Hostname: page-component-848d4c4894-m9kch Total loading time: 0 Render date: 2024-05-19T12:59:22.139Z Has data issue: false hasContentIssue false

Cell Loss from the Nucleus Basalis of Meynert in Alzheimer's Disease

Published online by Cambridge University Press:  18 September 2015

R. Doucette*
Affiliation:
Department of Anatomy, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan
M. Fisman
Affiliation:
Department of Psychiatry, London Psychiatric Hospital, London, Ontario
V.C. Hachinski
Affiliation:
Department of Clinical Neurological Sciences, University Hospital, London, Ontario
H. Mersky
Affiliation:
Department of Psychiatry, London Psychiatric Hospital, London, Ontario
*
Department of Anatomy, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N 0X0
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

We examined the degree of neuronal loss from the nucleus basalis of Meynert (nbM) in two groups of Alzheimer patients differing in the degree of intellectual impairment. Significant cell loss from the nbM was found only in the more severely demented group of patients. Mean cell counts (per lOu, paraffin section) were compiled separately for the anterior, intermediate and posterior subdivisions of the human nbM in three groups of subjects: Group 1 (N = 4) was severely demented and was untestable on the Extended Scale for Dementia (ESD) for at least the last two years of life; Group 2 (N = 4) was less demented and had completed at least one ESD test within 12 months of death; Group 3 (five controls) had died of non-neurological causes. In Group 2 there was a small (but insignificant) trend toward cell loss in the anterior subdivision, and a normal complement of neurons in both the intermediate and posterior subdivisions. There was, however, significant cell loss from all subdivisions of Group 1. How these cell counts may relate to the severity of the dementia is discussed.

Type
Cellular Clues to Pathogenesis
Copyright
Copyright © Canadian Neurological Sciences Federation 1986

