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Year : 2021  |  Volume : 69  |  Issue : 1  |  Page : 32--41

Alzheimer's Disease in the Down Syndrome: An Overview of Genetics and Molecular Aspects


Genetics and Molecular Biology Research Unit (UPGEM), Department of Molecular Biology, São José do Rio Preto Medical School (FAMERP), São José do Rio Preto – SP, Brazil

Correspondence Address:
Érika C Pavarino
Genetics and Molecular Biology Research Unit (UPGEM), São José do Rio Preto Medical School (FAMERP), São José do Rio Preto – SP
Brazil
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.310062

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The overexpression of the amyloid precursor protein (APP) gene, encoded on chromosome 21, has been associated in Down syndrome (DS) with the development of early-onset Alzheimer's disease (EOAD). The increase in APP levels leads to an overproduction of amyloid-β (Aβ) peptide that accumulates in the brain. In response to this deposition, microglial cells are active and generate cascade events that include release cytokines and chemokine. The prolonged activation microglial cells induce neuronal loss, production of reactive oxygen species, neuron death, neuroinflammation, and consequently the development of Alzheimer's disease (AD). The intrinsically deficient immune systems in people with DS result in abnormalities in cytokine levels, which possibly contribute to the development of neurodegenerative disorders such as AD. Knowledge about the biomarkers involved in the process of neurodegeneration and neuroinflamation is important for understanding the mechanisms involved in the incidence and the precocity of AD in individuals with DS.






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Online since 20th March '04
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