Abstract

In the present paper, we analyze the cell number within lamina X at the end stage of disease in a G93A mouse model of ALS; the effects induced by lithium; the stem-cell like phenotype of lamina X cells during ALS; the differentiation of these cells towards either a glial or neuronal phenotype. In summary we found that G93A mouse model of ALS produces an increase in lamina X cells which is further augmented by lithium administration. In the absence of lithium these nestin positive stem-like cells preferentially differentiate into glia (GFAP positive), while in the presence of lithium these cells differentiate towards a neuron-like phenotype (βIII-tubulin, NeuN, and calbindin-D28K positive). These effects of lithium are observed concomitantly with attenuation in disease progression and are reminiscent of neurogenetic effects induced by lithium in the subependymal ventricular zone of the hippocampus.

Highlights

  • Plastic changes were described in the spinal cord in the course of amyotrophic lateral sclerosis [1, 2]

  • In summary we found that G93A mouse model of ALS produces an increase in lamina X cells which is further augmented by lithium administration

  • In the absence of lithium these nestin positive stem-like cells preferentially differentiate into glia (GFAP positive), while in the presence of lithium these cells differentiate towards a neuronlike phenotype

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Summary

Introduction

Plastic changes were described in the spinal cord in the course of amyotrophic lateral sclerosis [1, 2] These consist of various morphological effects involving both resident cells such as neurons and glia and nonresident inflammatory cells. The sprouting of axon collaterals from spared motor neuron at the level of the peripheral muscles is well described [3, 4]. This is consistent during the disease course and it represents a marker of disease when it is detected by using electromyography. In keeping with stem cells, only a few studies focused on the occurrence of adult stem cells in ALS spinal cord

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