Membrane surface ruffling in cells that over-express Alzheimer amyloid beta/A4 C-terminal peptide.
Deposition of beta/A4 amyloid in brain is a defining characteristic of Alzheimer disease (AD); however, the extent to which amyloid deposits may interfere with normal cellular processes is incompletely understood. We examined this issue by means of PC12 cells. After transfection with DNA coding for 97 amino acids of the beta/A4 C-terminal region of the amyloid precursor protein, beta/A4 antigen was visible at the cell membrane. We report that normal unstimulated PC12 cells exhibit ruffling activity at the cell surface when plated on a plastic substrate. Relative to control cells, however, those that over-expressed the beta/A4 C-terminal peptide had significantly higher levels of ruffling activity, suggesting a structural and/or functional membrane modification. Similar cellular alterations, if present, in Alzheimer brain cells, may indicate disturbances in membrane-associated functions, including intercellular communication.
Maestre
G E
GE
Department of Psychiatry, Harvard Medical School, Boston, MA 02115.
Tate
B A
BA
Majocha
R E
RE
Marotta
C A
CA
D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000096:biosynthesis*; D000818:Animals; D002462:Cell Membrane / Q000502:physiology / Q000648:ultrastructure*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D016716:PC12 Cells / Q000378:metabolism
D016229:Amyloid beta-Peptides; D009419:Nerve Tissue Proteins