Dendritic changes in the basal nucleus of meynert and in the diagonal band nucleus in Alzheimer's disease—A quantitative Golgi investigation

Arendt, Thomas; Zvegintseva, H G; Leontovich, T. A.

doi:10.1016/0306-4522(86)90141-7

Cited by 114 publications

(46 citation statements)

References 42 publications

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“…Morphological analysis of VAChT-IR neurons followed a method adapted from a study by Arendt et al (1986), in which they used branch order to describe morphological differences in human basal forebrain neurons. A centrifugal ordering system was used to establish branch order in a neuron (Fig.…”

Section: Methodsmentioning

confidence: 99%

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Dominguez¹,

Jalali²,

Lacalle³

2004

J. Neurosci.

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In the present study, we examined the ability of estrogen to enhance cholinergic neurite arborization in vitro and identified the signal transduction cascade associated with this effect. Basal forebrain primordia collected from rat pups on postnatal day 1 were cultured for 2 weeks and then treated with 5 nM 17␤-estradiol for 24 hr. Cholinergic neurons were identified immunocytochemically with an antibody against the vesicular acetylcholine transporter and digitally photographed. Morphological analysis indicated that female cultures respond to estrogen treatment with an increase in total neurite length per neuron (4.5-fold over untreated controls) and in total branch segment number per neuron (2.3-fold over controls). In contrast, there was no change in total neurite length per neuron in male cultures, and we also observed a decrease in total branch segment number per neuron (0.5-fold below controls). Detailed histograms indicated that estrogen increases primary and secondary branch length and number and also increases terminal neuritic branches to the seventh order in female cultures. In a second set of experiments, we investigated the signal transduction cascade involved in this response, and found that an upstream extracellular signal-regulated kinase (ERK) inhibitor blocked the ability of estrogen to enhance outgrowth in female cultures. Our study provides strong evidence in support of the fact that the ERK pathway is required for estrogen-induced structural plasticity in the cholinergic system of female rats. Understanding the intracellular processes that underlie the response of cholinergic neurons to estrogen provides a necessary step in elucidating how cholinergic neurons can be particularly susceptible to degeneration in postmenopausal women.

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Section: Methodsmentioning

confidence: 99%

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Dominguez¹,

Jalali²,

Lacalle³

2004

J. Neurosci.

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“…Under certain conditions, however, these compensational processes might be maladaptive and eventually even contribute to the development and progression of the disease. This seems to be the situation in Alzheimer's disease (AD) (Geddes et al, 1985;Arendt et al, 1986;Butcher and Woolf, 1989), where an aberrant dendritic growth is observed (Scheibel and Tomiyasu, 1978;Ferrer et al, 1983;Arendt et al, 1986Arendt et al, , 1995bIhara et al, 1988;McKee et al, 1989) instead of the regular dendritic growth seen during aging and in a variety of related degenerative disorders (Buell and Coleman, 1979;Graveland et al, 1985;Coleman and Flood, 1987;Arendt et al, 1995b,c).…”

Section: Abstract: Alzheimer's Disease; Apolipoprotein E; Degeneratimentioning

confidence: 99%

“…Reconstruction of neurons and quantitative measurements were made in three dimensions with reference to a defined Cartesian system of axis by digitizing the neuron directly from serial sections with help of a semiautomatic image analyzing system (Orthoplan-3D, Leitz Wetzlar and analySIS, Münster, Germany). From the digitized image, the total dendritic length per neuron and the number of dendritic segments of each order using the centrifugal ordering system were calculated (Arendt et al, 1986(Arendt et al, , 1995a. No correction for tissue shrinkage was made.…”

Section: Methodsmentioning

confidence: 99%

Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

Arendt¹,

Schindler²,

Brückner³

et al. 1997

J. Neurosci.

309

174

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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 ⑀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 ⑀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 ⑀4 allele was very weak in the presence of one ⑀4 allele and completely lost in patients homozygous for the ⑀4 allele.The results provide direct evidence that neuronal reorganization is affected severely in patients with Alzheimer's disease carrying the apoE ⑀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.

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“…Indeed, several lines of evidence suggest that neuronal hypertrophy is inherent to AD. As such, nuclear hypertrophy and increases in cell size and dendritic arborization have been described in neurons from the nucleus basalis of Meynert of AD brain, 64,65 a region susceptible of suffering neurodegeneration in this disease. Furthermore, expression of the Swedish mutant form of APP in transgenic mice has been shown to induce cell cycle re-entry and increases of size in cortical neurons.…”

Section: Somatic Tetraploidy and Hypertrophy In Ad-affected Neuronsmentioning

confidence: 94%

A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75^NTR

Frade

López-Sánchez²

2010

Cell Cycle

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Dendritic changes in the basal nucleus of meynert and in the diagonal band nucleus in Alzheimer's disease—A quantitative Golgi investigation

Cited by 114 publications

References 42 publications

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75^NTR

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Dendritic changes in the basal nucleus of meynert and in the diagonal band nucleus in Alzheimer's disease—A quantitative Golgi investigation

Cited by 114 publications

References 42 publications

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75NTR

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Product

Resources

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A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75^NTR