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Publication : APOE genotype and sex modulate Alzheimer's disease pathology in aged EFAD transgenic mice.

First Author  Balu D Year  2023
Journal  Front Aging Neurosci Volume  15
Pages  1279343 PubMed ID  38020764
Mgi Jnum  J:343135 Mgi Id  MGI:7562823
Doi  10.3389/fnagi.2023.1279343 Citation  Balu D, et al. (2023) APOE genotype and sex modulate Alzheimer's disease pathology in aged EFAD transgenic mice. Front Aging Neurosci 15:1279343
abstractText  Increasing evidence supports that age, APOE and sex interact to modulate Alzheimer's disease (AD) risk, however the underlying pathways are unclear. One way that AD risk factors may modulate cognition is by impacting amyloid beta (Abeta) accumulation as plaques, and/or neuroinflammation Therefore, the goal of the present study was to evaluate the extent to which age, APOE and sex modulate Abeta pathology, neuroinflammation and behavior in vivo. To achieve this goal, we utilized the EFAD mice, which express human APOE3 or APOE4 and have five familial AD mutations (FAD) that result in Abeta42 overproduction. We assessed Abeta levels, reactive glia and Morris water maze performance in 6-, 10-, 14-, and 18-month-old EFAD mice. Female APOE4 mice had the highest Abeta deposition, fibrillar amyloid deposits and neuroinflammation as well as earlier behavior deficits. Interestingly, we found that female APOE3 mice and male APOE4 mice had similar levels of pathology. Collectively our data support that the combination of APOE4 and female sex is the most detrimental combination for AD, and that at older ages, female sex may be equivalent to APOE4 genotype.
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