L A Hansen1, S E Daniel, G K Wilcock, S Love. 1. Department of Pathology, University of California, San Diego, La Jolla 92093-0624, USA. lahansen@UCSD.edu
Abstract
OBJECTIVES: Dementia in Alzheimer's disease correlates closely with loss of neocortical synapses. Similar synaptic loss has been shown in patients whose Alzheimer's disease is also associated with neocortical and brain stem Lewy bodies. The aim was to determine if dementia in Lewy body disease was associated with diminished concentrations of midfrontal cortex synaptophysin. METHODS: An immunobinding assay was used to measure synaptophysin in postmortem samples of midfrontal cortex from 89 patients with Alzheimer's disease (ages 59-100, mean 79), 22 with combined Lewy body disease and Alzheimer's disease (ages 69-103, mean 79), 15 demented patients with "pure" Lewy body disease (ages 57-80, mean 74), nine with neocortical and brain stem Lewy bodies who had Parkinson's disease but were not demented (ages 68-85, mean 79), and 20 neurologically normal controls (ages 58-89, mean 75). The diagnosis was confirmed in all cases by detailed neuropathological examination of the contralateral hemibrain. Seven of the patients in the pure Lewy body disease with dementia group had initially presented with parkinsonism and eight with dementia. RESULTS: Synaptophysin concentrations (arbitrary units (AU)/microg) in patients with Alzheimer's disease (mean 79 (SD 28)) or combined Lewy body disease and Alzheimer's disease (mean 83 (SD 33)) were significantly lower than in controls (mean 115 (SD 29)) (p=0.002). Synaptophysin concentrations in demented patients with pure Lewy body disease (mean 106 SD 39) and patients with Lewy body disease who were not demented (mean 101 (SD 18)) did not differ significantly from control values or from each other. CONCLUSION: Loss of midfrontal cortex synapses probably contributes to dementia in Lewy body disease when Alzheimer's disease is also present but not to the dementia of pure Lewy body disease.
OBJECTIVES:Dementia in Alzheimer's disease correlates closely with loss of neocortical synapses. Similar synaptic loss has been shown in patients whose Alzheimer's disease is also associated with neocortical and brain stem Lewy bodies. The aim was to determine if dementia in Lewy body disease was associated with diminished concentrations of midfrontal cortex synaptophysin. METHODS: An immunobinding assay was used to measure synaptophysin in postmortem samples of midfrontal cortex from 89 patients with Alzheimer's disease (ages 59-100, mean 79), 22 with combined Lewy body disease and Alzheimer's disease (ages 69-103, mean 79), 15 demented patients with "pure" Lewy body disease (ages 57-80, mean 74), nine with neocortical and brain stem Lewy bodies who had Parkinson's disease but were not demented (ages 68-85, mean 79), and 20 neurologically normal controls (ages 58-89, mean 75). The diagnosis was confirmed in all cases by detailed neuropathological examination of the contralateral hemibrain. Seven of the patients in the pure Lewy body disease with dementia group had initially presented with parkinsonism and eight with dementia. RESULTS:Synaptophysin concentrations (arbitrary units (AU)/microg) in patients with Alzheimer's disease (mean 79 (SD 28)) or combined Lewy body disease and Alzheimer's disease (mean 83 (SD 33)) were significantly lower than in controls (mean 115 (SD 29)) (p=0.002). Synaptophysin concentrations in demented patients with pure Lewy body disease (mean 106 SD 39) and patients with Lewy body disease who were not demented (mean 101 (SD 18)) did not differ significantly from control values or from each other. CONCLUSION: Loss of midfrontal cortex synapses probably contributes to dementia in Lewy body disease when Alzheimer's disease is also present but not to the dementia of pure Lewy body disease.
Authors: E K Perry; I McKeith; P Thompson; E Marshall; J Kerwin; S Jabeen; J A Edwardson; P Ince; G Blessed; D Irving Journal: Ann N Y Acad Sci Date: 1991 Impact factor: 5.691
Authors: R D Terry; E Masliah; D P Salmon; N Butters; R DeTeresa; R Hill; L A Hansen; R Katzman Journal: Ann Neurol Date: 1991-10 Impact factor: 10.422
Authors: G Lennox; J Lowe; M Landon; E J Byrne; R J Mayer; R B Godwin-Austen Journal: J Neurol Neurosurg Psychiatry Date: 1989-11 Impact factor: 10.154
Authors: L Hansen; D Salmon; D Galasko; E Masliah; R Katzman; R DeTeresa; L Thal; M M Pay; R Hofstetter; M Klauber Journal: Neurology Date: 1990-01 Impact factor: 9.910
Authors: E K Perry; E Marshall; R H Perry; D Irving; C J Smith; G Blessed; A F Fairbairn Journal: Alzheimer Dis Assoc Disord Date: 1990 Impact factor: 2.703
Authors: E K Perry; M Curtis; D J Dick; J M Candy; J R Atack; C A Bloxham; G Blessed; A Fairbairn; B E Tomlinson; R H Perry Journal: J Neurol Neurosurg Psychiatry Date: 1985-05 Impact factor: 10.154
Authors: Stephanie Lessig; Kiren Ubhi; Douglas Galasko; Anthony Adame; Emiley Pham; Kelly Remidios; Michael Chang; Lawrence A Hansen; Eliezer Masliah Journal: Neuroreport Date: 2010-08-04 Impact factor: 1.837
Authors: Chandresh R Gajera; Rosemary Fernandez; Nadia Postupna; Kathleen S Montine; Edward J Fox; Dmitry Tebaykin; Michael Angelo; Sean C Bendall; C Dirk Keene; Thomas J Montine Journal: J Neurosci Methods Date: 2018-11-20 Impact factor: 2.390
Authors: Leslie Crews; Brian Spencer; Paula Desplats; Christina Patrick; Amy Paulino; Edward Rockenstein; Lawrence Hansen; Anthony Adame; Douglas Galasko; Eliezer Masliah Journal: PLoS One Date: 2010-02-19 Impact factor: 3.240