The increased activity of BACE1 correlates with oxidative stress in Alzheimer’s disease
| Autor: | Alessandra Piccini, Nicola Traverso, Stefania Patriarca, Gabriella Cirmena, Roberta Borghi, Anna Garuti, Massimo Tabaton, Patrizio Odetti, Daniela Storace |
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| Jazyk: | angličtina |
| Rok vydání: | 2007 |
| Předmět: |
Aging
medicine.medical_specialty Frontal cortex Peptide Disease Oxidative phosphorylation medicine.disease_cause Lipid peroxidation chemistry.chemical_compound Alzheimer Disease Internal medicine mental disorders Gene expression medicine Aspartic Acid Endopeptidases Humans Aged chemistry.chemical_classification Aged 80 and over Cerebral Cortex Amyloid beta-Peptides General Neuroscience Gene Expression Profiling Middle Aged Oxidative Stress Enzyme Endocrinology chemistry Case-Control Studies Neurology (clinical) Lipid Peroxidation Geriatrics and Gerontology Amyloid Precursor Protein Secretases Oxidative stress Developmental Biology |
| Popis: | We evaluated expression, protein levels and activity of the Beta-site cleaving enzyme (BACE1) as well as the amount of products of lipid peroxidation in frontal cortex of three groups of cases: sporadic Alzheimer's disease (AD); control subjects (CTR); cognitively normal subjects with abundant amyloid plaques (NA). We found a significant increase of BACE1 activity and products of lipid peroxidation in brain tissue of AD cases, with normal gene expression, and non-significant elevation of protein levels. CTR and NA samples showed similar levels of BACE1 activity and oxidative products. BACE1 activity and the amount of oxidative products were significantly correlated in all cases.Moreover, both BACE1 activity and the level of 4-hydroxynonenal were correlated with the amount of Beta-amyloid pyroglutamated 3-42, the more toxic Beta-amyloid peptide that is characteristic of AD. These findings suggest that BACE1 activity reflects the type of ABeta species, rather than the Beta-amyloid plaques load. Hence, the increase of BACE1 activity occurring in sporadic AD is likely the effect, rather the cause, of ABeta accumulation and oxidative stress. |
| Databáze: | OpenAIRE |
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