Neuropraxis

, 15:113 | Cite as

De rol van de pariëtaalkwab in de vroege fase van de ziekte van Alzheimer

  • Heidi Jacobs
Article
  • 131 Downloads

Met de vergrijzing in de maatschappij neemt ook de hoeveelheid patiënten met de ziekte van Alzheimer toe. De incidentie van het aantal patiënten met de ziekte van Alzheimer wereldwijd zal stijgen van 25 miljoen naar 114 miljoen patiënten in 2050 (Wimo, Winblad, Aguero-Torres & von Strauss, 2003). Niet enkel zullen er meer patiënten zijn die lijden onder de gevolgen van deze ziekte, ook de omgeving wordt ermee geconfronteerd. Inzicht krijgen in de oorzaak van deze ziekte en het tijdig kunnen stellen van een diagnose wordt steeds belangrijker.

Abstract

Background:

In view of the aging population in our society, the number of people suffering from Alzheimer’s disease (AD) is expected to increase immensely. This dementia is characterized by cognitive disorders, behavioural problems and interference with daily life activities. The cause of this disease is still not fully understood and consequently, the early diagnosis lacks accuracy. Because of the involvement of the medial temporal lobe regions in the formation of new memories, this region has received much attention the last decades. However, new imaging methods suggest the involvement of other cortical regions such as the parietal lobe in the pathogenesis of AD.

Methods:

Structural as well as functional MRI studies examining changes in the parietal lobe regions in early Alzheimer disease are discussed.

Results:

These studies indicated that the parietal lobe shows changes in the grey and white matter in the early stages of the disease. There is an increase in brain activity, possibly reflecting compensatory mechanisms to counteract a disconnection between medial temporal regions and the posterior cingulate gyrus.

Conclusions:

Structural and functional connectivity might provide new biomarkers for the early detection of Alzheimer’s disease. Neuroimaging will probably gain a more prominent role in the clinical setting.

