Common Ground: Both studies aim to uncover potential therapeutic targets for Alzheimer’s disease by investigating mechanisms that influence neuronal function and neuroprotection.
Key Differences: The current study focuses on the role of BRI2 proteolytic fragments in neuronal differentiation and inhibition of Aβ42 aggregation, while the recommended study examines the interaction between CB1R and NMDAR subunits in modulating synaptic function and neuroprotection.
Methodologies: The current study uses morphometric analysis and aggregation assays with SH-SY5Y cells and primary neuronal cultures. The recommended study utilizes transfected HEK-293T cells, cortical neurons, and the 5XFAD mice model to study cellular signaling and interactions.
Complementary Aspects: The current study provides insights into cellular uptake and stability of therapeutic peptides, whereas the recommended study elucidates neuroprotective signaling pathways at the molecular level.
Potential Impact: Combining findings could accelerate the development of treatments targeting neuronal differentiation and synapse protection in Alzheimer's disease.

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