
Promiscus Amyloid
Although genetic evidence puts the amyloid peptide (β-amyloid or Aβ) center stage in Alzheimer's disease (AD), it remains far from clear how this 4-kD protein fragment compromises neuronal function (1). On page 1399 of this issue, Kim et al. identify two new receptors for aggregated Aβ: the mouse paired immunoglobulin-like receptor B (PirB) and its human ortholog, leukocyte immunoglobulin-like receptor LilrB2 (2). The binding interaction triggers a signaling cascade that compromises the actin cytoskeleton of neurons and ultimately causes synaptic loss in a mouse model of AD.
I chose this article because on Friday I saw this article on Multiple Sclerosis and I taught this article was related but as I discovered it is not. I still did this article about this because I have been always fascinated by genetics and germs.
I think this is an important piece of information because now that we know another possible cause for Alzheimer we can develop a cure for it. I think this is important news because we can study the Promiscus Amyloid's components to figure out if any of them contain a new thing.
Information from: Promiscus Amyloid
By Malik A.
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