A double transgenic Tg2576 and homozygous CRHR1 knockout mouse line (supplemented with corticosterone for health maintenance) showed highly significant decreases (>60%) in basal levels of Aβ40, Aβ42, and APP C-Terminal Fragment (α and β) levels in the brain, suggesting that a CRHR1-mediated mechanism contributes to an appreciable amount of Aβ processing [ 51 ].
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