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Academia Mexicana de Neurología, A.C.

2015, Number 1

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Rev Mex Neuroci 2015; 16 (1)

Protein misfolding and neurodegeneration

Rodríguez-Leyva I, Calderón-Garcidueñas AL, Jiménez-Capdeville ME

Language: Spanish
References: 56
Page: 51-72
PDF size: 361.81 Kb.


ABSTRACT

In some way, neurodegenerative diseases are all proteinopathies. Although the main risk factor is aging, both genetics and environmental factors (trauma, pesticides, herbicides) are involved through epigenetic mechanisms in the development of proteinopathies. A range of possibilities for their presentation occurs, from absolute genetic risk (Huntington’s disease) until the almost exclusive environmental factor (pugilistic dementia). Similarly, the complex range of symptoms and signs of these diseases contribute to flawed diagnosis (Parkinson’s disease and supranuclear progressive paralysis, for example). Several authors propose that diseases thought until now to be different, may be exactly the same (Parkinson’s disease and Lewy Body Dementia). Their pathophysiology is similar, starting from functional or structural proteins that become misfolded, dysfunctional and insoluble. These proteins become toxic, leading to neuronal death with the consequent inflammation in cortical, subcortical, basal ganglia, brain stem and spinal cord nuclei, and even peripheral nervous system structures. This progression could explain the manifestations that may result in the characteristic semiology of each neurodegenerative disease.


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