Amyloid precursor protein (APP) is a key molecule in Alzheimer's disease (AD) due to its role as a precursor to the amyloid β (Aβ) peptide, central to the amyloid cascade hypothesis. APP is processed by secretases, primarily β- and γ-secretases, to generate Aβ, which contributes to AD pathology. APP also has other functions, including trophic effects on neurons, cell adhesion, and signaling. The APP gene family includes APLP1, APLP2, Appl, and apl-1, all encoding type I membrane proteins. APP processing involves cleavage in the extracellular and transmembrane domains, leading to the release of Aβ and p3 peptides. APP is trafficked through various cellular compartments, with its processing influenced by factors such as phosphorylation and interactions with cytosolic adaptors. APP's role in neuronal development and function is also significant, with evidence suggesting that its dysfunction may contribute to AD pathogenesis. APP-deficient mice show limited phenotypic effects, indicating that other factors are involved in AD. However, APP's role in synaptic formation, neuronal migration, and synapse function is crucial. The study highlights the importance of understanding APP's normal functions to develop therapeutic strategies for AD.Amyloid precursor protein (APP) is a key molecule in Alzheimer's disease (AD) due to its role as a precursor to the amyloid β (Aβ) peptide, central to the amyloid cascade hypothesis. APP is processed by secretases, primarily β- and γ-secretases, to generate Aβ, which contributes to AD pathology. APP also has other functions, including trophic effects on neurons, cell adhesion, and signaling. The APP gene family includes APLP1, APLP2, Appl, and apl-1, all encoding type I membrane proteins. APP processing involves cleavage in the extracellular and transmembrane domains, leading to the release of Aβ and p3 peptides. APP is trafficked through various cellular compartments, with its processing influenced by factors such as phosphorylation and interactions with cytosolic adaptors. APP's role in neuronal development and function is also significant, with evidence suggesting that its dysfunction may contribute to AD pathogenesis. APP-deficient mice show limited phenotypic effects, indicating that other factors are involved in AD. However, APP's role in synaptic formation, neuronal migration, and synapse function is crucial. The study highlights the importance of understanding APP's normal functions to develop therapeutic strategies for AD.