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The pathophysiological mechanisms underlying the onset and inexorable progressionof the late‑onset form of Alzheimer's disease (AD) are still the object of controversy.This review takes stock of some most recent advancements of this field concerningthe complex roles played by the amyloid‑β (Aβ)‑binding p75 neurotrophin receptor(p75NTR) and calcium‑sensing receptor (CaSR) and by the primary cilia in AD. Apartfrom their physiological roles, p75NTR is more intensely expressed in the hippocampusof human AD brains and Aβ‑bound p75NTR triggers cell death, whereas Aβ‑bound CaSRsignalling induces the de novo synthesis and release of nitric oxide (NO), vascularendothelial growth factor (VEGF)‑A and Aβ peptides (Aβs), particularly on thepart of normal adult human astrocytes. The latter effect could significantly increasethe pool of Aβ‑ and NO‑producing nerve cells favouring the progressive spreadof a self‑sustaining and self‑reinforcing 'infectious' mechanism of neural andvascular (i.e. blood-brain barrier) cell damage. Interestingly, primary ciliaconcentrate p75NTR receptors in their membranes and are abnormally structured/damagedin transgenic (Tg) AD‑model mice, which could impact on the adult neurogenesisoccurring in the dentate gyrus's subgranular zone (SGZ) that is necessary fornew memory encoding, thereby favouring typical AD cognitive decline. Altogether,these findings may pave the way to novel therapeutic approaches to AD, particularlyin its mild cognitive impairment (MCI) and pre‑MCI stages of development.

Alzheimer’s disease: An update of the roles of receptors, astrocytes and primary cilia (Review)