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. 2013 Aug 15;14(8):16817–16835. doi: 10.3390/ijms140816817

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© 2013 by the authors; licensee MDPI, Basel, Switzerland

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

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A schematic representation of TMT-induced gene activation in (a) mice; (b) rats; and (c) PC12 cells. (a) Results obtained in mice indicate the significant and early involvement of genes related to apoptosis, neuroinflammation and neurogenesis; (b) The studies performed in the rat model reflect an involvement of calcium homeostasis dysregulation and mitochondrial damage. The contribution of the authophagic pathway may be hypothesized, but genes related to neuroinflammation are not unambiguously modulated in the early phases of TMT-induced neurodegeneration; and (c) the study performed in PC12 cells evidences the activation of oxidative metabolism of glucose, cholesterol and fatty acids, along with the early activation of genes involved in apoptosis and stress-related pathways.

A schematic representation of TMT-induced gene activation in (a) mice; (b) rats; and (c) PC12 cells. (a) Results obtained in mice indicate the significant and early involvement of genes related to apoptosis, neuroinflammation and neurogenesis; (b) The studies performed in the rat model reflect an involvement of calcium homeostasis dysregulation and mitochondrial damage. The contribution of the authophagic pathway may be hypothesized, but genes related to neuroinflammation are not unambiguously modulated in the early phases of TMT-induced neurodegeneration; and (c) the study performed in PC12 cells evidences the activation of oxidative metabolism of glucose, cholesterol and fatty acids, along with the early activation of genes involved in apoptosis and stress-related pathways.