Decreased protein levels of stathmin in adult brains with Down syndrome and Alzheimer's disease.
J Neural Transm Suppl
; (61): 281-8, 2001.
Article
en En
| MEDLINE
| ID: mdl-11771751
ABSTRACT
Stathmin, distributed in neurons with high abundance, acts as an intracellular relay, integrating various transduction pathways triggered by extracellular 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), particularly, in neurofibrillary tangle (NFT) formation. Here we evaluated protein levels of stathmin in adult brain from patients with AD and Down syndrome (DS) showing AD-like pathology by applying proteomic technologies with two-dimensional (2-D) gel electrophoresis, matrix-assisted laser desorption ionization mass spectroscopy (MALDI-MS) identification and specific software for quantification of proteins. Significantly decreased protein levels of stathmin 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 significantly 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 fetal brain. Stathmin was not significantly changed between fetal DS brain and controls. We suggest that the decreased protein level of stathmin in brains is associated with tangle formation and microtubule instability in DS as well as AD, but stathmin is not involved in the abnormal development of fetal DS brain.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Fosfoproteínas
/
Encéfalo
/
Síndrome de Down
/
Enfermedad de Alzheimer
/
Proteínas de Microtúbulos
Límite:
Adult
/
Aged
/
Humans
/
Middle aged
Idioma:
En
Revista:
J Neural Transm Suppl
Año:
2001
Tipo del documento:
Article
País de afiliación:
Austria