Literatuur

  1. Bokde, A.L., Karmann, M., Born, C., Teipel, S.J., Omerovic, M., Ewers, M., et al. (2010). Altered brain activation during a verbal working memory task in subjects with amnestic mild cognitive impairment. Journal of Alzheimers Disease, 21,1, 103–118.Google Scholar
  2. Braak, H. & Braak, E. (1991). Neuropathological stageing of Alzheimer-related changes. Acta Neuropathologica (Berlin), 82,4, 239–259.CrossRefGoogle Scholar
  3. Braak, H. & Braak, E. (1996). Development of Alzheimer-related neurofibrillary changes in the neocortex inversely recapitulates cortical myelogenesis. Acta Neuropathologica (Berlin), 92,2, 197–201.CrossRefGoogle Scholar
  4. Braak, H. & Braak, E. (1997). Frequency of stages of Alzheimer-related lesions in different age categories. Neurobiology of Aging, 18,4, 351–357.PubMedCrossRefGoogle Scholar
  5. Buckner, R.L., Andrews-Hanna, J.R. & Schacter, D.L. (2008). The brain’s default network: anatomy, function, and relevance to disease. Annals of the New York Academy of Sciences, 1124, 1–38.PubMedCrossRefGoogle Scholar
  6. Cavanna, A.E. & Trimble, M.R. (2006). The precuneus: a review of its functional anatomy and behavioural correlates. Brain, 129(Pt 3), 564–583.PubMedCrossRefGoogle Scholar
  7. Clement, F. & Belleville, S. (2010). Compensation and disease severity on the memory-related activations in mild cognitive impairment. Biological Psychiatry, 68,10, 894–902.PubMedCrossRefGoogle Scholar
  8. Culham, J.C. & Kanwisher, N.G. (2001). Neuroimaging of cognitive functions in human parietal cortex. Current Opinion in Neurobiology, 11,2, 157–163.PubMedCrossRefGoogle Scholar
  9. Cummings, J.L. (2004). Alzheimer’s disease. New England Journal of Medicine, 351,1, 56–67.PubMedCrossRefGoogle Scholar
  10. Dickerson, B.C. & Sperling, R.A. (2008). Functional abnormalities of the medial temporal lobe memory system in mild cognitive impairment and Alzheimer’s disease: insights from functional MRI studies. Neuropsychologia, 46,6, 1624–1635.PubMedCrossRefGoogle Scholar
  11. Dubois, B., Feldman, H.H., Jacova, C., Cummings, J.L., Dekosky, S.T., Barberger-Gateau, P., et al. (2010). Revising the definition of Alzheimer’s disease: a new lexicon. Lancet Neurology, 9,11, 1118–1127.PubMedCrossRefGoogle Scholar
  12. Echavarri, C., Aalten, P., Uylings, H B., Jacobs, H.I., Visser, P.J., Gronenschild, E.H., et al. (2010). Atrophy in the parahippocampal gyrus as an early biomarker of Alzheimer’s disease. Brain Structure and Function, DOI 10.1007/s00429-010-0283-8.Google Scholar
  13. Fleisher, A.S., Sun, S., Taylor, C., Ward, C.P., Gamst, A.C., Petersen, R.C., et al. (2008). Volumetric MRI vs clinical predictors of Alzheimer disease in mild cognitive impairment. Neurology, 70,3, 191–199.PubMedCrossRefGoogle Scholar
  14. Herholz, K., Carter, S.F. & Jones, M. (2007). Positron emission tomography imaging in dementia. The British Journal of Radiology, 80 Spec No 2, S160–S167.PubMedCrossRefGoogle Scholar
  15. Jack, C.R. Jr., Knopman, D.S., Jagust, W.J., Shaw, L.M., Aisen, P.S., Weiner, M.W., et al. (2010). Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade. Lancet Neurology, 9,1, 119–128.PubMedCrossRefGoogle Scholar
  16. Jacobs, H.I.L. (2011). Parietal matters in early Alzheimer’s disease: evidence from structural and functional MRI. Maastricht University, Maastricht.Google Scholar
  17. Jacobs, H.I.L., Boxtel, M.P.J. van, Uylings, H.B.M., Gronenschild, E.H.B.M., Verhey, F.R. & Jolles, J. (2010). Atrophy of the parietal lobe in preclinical dementia. Brain and Cognition, doi:10.1016/j.bandc.2010.11.003.Google Scholar
  18. Jacobs, H.I.L., Boxtel, M.P.J. van, Elst, W. van der, Burgmans, S., Smeets, F., Gronenschild, E.H.B.M., et al. (2011). Increasing the diagnostic accuracy of medial temporal lobe atrophy in Alzheimer’s disease. Journal of Alzheimers Disease, In druk.Google Scholar
  19. Jacobs, H.I.L., Visser, P.J., Boxtel, M.P. van, Frisoni, G.B., Tsolaki, M., Papapostolou, P., et al. (2010). The association between white matter hyperintensities and executive decline in mild cognitive impairment is network dependent. Neurobiology of Aging.Google Scholar
