Down syndrome and Alzheimer's disease: Oxidative stress in the neurodegenerative process

Autor(es)

Cordeiro, Augusto Magno Tranquezi ; Singulani, Monique Patricio ; Talib, Leda Leme ; Forlenza, Orestes Vicente

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF ALZHEIMER'S DISEASE; v. N/A, p. 10-pg., 2025-04-03.

Resumo

Background: Individuals with Down syndrome (DS) generally show neuropathological features of Alzheimer disease (AD). The trisomy of chromosome 21 causes an imbalance of antioxidant systems, which can be linked to AD pathophysiology. Objective: Verify the difference between the activity of antioxidant enzymes and products of the oxidation process in peripheral blood in non-trisomic (NT) and trisomic (DS) adults and elders and respective associations with cognitive impairment. Methods: A total of 120 subjects were included in this study. Sociodemographic and clinical information were collected as per protocol for participants in DS and NT groups. The cognitive state of the DS participants was established according to the Brazilian version of the Cambridge Examination for Mental Disorders of Older People with Down's syndrome and Others with Intellectual Disabilities (CAMDEX-DS). The CAMDEX interview was used for this purpose for participants in the NT group. Plasma samples were collected to evaluate protein carbonyl content, superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), malondialdehyde (MDA), and 4-hydroxy-2-nonenal (HNE). Results: We found increased levels of SOD and CAT activity in the DS group. When the groups were stratified by cognitive decline, elevated levels of SOD and CAT activity were found both in DS groups with and without decline. The activity of GPx was similar between the groups, as well as MDA and HNE. Conclusion: The results suggest that alterations of the antioxidative processes can be implicated in the onset of neurodegeneration observed in individuals with DS. (AU)

• Processo FAPESP: 21/06378-1 - Análise do envolvimento do lítio nos marcadores mitocondriais na Doença de Alzheimer
• Beneficiário: Monique Patricio Singulani
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 14/50873-3 - INCT 2014: Instituto Nacional de Biomarcadores em Neuropsiquiatria (INBioN)
• Beneficiário: Wagner Farid Gattaz
• Modalidade de apoio: Auxílio à Pesquisa - Temático