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- W2004138830 abstract "identified. Three of these, the amyloid precursor protein [APP] 2 and the presenilin 1 and 2 [PS1 and PS2] genes 3–5 , were identified using the classical Mendelian positional cloning paradigm most prominently applied in the 1990’s. This success was facilitated by highlypenetrant autosomal dominant inheritance in early-onset AD families. While these three genes explain the majority of early-onset familial AD and their identification represents a tremendous accomplishment, collectively they account for less than 2% of all AD cases. The genetic architecture underlying the far more common late-onset AD (LOAD; age at onset ≥ 60 years of age) 6 is much more complex. The sibling recurrence risk (λs)for AD is surprisingly consistent across studies 7–9 with a range of about 4–5. The confluence of biology 10, 11 and genetic mapping 12 facilitated the identification of the association between" @default.
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- W2004138830 date "2009-11-01" @default.
- W2004138830 modified "2023-09-25" @default.
- W2004138830 title "Beyond proof of principle: new genes for Alzheimer's disease through collaboration" @default.
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- W2004138830 doi "https://doi.org/10.1016/s1474-4422(09)70277-7" @default.
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