  20. Jhoo, J.H., Lee, D.Y., Choo, I.H., Seo, E.H., Oh, J.S., Lee, J.S., et al. (2010). Discrimination of normal aging, MCI and AD with multimodal imaging measures on the medial temporal lobe. Psychiatry Research, 183,3, 237–243.PubMedCrossRefGoogle Scholar
  21. Koch, W., Teipel, S., Mueller, S., Benninghoff, J., Wagner, M., Bokde, A.L., et al. (2010). Diagnostic power of default mode network resting state fMRI in the detection of Alzheimer’s disease. Neurobiology of Aging.Google Scholar
  22. Korczyn, A.D. (2008). The amyloid cascade hypothesis. Alzheimers & Dementia, 4,3, 176–178.CrossRefGoogle Scholar
  23. Le Bihan, D. (2003). Looking into the functional architecture of the brain with diffusion MRI. Nature Reviews Neuroscience, 4,6, 469–480.PubMedCrossRefGoogle Scholar
  24. Matsuda, H. (2007). Role of neuroimaging in Alzheimer’s disease, with emphasis on brain perfusion SPECT. Journal of Nuclear Medicine, 48,8, 1289–1300.PubMedCrossRefGoogle Scholar
  25. Mentis, M.J., Alexander, G.E., Krasuski, J., Pietrini, P., Furey, M.L., Schapiro, M.B., et al. (1998). Increasing required neural response to expose abnormal brain function in mild versus moderate or severe Alzheimer’s disease: PET study using parametric visual stimulation. American Journal of Psychiatry, 155,6, 785–794.PubMedGoogle Scholar
  26. Nieuwenhuys, R., Voogd, J. & van Huijzen, C. (2008). The Human Nervous System (4th ed.). Berlin, Heidelberg, New York: Springer Verlag.Google Scholar
  27. Petersen, R.C. & Negash, S. (2008). Mild cognitive impairment: an overview. CNS Spectrums, 13,1, 45–53.PubMedGoogle Scholar
  28. Raichle, M.E., MacLeod, A.M., Snyder, A.Z., Powers, W.J., Gusnard, D.A. & Shulman, G.L. (2001). A default mode of brain function. Proceedings of the National Academy of Sciences of the USA, 98,2, 676–682.PubMedCrossRefGoogle Scholar
  29. Roebroeck, A., Formisano, E. & Goebel, R. (2005). Mapping directed influence over the brain using Granger causality and fMRI. Neuroimage, 25,1, 230–242.PubMedCrossRefGoogle Scholar
  30. Salat, D.H., Tuch, D.S., Kouwe, A.J. van der, Greve, D.N., Pappu, V., Lee, S.Y., et al. (2010). White matter pathology isolates the hippocampal formation in Alzheimer’s disease. Neurobiology of Aging, 31,2, 244–256.PubMedCrossRefGoogle Scholar
  31. Singh, V., Chertkow, H., Lerch, J.P., Evans, A.C., Dorr, A.E. & Kabani, N.J. (2006). Spatial patterns of cortical thinning in mild cognitive impairment and Alzheimer’s disease. Brain, 129(Pt 11), 2885–2893.PubMedCrossRefGoogle Scholar
  32. Thal, D.R., Rub, U., Orantes, M. & Braak, H. (2002). Phases of A beta-deposition in the human brain and its relevance for the development of AD. Neurology, 58,12, 1791–1800.PubMedGoogle Scholar
  33. Wilson, R.S., Leurgans, S.E., Boyle, P.A. & Bennett, D.A. (2011). Cognitive decline in prodromal Alzheimer disease and mild cognitive impairment. Archives of Neurology, 68,3, 351–356.PubMedCrossRefGoogle Scholar
  34. Wimo, A., Winblad, B., Aguero-Torres, H. & Strauss, E. von (2003). The magnitude of dementia occurrence in the world. Alzheimer Disease and Associated Disorders, 17,2, 63–67.PubMedCrossRefGoogle Scholar
  35. Woodard, J.L., Seidenberg, M., Nielson, K.A., Antuono, P., Guidotti, L., Durgerian, S., et al. (2009). Semantic memory activation in amnestic mild cognitive impairment. Brain, 132(Pt 8), 2068–2078.PubMedCrossRefGoogle Scholar
  36. Yoshita, M., Fletcher, E., Harvey, D., Ortega, M., Martinez, O., Mungas, D.M., et al. (2006). Extent and distribution of white matter hyperintensities in normal aging, MCI, and AD. Neurology, 67,12, 2192–2198.PubMedCrossRefGoogle Scholar

Copyright information

© Bohn, Stafleu van Loghum 2011

Authors and Affiliations

  • Heidi Jacobs
    • 1
  1. 1.School for Mental Health and Neuroscience, Alzheimer Center LimburgUniversiteit MaastrichtMaastrichtThe Netherlands

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