in vitro and
in vivo (APPswe/PS1dE9 mouse model of Alzheimer’s disease) experiments that show increased mast cell hemichannel activity after treatment with amyloid peptide (Ab
25–35), with subsequent degranulation response and enhanced histamine release [2]. The number of mast cells in hippocampal and cortical areas increased drastically even before amyloid plaque deposits became evident, suggesting that mast cells are one of the first brain cells to recognize and respond to amyloid peptides, and thus may play a critical role in the onset and progression of Alzheimer’s disease. Treatment with masitinib was shown to totally prevent the amyloid-induced hemichannel-dependent mast cell activity in bone marrow-derived mast cells and brain mast cells. The authors concluded that hemichannel expressed by mast cells might serve as a molecular target with which to develop therapeutic treatments that could delay the onset and progression of Alzheimer’s disease.