Effect of the inflammation on the aggregation of the tau and amyloid-β polypeptides in the pyramidal neurons on the hippocampus of a triple transgenic murine model for the Alzheimer’s disease

Alzheimer’s Disease (AD) is the most important form of dementia. It represents 70% of all dementia cases worldwide. On a molecular level, AD is characterized by the presence of two fibrillar lesions: the neurofibrillary tangles (NFT) due to the oligomerization of pathological forms caused by post-translational modifications (PTMs) of protein Tau and; the aggregation of peptide amyloid-β (Aβ), product of a bad-processing of amyloid precursor protein (APP) forming neuritic plaques (NP). The triple transgenic mice (3xTg-AD) presents some pathological species of Tau and Aβ aggregations. 3xTg-AD mice received an ethanol treatment to evaluate the generation of proteolyzed forms of Tau through the induction of an exacerbated neurotoxic state Caspase 3 activity was observed accompanied by an increment of NPs in the hippocampus, as well as, the presence of neurofibrillary aggregations of Tau and Aβ.

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