Hostname: page-component-586b7cd67f-dlnhk Total loading time: 0 Render date: 2024-11-25T07:19:29.323Z Has data issue: false hasContentIssue false
  • English
  • Français

Acute tryptophan depletion and Lewy body dementias

Published online by Cambridge University Press:  18 March 2016

Janet L. Mace ,
Richard J. Porter ,
John C. Dalrymple-Alford ,
Chris Collins  and
Tim J. Anderson
Janet L. Mace
Affiliation:
Department of Medicine and Pharmacology, The University of Western Australia, Perth, Australia
Richard J. Porter*
Affiliation:
Department of Psychological Medicine, University of Otago, Christchurch, New Zealand
John C. Dalrymple-Alford
Affiliation:
Department of Psychology, University of Canterbury, Christchurch, New Zealand New Zealand Brain Research Institute, Christchurch, New Zealand
Chris Collins
Affiliation:
Psychiatric Services for the Elderly, Princess Margaret Hospital, Christchurch, New Zealand
Tim J. Anderson
Affiliation:
New Zealand Brain Research Institute, Christchurch, New Zealand Department of Medicine, University of Otago, Christchurch, New Zealand
*
Correspondence should be addressed to: Professor R. J. Porter, Department of Psychological Medicine, University of Otago, Christchurch, PO Box 4345 Christchurch, New Zealand. Phone: +64 3 372 0400; Fax: +64 3 372 0407. Email: [email protected].
Get access Rights & Permissions [Opens in a new window]

Abstract

Background:

Studies using acute tryptophan depletion (ATD) to examine the effects of a rapid reduction in serotonin function have shown a reduction in global cognitive status during ATD in Alzheimer's disease (AD) and Parkinson's disease (PD). Based on the severe cholinergic loss evident in dementia with Lewy bodies (DLB) and Parkinson's disease and dementia (PDD), we predicted that a reduction of global cognitive status during ATD would be greater in these conditions than in AD.

Methods:

Patients having DLB or PDD underwent ATD in a double-blind, placebo-controlled, randomized, counterbalanced, crossover design.

Results:

While the study intended to test 20 patients, the protocol was poorly tolerated and terminated after six patients attempted, but only four patients – three with DLB and one with PDD – completed the protocol. The Modified Mini-Mental State Examination (3MSE) score was reduced in all three DLB patients and unchanged in the PDD and dementia patient during ATD compared with placebo.

Conclusions:

This reduction in global cognitive function and the poor tolerability may fit with the hypothesis that people with dementia with Lewy bodies have sensitivity to the effects of reduced serotonin function.

Keywords

Parkinson's diseasedementiamemorycognitive disordersdementia with Lewy bodies
Type
Research Article
Information
International Psychogeriatrics , Volume 28 , Issue 9 , September 2016 , pp. 1487 - 1491
Copyright
Copyright © International Psychogeriatric Association 2016 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Bohnen, N. I., Kaufer, D. I., Hendrickson, R., Constantine, G. M., Mathis, C. A. and Moore, R. Y. (2007). Cortical cholinergic denervation is associated with depressive symptoms in Parkinson's disease and parkinsonian dementia. Journal of Neurology, Neurosurgery, and Psychiatry, 78, 641–643.CrossRefGoogle ScholarPubMed
Bohnen, N. I. et al. (2003). Cortical cholinergic function is more severely affected in parkinsonian dementia than in Alzheimer disease: an in vivo positron emission tomographic study. Archives of Neurology and Psychiatry, 60, 1745–1748.Google Scholar
Emre, M. et al. (2007). Clinical diagnostic criteria for dementia associated with Parkinson's disease. Movement Disorders, 22, 1689–1707; quiz 1837.Google Scholar
Hoehn, M. M. and Yahr, M. D. (1967). Parkinsonism: onset, progression and mortality. Neurology, 17, 427–442.CrossRefGoogle ScholarPubMed
Mace, J. L., Porter, R. J., Dalrymple-Alford, J. C. and Anderson, T. J. (2010a). The effects of acute tryptophan depletion on mood in patients with Parkinson's disease and the healthy elderly. Journal of Psychopharmacology, 24, 615–619.Google Scholar
Mace, J. L., Porter, R. J., Dalrymple-Alford, J. C., Wesnes, K. A. and Anderson, T. J. (2010b). Effects of acute tryptophan depletion on neuropsychological and motor function in Parkinson's disease. Journal of Psychopharmacology, 24, 1465–1472.CrossRefGoogle ScholarPubMed
Mace, J. L., Porter, R. J., Dalrymple-Alford, J. C., Wesnes, K. A. and Anderson, T. J. (2011). The effects of acute tryptophan depletion on neuropsychological function, mood and movement in the healthy elderly. Journal of Psychopharmacology, 25, 1337–1343.Google Scholar
McKeith, I. G. et al. (1996). Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. Neurology, 47, 1113–1124.Google Scholar
Nelson, H. E. (1982). National Adult Reading Test Manual, Windsor: NFER-Nelson.Google Scholar
Porter, R. J., Bourke, C. and Gallagher, P. (2007). Neuropsychological impairment in major depression: its nature, origin and clinical significance. Australian and New Zealand Journal of Psychiatry, 41, 115–128.CrossRefGoogle ScholarPubMed
Porter, R. J., Lunn, B. S. and O'Brien, J. T. (2003). Effects of acute tryptophan depletion on cognitive function in Alzheimer's disease and in the healthy elderly. Psychological Medicine, 33, 41–49.Google Scholar
Porter, R. J., Lunn, B. S., Walker, L. L., Gray, J. M., Ballard, C. G. and O'Brien, J. T. (2000). Cognitive deficit induced by acute tryptophan depletion in patients with Alzheimer's disease. American Journal of Psychiatry, 157, 638–640.CrossRefGoogle ScholarPubMed
Porter, R. J., Phipps, A. J., Gallagher, P., Scott, A., Stevenson, P. S. and O'Brien, J. T. (2005). Effects of acute tryptophan depletion on mood and cognitive functioning in older recovered depressed subjects. American Journal of Geriatric Psychiatry, 13, 607–615.Google Scholar
Price, L. H., Malison, R. T., McDougle, C. J., McCance-Katz, E. F., Owen, K. R. and Heninger, G. R. (1997). Neurobiology of tryptophan depletion in depression: effects of m-chlorophenylpiperazine (mCPP). Neuropsychopharmacology, 17, 342–350.Google Scholar
Scholtissen, B., Verhey, F. R., Adam, J. J., Prickaerts, J. and Leentjens, A. F. (2006). Effects of acute tryptophan depletion on cognition, memory and motor performance in Parkinson's disease. Journal of the Neurological Sciences, 248, 259–265.Google Scholar
Teng, E. L. and Chui, H. C. (1991). Manual for the Administration and Scoring of the Modified Mini-Mental State (3MS) test., Los Angeles: University of Southern California School of Medicine.Google Scholar
Tiraboschi, P. et al. (2002). Early and widespread cholinergic losses differentiate dementia with Lewy bodies from Alzheimer disease. Archives of General Psychiatry, 59, 946–951.Google Scholar
Walker, M. P. et al. (2000). The clinician assessment of fluctuation and the one day fluctuation assessment scale. Two methods to assess fluctuating confusion in dementia. British Journal of Psychiatry, 177, 252–256.CrossRefGoogle ScholarPubMed
Young, S. N. (2013). Acute tryptophan depletion in humans: a review of theoretical, practical and ethical aspects. Journal of Psychiatry and Neuroscience, 38, 294–305.CrossRefGoogle ScholarPubMed