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By Suzanne De La Monte

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Extra info for The Clinical Spectrum of Alzheimer’s Disease The Charge Toward Comprehensive Diagnostic and Therapeutic Strategies

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2006) Alpha-1-antichymotrypsin (ACT or SERPINA3) polymorphism may affect age-at-onset and disease duration of Alzheimer’s disease. , et al. (2009) CSF biomarkers predict rate of cognitive decline in Alzheimer disease. , & Dubois, B. (2008) VBM anticipates the rate of progression of Alzheimer disease: a 3-year longitudinal study. , & Bäckman, L. (2010) The Influence of Vascular Disease on Cognitive Performance in the Preclinical and Early Phases of Alzheimer’s Disease. , et al. (2010) Association between the RAGE G82S polymorphism and Alzheimer’s disease.

Barba I, Fernandez-Montesinos R, Garcia-Dorado D, et al. (2008) Alzheimer’s Disease beyond the genomic era:nuclear magnetic resonance (NMR) spectroscopy-based metabolomics. J cell Mol Med 12(5A): 1477-85. Beach T, Leung D, Bryden L, et al. (2008) Sorl1 as an Alzheimer's disease predisposition gene? , 5(2):60-4. Beecham GW, Martin ER, Li YJ, et al. (2009) Genome-wide association study implicates a chromosome 12 risk locus for late-onset Alzheimer disease. Am J Hum Genet, 84:3543. Bergem AL, Engedal K, Kringlen E.

These peptides aggregate to form amyloid plaques. Given their rarity, these three gene mutations contribute minimally to the estimated 60% heritability of AD. The importance of these rare mutations lies in the identification of pathogenic pathways, specifically those involving the catabolism of APP. Hence accumulation of Aβ40 and Aβ42 is attributed to increased activity of the β and γ secretases in familial cases of AD with APP, PSEN1 and PSEN2 gene mutations. However environmental or other non-genetic or epigenetic factors may also affect the activities of the secretases.

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