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Commentary

Published online by Cambridge University Press:  02 January 2018

D. Neill
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The article by Byrne gives a general overview of dementia with Lewy bodies (LBD) and discusses treatment in terms of modulation of neurotransmitter systems, treatment of psychotic symptoms and extrapyramidal features. However, as is the case with Alzheimer's disease, the dementia is related to underlying pathological processes which result in death and/or malfunction of neurons. Prevention or amelioration of this neuronal loss is therefore the ultimate aim of treatment. Such treatment is not yet available and the possibility of its development is likely to depend on further elucidation of the underlying pathological process. The relationship of LBD to Alzheimer's disease and Parkinson's disease should be considered, as this is important for the determination of the underlying pathological processes in LBD.

Type
Article Commentary
Information
Advances in Psychiatric Treatment , Volume 4 , Issue 6 , November 1998 , pp. 364 - 366
Copyright
Copyright © The Royal College of Psychiatrists 1998 

References

Galasko, D., Saitoh, T., Xia, T. et al (1995) The apolipoprotein E allele eP4 is over-represented in patients with the Lewy body variant of Alzheimer's disease. Neurology, 44, 1950–1951.Google Scholar
Halliday, G., Brooks, W., Arthur, H. et al (1997) Further evidence for an association between a mutation in the APP gene and Lewy body formation. Neuroscience Letters, 227, 49–52.CrossRefGoogle ScholarPubMed
Kosaka, K., Iseki, E., Odawara, T. et al (1996) Cerebral type of Lewy body disease. Neuropathology, 16, 32–35.Google Scholar
Marder, K., Maestre, G., Cote, L. et al (1994) The apolipoprotein e4 allele in Parkinson's disease with and without dementia. Neurology, 44, 1330–1331.Google Scholar
McKenzie, J. E., Edwards, R. J., Gentleman, S. M. et al (1996) A quantitative comparison of plaque types in Alzhiemer's disease and senile dementia of the Lewy body type. Acta Neuropathologica, 91, 526–529.Google Scholar
Polymeropoulos, M. H., Lavedan, C., Leroy, E. et al (1997) Mutation in the α-synuclein gene identified in families with Parkinson's disease. Science, 276, 2045–2047.Google Scholar
Reyes, M. G., Faraldi, F., Chandran, R. et al (1996) Histopathology of the substantia nigra in Alzheimer's disease. Panminerva Medica, 38, 8–14.Google Scholar
Saitoh, T., Xia, M. S., Chen, X. et al (1995) The CYP2D6B mutant allele is overrepresented in the Lewy body variant of Alzheimer's disease. Annals of Neurology, 37, 110–112.Google Scholar
Schmidt, M. L., Martin, J. A., Lee, V. M. et al (1996) Convergence of Lewy bodies and neurofibrillary tangles in amygdala neurons of Alzheimer's disease and Lewy body disorders. Acta Neuropathologica, 91, 475–481.Google Scholar
Smith, M. C., Mallory, M., Hansen, L. A. et al (1995) Fragmentation of the neuronal cytoskeleton in the Lewy body variant of Alzheimer's disease. Neuroreport, 6, 673–676.Google Scholar
Spillantini, M. G., Schmidt, M. L., Lee, V. M. et al (1997) Alpha-synuclein in Lewy bodies (letter). Nature, 388, 839–840.CrossRefGoogle Scholar
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