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P1–302: MTHFR and APOE polymorphisms in a case–control study of Alzheimer's disease
Author(s) -
Fernandez Liana L.,
Scheibe Rosane Machado
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.680
Subject(s) - methylenetetrahydrofolate reductase , apolipoprotein e , genotyping , genotype , medicine , allele , alzheimer's disease , disease , gastroenterology , oncology , genetics , biology , gene
aging. This observation is consistent with the idea that the gradual downregulation of NEP expression, resulting in a corresponding elevation in the steady-state levels of A , over a decade or more, may cause A accumulation that triggers the AD pathological cascade. Additionally, higher mRNA levels of IDE and NEP were detected in the human cerebellum than in the frontal cortex, which may partly explain why cerebellum exhibits only minor plaque pathology. Conclusions: These data suggest that ageand region-specific changes in the proteolytic clearance of A make an important contribution to pathogenic mechanisms in AD.