An article published by Science Magazine, talks about a deletion or a rare variant of a gene referred to as GGA3 and how it affects neurological pathways that are interrupted during late onset Alzheimers. In this study, when mice were subjected to a deletion of this gene, it disrupted axon movement of the BACE1 (β-site APP-cleaving enzyme 1). This resulted in a buildup of axons. This buildup of axons leads to damage in the brain. This damage is directly linked to damage that is observed and expressed with Alzheimers disease. This is specifically important because this process works independently of β-amyloid. β-amyloid has specifically been linked to Alzheimers because it makes up the plaque buildup in the brain. While this study was unable to identify the specific mechanisms that are triggered between the deletion of GGA and BACE1, they were still able to identify that the deletion or mutation has a direct affect.
This study is important to trying to find out the specific trigger for Alzheimers. Science is still unsure what exactly causes Alzheimers disease. Understanding neurological diseases can be very challenging because there are many pathways and complex protein cascades. Alzheimers is specifically difficult because it does not show signs in early stages of life and typically shows symptoms in older age. This is important in genetics because it makes it difficult to track through families. However, if we are able to detect this deletion or alteration in GGA3 gene it may allow us to see the risk of developing Alzheimers in later years. We may be able to have the opportunity to alter or manipulate this gene with CRISPR eventually.
Articles used: Science Mag and PubMed article about β-amyloid with BACE1
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