Oxidation of cytosolic proteins and expression of creatine kinase BB in frontal lobe in different neurodegenerative disorders

Citation
Mv. Aksenova et al., Oxidation of cytosolic proteins and expression of creatine kinase BB in frontal lobe in different neurodegenerative disorders, DEMENT G C, 10(2), 1999, pp. 158-165
Citations number
54
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
DEMENTIA AND GERIATRIC COGNITIVE DISORDERS
ISSN journal
14208008 → ACNP
Volume
10
Issue
2
Year of publication
1999
Pages
158 - 165
Database
ISI
SICI code
1420-8008(199903/04)10:2<158:OOCPAE>2.0.ZU;2-T
Abstract
The presence of the biomarkers of oxidative damage, protein carbonyl format ion and the inactivation of oxidatively sensitive brain creatine kinase (CK BE, cytosolic isoform), were studied in frontal lobe autopsy specimens obt ained from patients with different age-related neurodegenerative diseases: Alzheimer's disease (AD), Pick's disease (PkD), diffuse Lewy body disease ( DLBD), Parkinson's disease (PD), and age-matched control subjects. The CK a ctivity was significantly reduced in the frontal lobe of AD, PkD and DLBD s ubjects, and CK BB-specific mRNA was significantly reduced in AD and DLBD. Protein carbonyl content was significantly increased in AD, PkD and DLBD. T he results of this study confirm that the presence of biomarkers of oxidati ve damage is related to the presence of histopathological markers of neurod egeneration. Our data suggest that oxidative damage contributes to the deve lopment of the symptoms of frontal dysfunction in AD, PkD and DLBD. The dev elopment of frontal dysfunction in idiopathic PD might be secondary to oxid ative damage and neuronal loss primarily located in the nigrostriatal syste m. The results of CK BE expression analysis demonstrate that the loss of th e isoenzyme in different neurodegenerative diseases is likely the consequen ce of its posttranslational modification, possibly oxidative damage. Change s in CK BE expression may be an early indicator of oxidative stress in neur ons.