Decreased protein levels of stathmin in adult brains with Down syndrome and Alzheimer's disease

Stathmin, distributed in neurons with high abundance, acts as an intracellu lar relay, integrating various transduction pathways triggered by extracell ular signals and it is involved in physiological regulation of microtubule destabilization. Stathmin has been also shown to be a critical molecule in pathology of neurodegeneration such as Alzheimer's disease (AD), particular ly, in neurofibrillary tangle (NFT) formation. Here we evaluated protein le vels of stathmin in adult brain from patients with AD and Down syndrome (DS ) showing AD-like pathology by applying proteomic technologies with two-dim ensional (2-D) gel electrophoresis, matrix-assisted laser desorption ioniza tion mass spectroscopy (MALDI-MS) identification and specific software for quantification of proteins. Significantly decreased protein levels of stath min were observed in frontal (2.12 +/- 1.17, n = 6) and temporal (3.05 +/- 2.81, n = 10) cortices of AD compared to controls (frontal cortex: 4.41 +/- 1.70, n = 8; temporal cortex: 5.26 +/- 2.26, n = 13). Stathmin was also si gnificantly decreased in frontal (2.47 +/- 1.11, n = 7) and temporal (2.02 +/- 1.18, n = 9) cortices of DS. We also investigated stathmin levels in fe tal brain. Stathmin was not significantly changed between fetal DS brain an d controls. We suggest that the decreased protein level of stathmin in brai ns is associated with tangle formation and microtubule instability in DS as well as AD, but stathmin is not involved in the abnormal development of fe tal DS brain.