The ability of a cationic lipid to deliver plasmid DNA (pDNA) in presence o
f the neurotoxic fragment of amyloid beta -peptide was evaluated. Pre-treat
ment of cells with beta AP (25-35) peptide resulted in a modest increase in
transgene expression. When beta AP (25-35) peptide was mixed with the pDNA
/liposome complex and used, the complexes lost their ability to transfect.
However, the reverse sequenced beta AP (35-25) peptide demonstrated no sign
ificant differences in transgene expression in pre-treated cells, and in ce
lls where PAP (35-25) peptide was mixed with pDNA/liposome complexes and tr
ansfected. The amount of pDNA delivered to the cells was decreased in prese
nce of beta AP (25-35) as measured with flow cytometry using fluorescently
labeled liposomes. The decreased endocytosis may be due to their rod-like s
tructure formation as demonstrated by electron microscopy and atomic force
microscopy (AFM). These results demonstrate that beta AP (25-35) peptide ma
y interfere with gene delivery with cationic systems.