Alzheimer's disease (AD) is correlated with the presence of �/A4 peptides. These �/A4 peptides accumulate as filamentous aggregates in the AD brains and they are derived from APPs. The increased expression and/or over expression of this APPs results in the formation of �/A4 peptides.BMAA has been recently detected at high concentrations in the brain tissue of patients with AD. Ntera-2 cells (NT2) cell lines were used as a model system because they express endogenous levels of the protein precursor to the plaque forming amyloid beta peptide, called, APP.Our laboratory has investigated that APP proteolytic processing is decreased in the presence of varying concentrations of BMAA where the alpha-secretase cleaved APP-CTFalpha is lower in comparison to the control neurons. These results delineate a mechanism where BMAA alters and perhaps lowers the formation of the non-deleterious APP-CTF, paving the way for an alternative mechanism that produces the deleterious �/A4 peptides.

Effect of neurotoxin β-methylamino-L-alanine (BMAA) on proteolytic processing of amyloid precursor protein (APP) using in vitro model systems

245th National Meeting (2013)

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