Role of β-Amyloid in the Diagnosis of Neurodegenerative Diseases: Diffuse Lewy Body Disease Versus Alzheimer’s Disease
Deposition of β-amyloid senile plaques in the neuropil and the formation of intracellular neurofibrillary tangles are the histopathological hallmarks of both sporadic and familial forms of Alzheimer’s disease (AD). Excess β-amyloid, formed from abnormal processing of β-amyloid precursor protein (β-APP) coded for on chromosome 21, can also be found in aged individuals with Down’s syndrome (Trisomy 21) as well as in the recently described cases of diffuse Lewy body disease (DLBD) (Gibb et al., 1989; Kosaka, 1993; Kuzuhara and Yoshimura, 1993). Patients with the pure form of DLBD are characterized clinically by progressive dementia with fluctuating confusional states and visual hallucinations, followed later by Parkinsonian symptoms (Byrne et al., 1989; Forstl et al., 1993; Kosaka, et al., 1980; and Perry et al., 1993). Parkinsonism rarely is the presenting symptom. Neuropathological findings include Lewy bodies both in the neuromelanin containing cells of the substantia nigra as well as in the neocortex but few, if any, neurofibrillary tangles. The occurrence of DLBD as well as the Lewy body variant of AD (LBVAD) is not as rare as previously thought (Gibb et al., 1989; Forstl et al., 1993). The LBVAD has features of both DLBD and AD. It has been found that, when combined, both types of Lewy body disease are the second leading cause of non-vascular dementia following classical AD.
KeywordsLewy Body Neurofibrillary Tangle Brodmann Area Neuritic Plaque Lewy Body Dementia
Unable to display preview. Download preview PDF.
- Bancher, C., Lassmann, H., Budka, H., Jellinger, K., Grundke-Iqbal, I., Iqbal, K., Wiche, G., Seitelberger, F., and Wisniewski, H.M., 1989, An antigenic profile of Lewy bodies:Immunocytochemical indication for protein phosphorylation and ubiquitination, J. Neuropathol. Exp. Neurol. 48: 81–92.PubMedCrossRefGoogle Scholar
- Drewes, G., Lichtenberg-Kraag, B., Dozing, F., Mandelkow, E.-M., Biemat, J., Goris, J., Doree, M., and Mandelkow, E., 1992, Mitogen activated protein (MAP) kinase transforms tau protein into an Alzheimer-like state, EMBO J. 11:2131–2138.Google Scholar
- Gibb, W.R.G., Mountjoy, C.Q., Mann, D.M.A., and Lees, A.J., 1989, A pathological study of the association between Lewy body disease and Alzheimer’s disease, J. Neurol. Neurosurg. Psychiatry 52: 701–708.Google Scholar
- Kosaka, K., Matsushita, M., Oyanagi, S., and Mehraein, P., 1980, A clinicopathological study of the “Lewy body disease”, Psychiatr. Neurol. Jpn. 82: 292–311.Google Scholar
- Kosaka, K.,1993, Dementia and neuropathology in Lewy body disease, Adv. Neurol. 60:456–463. Kuzuhara, S., and Yoshimura, M., 1993, Clinical and neuropathological aspects of diffuse Lewy body diseasein in the elderly, Adv. Neurol. 60: 464–469.Google Scholar
- Lichtenberg-Kraag, B., Mandelkow, E.-M., Biemat, J., Steiner, B., Schroter, C., Gustke, N., Meyer, H.E., and Mandelkow, E., 1992, Phosphorylation-dependent epitopes of neurofilament antibodies on tau protein and relationship with Alzheimer tau, Proc. Natl. Acad. Sci. USA 89: 5384–5388.PubMedCrossRefGoogle Scholar
- Perry, E.K., Irving, D., Kerwin, J.M., McKeith, I.G., Thompson, P., Collerton, D., Fairbairn, A.F., Ince, P.G., Morris, C.M., Cheng, A.V., and Perry, R.H., 1993, Cholinergie transmitter and neurotrophic activities in Lewy body dementia: Similarity to Parkinson’s and distinction from Alzheimer’s disease, Alzheimer Dis. Assoc. Disord. 7: 69–79.Google Scholar