Down patients: Extracellular preamyloid deposits precede neuritic degeneration and senile plaques☆
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2011, Neurobiology of Learning and MemoryCitation Excerpt :Observations from human genetics earlier determined that some cases of familial AD show linkage to chromosome 21 (Tanzi et al., 1988), which was found to be the locus for the APP gene. An additional indication that APP might play a critical role in AD were the findings that it is overexpressed in Down syndrome (Podlisny, Lee, & Selkoe, 1987), which is caused by an extra chromosome 21, and that individuals with Down syndrome invariably develop AD (Giaccone et al., 1989; Lemere et al., 1996). Although APP is not overexpressed in AD (Podlisny et al., 1987), its metabolism is altered significantly by mutations that cause FAD.
Amyloid precursor protein (APP) processing genes and cerebrospinal fluid APP cleavage product levels in Alzheimer's disease
2011, Neurobiology of AgingCitation Excerpt :The majority of these mutations alter processing of APP so that the relative levels of Aβ42 are increased (Scheuner et al., 1996; Walker et al., 2005). Triplication of the APP gene, due to chromosome 21 trisomy in Down's syndrome, is associated with increased APP expression and amyloid plaque formation (Giaccone et al., 1989; Lemere et al., 1996; Englund et al., 2007). In addition, APP promoter polymorphisms have been associated with AD (Guyant-Marechal et al., 2007; Lv et al., 2008).
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Preliminary reports were presented at the Fifth Paulo Foundation International Symposium on Pathobiology of Alzheimer's Disease (Hanaasari, Espoo, Finland) June 17–19, 1988 and the First International Conference on Alzheimer's Disease and Related Disorders (Las Vegas, Nevada, USA), September 6–9, 1988.