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PMID: 8987775 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Plastic neuronal remodeling is impaired in patients with Alzheimer's disease carrying apolipoprotein epsilon 4 allele.

The Journal of neuroscience : the official journal of the Society for Neuroscience ·Vol. 17 ·No. 2 ·1997-01-15 ·Pages 516-29

Arendt T, Schindler C, Brückner MK, Eschrich K, Bigl V, Zedlick D, Marcova L

Abstract

A relationship between the apolipoprotein E (apoE) genotype and the risk to develop Alzheimer's disease has been established recently. Apolipoprotein synthesis is implicated in developmental processes and in neuronal repair of the adult nervous system. In the present study, we investigated the influence of the apolipoprotein polymorphism on the severity of neuronal degeneration and the extent of plastic dendritic remodeling in Alzheimer's disease. Changes in length and arborization of dendrites of Golgi-impregnated neurons in the basal nucleus of Meynert, locus coeruleus, raphe magnus nucleus, medial amygdaloid nucleus, pedunculopontine tegmental nucleus, and substantia nigra were analyzed after three-dimensional reconstruction. Patients with either one or two apoE epsilon 4 alleles not only showed a more severe degeneration in all areas investigated than in patients lacking the apoE 4 allele but also revealed significantly less plastic dendritic changes. ApoE epsilon 4 allele copy number, furthermore, had a significant effect on the pattern of dendritic arborization. Moreover, the relationship between the intensity of dendritic growth and both the extent of neuronal degeneration and the stage of the disease seen in patients lacking the apoE epsilon 4 allele was very weak in the presence of one epsilon 4 allele and completely lost in patients homozygous for the epsilon 4 allele. The results provide direct evidence that neuronal reorganization is affected severely in patients with Alzheimer's disease carrying the apoE epsilon 4 allele. This impairment of neuronal repair might lead to a more rapid functional decompensation, thereby contributing to an earlier onset and more rapid progression of the disease.

MeSH Terms
Aged Aged, 80 and over Alleles Alzheimer Disease/genetics,pathology Apolipoprotein E4 Apolipoproteins E/genetics Brain/pathology Choline O-Acetyltransferase/analysis Dendrites/ultrastructure Female Genotype Humans Male Nerve Degeneration/genetics,pathology Nerve Tissue Proteins/analysis Neuronal Plasticity/genetics Neurons/pathology Polymorphism, Genetic
Chemicals
Apolipoprotein E4 Apolipoproteins E Nerve Tissue Proteins Choline O-Acetyltransferase
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Arendt T
Department of Neurochemistry, Paul Flechsig Institute of Brain Research, Leipzig, Germany.
Schindler C
Brückner M K
Eschrich K
Bigl V
Zedlick D
Marcova L
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Article Info
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
Abbr.
J Neurosci
ISSN
0270-6474
Published
1997-01-15
Pages
516-29
Language
English
Region
United States
NLM ID
8102140
PMCID
PMC6573225
Subset
IM
External Links
PubMed source PMC Full Text View journal details
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