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.
journal_name
Int J Mol Scijournal_title
International journal of molecular sciencesauthors
Martínez-Cué C,Rueda Ndoi
10.3390/ijms21186906subject
Has Abstractpub_date
2020-09-20 00:00:00issue
18issn
1422-0067pii
ijms21186906journal_volume
21pub_type
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journal_title:International journal of molecular sciences
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journal_title:International journal of molecular sciences
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