The initial steps for Alzheimer disease can be clearly defined in familial Alzheimer disease (FAD). In this type of AD, mutations in APP and PS1/PS2 genes promote the appearance of β amyloid peptide and the onset of the disease. In FAD, no mutations for BACE1 protein have been found.

However, FAD accounts for probably, less than 1 percent of the total cases of AD, and the sporadic form is the most prevalent type of the disease. In this case, there is a hypothesis indicating that oxidative damage could be related to the onset of disease. This hypothesis is well supported by the recent work of Guglielmotto et al. (2009), indicating the involvement of reactive oxygen species (ROS), released by mitochondria, in BACE1 upregulation that will produce β amyloid peptide accumulation and neurodegeneration. This generation of ROS could be the consequence of risk factors for the disease, like hypoxia.

This is a well-performed work. The signaling pathways involved in the early hypoxic-dependent upregulation of BACE1 have been also...  Read more

The initial steps for Alzheimer disease can be clearly defined in familial Alzheimer disease (FAD). In this type of AD, mutations in APP and PS1/PS2 genes promote the appearance of β amyloid peptide and the onset of the disease. In FAD, no mutations for BACE1 protein have been found.

However, FAD accounts for probably, less than 1 percent of the total cases of AD, and the sporadic form is the most prevalent type of the disease. In this case, there is a hypothesis indicating that oxidative damage could be related to the onset of disease. This hypothesis is well supported by the recent work of Guglielmotto et al. (2009), indicating the involvement of reactive oxygen species (ROS), released by mitochondria, in BACE1 upregulation that will produce β amyloid peptide accumulation and neurodegeneration. This generation of ROS could be the consequence of risk factors for the disease, like hypoxia.

This is a well-performed work. The signaling pathways involved in the early hypoxic-dependent upregulation of BACE1 have been also described by Guglielmotto et al.

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