The pathophysiological mechanisms underlying the onset and inexorable 
progression of 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 concerning the 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. Apart from their physiological roles, p75NTR is more 
intensely expressed in the hippocampus of human AD brains and Aβ‑bound p75NTR 
triggers cell death, whereas Aβ‑bound CaSR signalling induces the de novo 
synthesis and release of nitric oxide (NO), vascular endothelial growth factor 
(VEGF)‑A and Aβ peptides (Aβs), particularly on the part of normal adult human 
astrocytes. The latter effect could significantly increase the pool of Aβ‑ and 
NO‑producing nerve cells favouring the progressive spread of a self‑sustaining 
and self‑reinforcing 'infectious' mechanism of neural and vascular (i.e. 
blood-brain barrier) cell damage. Interestingly, primary cilia concentrate 
p75NTR receptors in their membranes and are abnormally structured/damaged in 
transgenic (Tg) AD‑model mice, which could impact on the adult neurogenesis 
occurring in the dentate gyrus's subgranular zone (SGZ) that is necessary for 
new memory encoding, thereby favouring typical AD cognitive decline. Altogether, 
these findings may pave the way to novel therapeutic approaches to AD, 
particularly in its mild cognitive impairment (MCI) and pre‑MCI stages of 
development.