Fig. 8.

Proposed model of mToxin effects in the brain of AD mice (with emphasis upon α7AChR function). a The development of AD-like phenotype in mice is characterized by neuroinflammation, astrogliosis, gradual Aβ deposition, cholinergic deficits due to block of α7AChR by Aβ oligomeric and fibrillar species, followed by α7AChR internalization. Also, these processes eventuate in the downregulation of the MAPK/ERK pathway that exacerbates the cognitive decline. b mToxin competes with Aβ for the binding to α7AChR and modulates its activity. Also, the treatment leads to a reduction in astrogliosis and neuroinflammation, which subsequently moderates the APP transcription, translation, and processing rates. Likewise, the treatment eventuates in activation of ERK and memory improvement. Of note, neuronal nicotinic acetylcholine receptors are located preterminally, presynaptically, and postsynaptically. ACh released from presynaptic vesicles diffuse and activate presynaptic α7AChR as well as postsynaptic, which results in the recruiting of neurotransmitter reserves and modulation of its release. Accordingly, PPF demonstrate significantly improved ratios following the treatment with mToxin. BACE1-β-secretase