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Abstract: Down syndrome (DS), the most common cause of intellectual disability of genetic origin, is characterized by alterations in central nervous system morphology and function that appear from early prenatal stages. However, by the fourth decade of life, all individuals with DS develop neuropathology identical to that found in sporadic Alzheimer's disease (AD), including the development of amyloid plaques and neurofibrillary tangles due to hyperphosphorylation of tau protein, loss of neurons and synapses, reduced neurogenesis, enhanced oxidative stress, and mitochondrial dysfunction and neuroinflammation. It has been proposed that DS could be a useful model for studying the etiopathology of AD and to search for therapeutic targets. There is increasing evidence that the neuropathological events associated with AD are interrelated and that many of them not only are implicated in the onset of this pathology but are also a consequence of other alterations. Thus, a feedback mechanism exists between them. In this review, we summarize the signalling pathways implicated in each of the main neuropathological aspects of AD in individuals with and without DS as well as the interrelation of these pathways.
Fuente: International Journal of Molecular Sciences, 2020, 21(18), 6906
Publisher: MDPI
Year of publication: 2020
No. of pages: 38
Publication type: Article
DOI: 10.3390/ijms21186906
ISSN: 1661-6596,1422-0067
Publication Url: https://doi.org/10.3390/ijms21186906
Consult in UCrea Read publication
CARMEN MARTINEZ-CUE PESINI
NOEMI RUEDA REVILLA
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