Avid Bioservices Inc (CDMO)

[freethemice]

PS and Alzheimer's Disease, a role for Bavituximab?
This paper suggests that exposed PS on neuronal cells
may be involved in Alzheimer's. Is it possible that bavi
could get into the brain and treat AD? Has anyone heard
more about this?
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Peptides 23 (2002) 1249–1263

Annexin 5 and apolipoprotein E2 protect against Alzheimer’s
amyloid-{beta}-peptide cytotoxicity by competitive inhibition
at a common phosphatidylserine interaction site

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Abstract

Amyloid-beta-protein ({beta}A/4, A{beta}P) accumulates in the brains of patients with Alzheimer’s disease (AD), regardless of genetic etiology, and
is thought to be the toxic principle responsible for neuronal cell death. The {epsilon}4 allele of apoE has been linked closely to earlier onset of AD
and increased deposition of the amyloid peptide, regardless of the clinical status of AD, while the apoE {epsilon}2 allele is generally protective.
We have previously hypothesized that the cell target for amyloid peptide might be the apoptotic signal molecule phosphatidylserine (PS).
We report here that annexin 5, a specific ligand for PS, not only blocks amyloid peptide A{beta}P[1–40] cytotoxicity, but competitively inhibits
A{beta}P[1–40]-dependent aggregation of PS liposomes. In addition, we find that apoE2, but not apoE4, can not only perform the same protective
effect on cells exposed to A{beta}P[1–40], but can also competitively inhibit PS liposome aggregation and fusion by the amyloid peptide.
Altogether, the in vivo and in vitro results reported here provide fundamental insight to the process by which amyloid targets specific
neurons for destruction, and suggest that PS may be a surface “receptor” site for A
P binding. These results also provide a biochemical
mechanism by which the apoE {epsilon}2 allele, but not apoE {epsilon}4, can be protective towards the incidence and progression of Alzheimer’s disease.