990; 28: 799–804.

    Article  PubMed  CAS  Google Scholar 

  43. Kuhl DE, Metter EJ, Riege WH et al. Effects of human aging on patterns of local cerebral glucose utilization determined by the (18 F) flurodeoxyglucose method. J Cereb Blood Flow Metab 1982; 2: 163–171.

    Article  PubMed  CAS  Google Scholar 

  44. Martin WRW, Palmer MR, Patlak CS et al. Nigrostriatal function in humans studied with positron emission topography. Ann Neurol 1989; 26: 535–542.

    Article  PubMed  CAS  Google Scholar 

  45. Calne D, Calne JS. Normality and disease. Can J Neurol Sci 1988; 14: 3–14.

    Google Scholar 

  46. Mann DMA, Jones D, Prinja D et al. The prevalence of amyloid (A4) protein deposits within the cerebral and cerebellar cortex in Down’s syndrome and Alzheimer’s disease. Acta Neuropathol 1990; 80: 318–327.

    Article  PubMed  CAS  Google Scholar 

  47. Torvik A, Torp S, Lindboe CF. Atrophy of the cerebellar vermis in aging. A morphometric and histologie study. J Neurol Sci 1986; 76: 283–294.

    Article  PubMed  CAS  Google Scholar 

  48. Selkoe DJ, Bell DS, Podlisny MB et al. Conservation of brain amyloid proteins in aged mammals and humans with Alzheimer’s disease. Science 1987; 235: 873–877.

    Article  PubMed  CAS  Google Scholar 

  49. Walker LC, Kitt CA, Schwam E et al. Senile plaques in aged squirrel monkeys. Neurobiol Aging 1987; 8: 291–296.

    Article  PubMed  CAS  Google Scholar 

  50. Struble RG, Price DL, Cork LC et al. Senile plaques in cortex of aged normal monkeys. Brain Res 1985; 361: 267–275.

    Article  PubMed  CAS  Google Scholar 

  51. Cork LC, Powers RE, Selkoe DJ et al. Neurofibrillary tangles and senile plaques in aged bears. J Neuropathol Exp Neurol 1988; 47: 629–641.

    Article  PubMed  CAS  Google Scholar 

  52. Giaccone G, Verga L, Finazzi M et al. Cerebral preamyloid deposits and congophilic angiopathy in aged dogs. Neurosci Lett 1990; 114: 178–183.

    Article  PubMed  CAS  Google Scholar 

  53. Wisniewski T, Lalowski M, Bobik M et al. Amyloid β1–42 deposits do not lead to Alzheimer’s neuritic plaques in aged dogs. Biochem J 1996; 313: 575–580.

    PubMed  CAS  Google Scholar 

  54. Wegiel J, Wisniewski HM, Dziewiatkowski J et al. Fibrillar and non-fibrillary amyloid in the brain of aged dogs. In: Iqbal K, Mortimer JA, Winblad B et al., eds. Research Advances in Alzheimer’s Disease and Related Disorders. John Wiley & Sons Ltd, 1995: 703–707.

    Google Scholar 

  55. Volloch V. Possisble mechanism for resistance to Alzheimer’s disease (AD) in mice suggests new approach to generate a mouse model for sporadic AD and may explain familial resistance to AD in man. Neurodegeneration (In press).

    Google Scholar 

  56. Coleman PD, Flood DG. Neurone numbers and dendritic extent in normal aging and Alzheimer’s disease. Neurobiol Aging 1987; 8: 521–545.

    Article  PubMed  CAS  Google Scholar 

  57. Rogers J, Magistretti PJ, Bolis LC. Animal models for aging research. Neurobiol Aging 1991; 12: 619–701.

    Article  Google Scholar 

  58. Coleman PD, Finch C, Joseph J. The need for multiple time points in aging studies. Neurobiol Aging 1990; 11: 1–2.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. University of Manchester, Manchester, UK

    David M. A. Mann PhD, FRCPath

Authors
  1. David M. A. Mann PhD, FRCPath
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

Copyright information

© 1997 Springer Science+Business Media Dordrecht

About this chapter

Cite this chapter

Mann, D.M.A. (1997). Relationships Between Aging and Neurodegenerative Disease. In: Sense and Senility: The Neuropathology of the Aged Human Brain. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6001-2_5

Download citation

  • DOI: https://doi.org/10.1007/978-1-4615-6001-2_5

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7749-8

  • Online ISBN: 978-1-4615-6001-2

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics

Search

Navigation