Inter-Dependent Mechanisms Behind Cognitive Dysfunction, Vascular Biology and XXXX in Down Syndrome: Multi-Faceted Roles of @entity477 .

@entity1 @entity303 @entity477 @entity1467 @entity195 @entity717 @entity70806
UNASSIGNED: @entity1 with Down syndrome (DS) virtually all develop @entity717 ( @entity717 ) of varying degree of severity, and also have a high risk of early @entity195 ( @entity195 ). @entity717 prior to the onset of @entity303 , and its relationship to the onset of @entity303 in DS is a complex phenomenon influenced by many factors, and scarcely understood. Unraveling the causative factors and modulators of these processes remains a challenge, with potential to be informative for both @entity717 and @entity195 , for the development of early biomarkers and/or therapeutic approaches. We review the potential relative and inter-connected roles of the chromosome 21 gene for @entity477 ( @entity477 ), in both pathological conditions. Rare non-DS @entity1 with duplication of @entity477 ( @entity70806 ) get familial early onset @entity195 (FEOAD) with virtually 100% penetrance and prominent cerebrovascular pathology, but don't suffer from @entity717 before @entity303 onset. All of these features appear to be radically different in DS. On the other hand, rare individuals with @entity1467 (T21) (with @entity477 , but not DS-critical region in trisomy) have been described having @entity717 . Likewise, partial T21 DS (without @entity477 trisomy) show a range of @entity717 , but no @entity195 pathology. We review the multi-faceted roles of @entity477 that might affect cognitive functioning. Given the fact that both Ab secretion and synaptic maturation/plasticity are dependent on neuronal activity, we explore how this conflicting inter-dependency might affect cognitive pathogenesis in a dynamic way in DS, throughout the lifespan of an individual.