References

1.Blessed, G, Tomlinson, BE and Roth, M.The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects. Brit J Psych 1986; 114: 797811.CrossRefGoogle Scholar
2.Wilcock, GK and Esiri, MM.Plaques, tangles and dementia: A quantitative study. J Neurol Sci 1982; 56; 343356.CrossRefGoogle ScholarPubMed
3.Arendt, T, Bigl, V, Tennstedt, A and Arendt, A.Correlation between cortical plaque count and neuronal loss in the nucleus basalis in Alzheimer’s disease. Neurosci Lett 1984; 48(1): 8186.CrossRefGoogle ScholarPubMed
4.Mann, DM, Yates, PO and Marcyniuk, B.Correlation between senile plaque and neurofibrillary tangle counts in cerebral cortex and neuronal counts in cortex and subcortical structures in Alzheimer’s Disease. Neurosci Lett 1985; 56: 5155.CrossRefGoogle ScholarPubMed
5.Hersch, EL.Development and application of the extended scale for dementia. J Amer Ger Soc 1979; 28: 348354.CrossRefGoogle Scholar
6.Kiernan, JA.Histological and Histochemical Methods”, Oxford: Pergamon Press.Google Scholar
7.Mesulam, M-M, Mufson, EJ, Levey, AI and Wainer, BH.Cholinergic innervation of cortex by the basal forebrain: Cytochemistry and cortical connections of the septal area, diagonal band nuclei, nucleus basalis (substantia innominata) and hypothalamus in the rhesus monkey. J Comp Neurol 1983; 214: 170197.CrossRefGoogle ScholarPubMed
8.Abercrombie, M.Estimation of nuclear population from microtome sections. Anat Rec 1946; 94: 239247.CrossRefGoogle ScholarPubMed
9.McGeer, PL, McGeer, EG, Suzuki, J, Dolman, CE and Higai, T.Aging, Alzheimer’s disease, and the cholinergic system of the basal forebrain. Neurol 1984; 34(6): 741745.CrossRefGoogle ScholarPubMed
10.Pearson, RC, Sofroniew, MV, Cuello, AC, Powell, TP, Eckenstein, F, Esiri, MM and Wilcock, G.Persistence of cholinergic neurons in the basal nucleus in a brain with senile dementia of the Alzheimer’s type demonstrated by immunohistochemical staining for choline acetyl-transferase. Brain Res 1983; 289: 375379.CrossRefGoogle Scholar
11.Nagai, I, McGeer, PL, Peng, JH, McGeer, EG and Dolman, CE.Choline acetyltransferase immunohistochemistry in brains of Alzheimer’s disease patients and controls. Neurosci Lett 1983; 36: 195199.CrossRefGoogle ScholarPubMed
12.Wilcock, GK, Esiri, MM, Bowen, DM and Smith, CC.Alzheimer’s disease: Correlation of cortical choline acetyltransferase activity with the severity of dementia and histological abnormalities. J Neurol Sci 1982; 57: 407417.CrossRefGoogle ScholarPubMed
13.Candy, JM, Perry, RH, Perry, EK, Irving, D, Blessed, G, Fairbairn, AF and Tomlinson, BE.Pathological changes in the nucleus of Meynert in Alzheimer’s and Parkinsons’s diseases. J Neurol Sci 1983; 277289.CrossRefGoogle ScholarPubMed
14.Ezrin-Waters, C and Resch, L.The nucleus basalis of Meynert. Can J Neurol Sci 1986; 13: 814.CrossRefGoogle ScholarPubMed
15.Perry, EK.The cholinergic hypothesis: Ten years on. Brit Med Bull 1986, 42: 6369.CrossRefGoogle Scholar
16.Whitehouse, PJ, Price, DL, Clark, AW, Coyle, JT and DeLong, MR.Alzheimer’s disease: Evidence for selective loss of cholinergic neurons in the nucleus basalis. Ann Neurol 1981; 10: 122126.CrossRefGoogle ScholarPubMed
17.Tagliavini, F and Pilleri, G.Basal nucleus of Meynert: A neuropathological study in Alzheimer’s disease, simple senile dementia, Pick’s disease and Huntington’s chorea. J Neurol Sci 1983; 62(1–3): 243260.CrossRefGoogle ScholarPubMed
18.Arendt, T, Bigl, V, Arendt, A and Tennstedt, A.Loss of neurons in the nucleus basalis of Meynert in Alzheimer’s disease, paralysis agitans and Korsakoff’s disease. Acta Neuropath 1983; 61: 101108.CrossRefGoogle ScholarPubMed
19.Mann, DM and Yates, PO.qIs the loss of cerebral cortical CAT activity in Alzheimer’s disease due to degeneration of ascending cholinergic nerve cells? J Neurol Neurosurg Psychiat 1982; 45: 936943.CrossRefGoogle Scholar
20.Whitehouse, PJ, Price, DL, Struble, RG, Clark, AW, Coyle, JT and DeLong, MR.Alzheimer’s disease and senile dementia: Loss of neurons in the basal forebrain. Science 1982; 215: 12371239.CrossRefGoogle ScholarPubMed
21.Perry, RH, Candy, JM, Perry, EK, Irving, D, Blessed, G, Fairburn, AF and Tomlinson, BE.Extensive loss of choline acetyltransferase activity is not reflected by neuronal loss in nucleus of Meynert in Alzheimer’s disease. Neurosci Lett 1982; 33: 311315.CrossRefGoogle Scholar
22.Wilcock, GK, Esiri, MM, Bowen, DM and Smith, CC.The nucleus basalis in Alzheimer’s disease: Cell counts and cortical biochemistry. Neuropath Appl Neurobiol 1983; 9: 175179.CrossRefGoogle ScholarPubMed
23.Mann, DM, Yates, PO and Marcyniuk, B.Changes in nerve cells of the nucleus basalis of Meynert in Alzheimer’s Disease and their relationship to aging and to the accumulation of lipofuscin pigment. Mech Ageing Devel 1984a; 25: 189204.CrossRefGoogle Scholar
24.Mann, DM, Yates, PO and Marcyniuk, B.Alzheimer’s presenile dementia, senile dementia of Alzheimer type and Down’s syndrome in middle age form an age related continuum of pathological changes. Neuropath Appl Neurobiol 1984b; 10(3): 185208.CrossRefGoogle ScholarPubMed
25.Mann, DM, Yates, PO and Marcyniuk, B.A comparison of changes in the nucleus basalis and locus coeruleus in Alzheimer’s disease. J Neurol Neurosurg Psychiat 1984c; 47(2): 201203.CrossRefGoogle ScholarPubMed
26.Chui, HC, Bondareff, W, Zarow, C and Slager, U.Stability of neuronal number in the human nucleus basalis of Meynert with age. Neurobiol of Aging 1984; 5: 8388.CrossRefGoogle ScholarPubMed
27.Bowen, DM, Allen, SJ, Benton, JS, et al. Biochemical assessment of serotonergic and cholinergic dysfunction and cerebral atrophy in Alzheimer’s Disease. J Neurochem 1983; 41: 261272.CrossRefGoogle ScholarPubMed
28.Arendt, T, Bigl, V, Tennstedt, A, et al. Neuronal loss in different parts of the nucleus basalis is related to neuritic plaque formation in cortical target areas in Alzheimer’s Disease. Neurosci 1985; 14: 114.CrossRefGoogle ScholarPubMed