The abstract is read at the publisher; the summary is JClub's.
Prenatal alcohol exposure in pregnant B6129 and 3xTg-AD mice increases APP C-terminal fragments and NICD in cortical lysates, linked to hippocampal learning and memory deficits.
- Why it matters: PAE is proposed as an early-life risk for AD/ADRD, but the developmental mechanisms connecting it to later cognitive problems remain unclear.
- What they did: Pregnant wild-type B6129 and 3xTg-AD mice received an ethanol-containing liquid diet during gestational days 13–15; cortical lysates were analyzed from birth to adulthood, and hippocampal-dependent behavior was tested at 3 and 6 months (wild-type) and at 4 months (3xTg-AD).
- The result: PAE disrupted gamma-secretase activity during development and the resulting molecular changes persisted, impairing learning and memory in wild-type mice at 3 and 6 months and worsening deficits in 4-month-old 3xTg-AD mice.
The findingWhy it mattersWhat they didThe result
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