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How Alzheimer's can Spread

Here's my last post before the American Thanksgiving, and living in Canada, you can read my old rant on the Black Friday that follows.

Anyway, ok, so here's a short post on a new study I came across that sheds light on how the toxic proteins associated with Alzheimer's--amyloid-beta--and how it gets transmitted.

Now just to be clear, this study looked at nerve cell to nerve cell, NOT person to person, so in NO way implies Alzheimer's is a communicable condition. I want to make that absolutely clear. Here is my take on an abbreviated abstract. If you're looking to do more research, follow the link to the source below, and you'll be taken to the full-text article. Enjoy!

The spreading of pathology through neuronal pathways is likely to be the cause of the progressive cognitive loss observed in Alzheimer's disease (AD) and other neurodegenerative diseases. The researchers had recently shown the propagation of AD pathology via cell-to-cell transfer of oligomeric amyloid beta (Aβ) residues 1-42 (oAβ1-42) using a model.

Now they show that different Aβ-isoforms can transfer from one cell to another. Thus, transfer is not restricted to a specific Aβ-isoform. Although different Aβ isoforms can transfer, differences in the cells' capacity to clear and/or degrade these aggregated isoforms result in vast differences in the net amounts ending up in the receiving cells and the net remaining Aβ can cause seeding and pathology in the receiving cells. This insufficient clearance and/or degradation by cells creates sizable intracellular accumulations of the aggregation-prone Aβ1-42 isoform, which further promotes cell-to-cell transfer; thus, oligomeric Aβ1-42 is a potentially toxic isoform.

Furthermore, cell-to-cell transfer is shown to be an early event that is seemingly independent of later appearances of cellular toxicity. This phenomenon could explain how seeds for the AD pathology could pass on to new brain areas and gradually induce AD pathology, even before the first cell starts to deteriorate, and how cell-to-cell transfer can act together with the factors that influence cellular clearance and/or degradation in the development of AD.

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Source: Spreading of amyloid-β peptides via neuritic cell-to-cell transfer is dependent on insufficient cellular clearance

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