Abstract

Advances in the understanding of genetic and molecular mechanisms and imaging technologies have opened a new window of research possibilities to address dynamic processes associated with neuroplasticity in physiologically intact models of neurodegenerative diseases. This review aims to: (i) establish the most relevant molecular mechanisms, as well as cellular and structural biomarkers in the study of neuroplasticity; (ii) introduce different neurodegenerative diseases in animal models that contribute to our knowledge of neuroplasticity; and (iii) illustrate the capabilities and limitations of current diffusion magnetic resonance imaging techniques to study cortical plasticity, as well as the use of alternative diffusion models.

Highlights

  • Upon the early 20th century, the rendition of the original Spanish works of 1899-1904 and French works of 1909-1911, Cajal (2002) already described in his publication structural modifications that imply the formation of new neural pathways through ramification and progressive growth of the dendritic terminals

  • A finer motor learning paradigm in mice with a Varian multi-channel 7.0T, 40 cm diameter bore magnet (30 directions with b = 1917 s/mm2, yielding a 130 μm isotropic voxel resolution) showed an increase in fractional anisotropy (FA) values located in the hippocampus (Scholz et al, 2015), underlying some of the grey matter (GM) microstructural changes occurring in these experimental paradigms. These results demonstrated the capabilities of diffusion magnetic resonance imaging (dMRI) techniques to unveil central nervous system (CNS) microstructural changes in specific GM areas associated with NP

  • During neurodevelopment and the adult age, the structural shape of the nervous system is continuously influenced by subtle functional modifications triggered by internal and external factors

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Summary

Introduction

Upon the early 20th century, the rendition of the original Spanish works of 1899-1904 and French works of 1909-1911, Cajal (2002) already described in his publication structural modifications that imply the formation of new neural pathways through ramification and progressive growth of the dendritic terminals (see Stahnisch and Nitsch 2002 and Lobato 2008). Molecular and cellular mechanisms of NP phenomena can be classified into other sorts: functional NP, which includes changes in the efficacy of synaptic transmissions such as long-term potentiation and the activation of silent synapses; and structural NP, associated to changes in cell structure, as well as mechanisms of axonal regeneration, collateralization and reactive synaptogenesis (BergadoRosado and Almaguer Melián, 2000) We will provide a further assessment of how such histological descriptors can vary in the context of different preclinical animal models of NDDs and the application of dMRI techniques to study the interconnected flexible structural and functional phenomena in intact physiological organisms (Fig. 1). The combination of different molecular, neuropathological, and imaging technologies will provide a further understanding of how the NP mechanisms operate, with a better application of this knowledge in the discovery of new neuroregenerative therapies in patients with NDDs

General molecular mechanisms of neuroplasticity
Glutamate receptors There are two types of glutamate receptors
Protein-kinases
Gangliosides
Steroids
Microstructural neuroplasticity
Axonal regeneration and plasticity
Gray matter neuroplasticity
Amyotrophic lateral sclerosis
Diffusion MRI: limitations and future directions in neuroplasticity and NDDs
Findings
Concluding remarks
Full Text
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