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- W2015808890 abstract "Down syndrome (DS) is one of the most frequent genetic abnormalities characterized by multiple pathological phenotypes. Indeed, currently life expectancy and quality of life for DS patients have improved, although with increasing age pathological dysfunctions are exacerbated and intellectual disability may lead to the development of Alzheimer's type dementia (AD). The neuropathology of DS is complex and includes the development of AD by middle age, altered free radical metabolism, and impaired mitochondrial function, both of which contribute to neuronal degeneration. Understanding the molecular basis that drives the development of AD is an intense field of research. Our laboratories are interested in understanding the role of oxidative stress as link between DS and AD. This review examines the current literature that showed oxidative damage in DS by identifying putative molecular pathways that play a central role in the neurodegenerative processes. In addition, considering the role of mitochondrial dysfunction in neurodegenerative phenomena, results demonstrating the involvement of impaired mitochondria in DS pathology could contribute a direct link between normal aging and development of AD-like dementia in DS patients." @default.
- W2015808890 created "2016-06-24" @default.
- W2015808890 creator A5008788895 @default.
- W2015808890 creator A5039202201 @default.
- W2015808890 date "2012-01-01" @default.
- W2015808890 modified "2023-10-17" @default.
- W2015808890 title "Oxidative Stress and Down Syndrome: A Route toward Alzheimer-Like Dementia" @default.
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- W2015808890 doi "https://doi.org/10.1155/2012/724904" @default.
- W2015808890 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3235450" @default.
- W2015808890 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22203843" @default.
- W2015808890 hasPublicationYear "2012" @default.
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