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In Alzheimer disease specifically, BDNF deficits are most pronounced in the hippocampus, entorhinal cortex, and prefrontal cortex, the regions earliest and hardest hit by the disease

This positioning places DSIP within sleep architecture modulation research rather than acute sleep induction mechanisms

These interactions activate integrin-linked kinase (ILK) signalling pathways, leading to enhanced Akt phosphorylation and downstream target activation

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