The 5× familial [[Alzheimer's disease]] (5×FAD) [[mice]] show alleviated mechanical [[allodynia]] which can be regained by genetic activation of [[anterior cingulate cortex]] (ACC) [[excitatory]] neurons. Furthermore, the lower peak neuronal [[excitation]], delayed response initiation, as well as the dendritic spine reduction of ACC [[pyramidal neuron]]s in 5×FAD mice, can be mimicked by [[Rac1]] or actin polymerization inhibitor in Wild-type (WT) mice. These findings indicate that abnormal pain sensitivity in Alzheimer's disease modeling mice is closely related to the variation of neuronal activity and dendritic spine loss in ACC pyramidal neurons, suggesting the crucial role of [[dendritic spine]] density in pain processing ((Cui Z, Guo Z, Wei L, Zou X, Zhu Z, Liu Y, Wang J, Chen L, Wang D, Ke Z. Altered pain sensitivity in 5×FAD mice is associated with the dendritic spine loss in ACC pyramidal neurons. Pain. 2022 Apr 6. doi: 10.1097/j.pain.0000000000002648. Epub ahead of print. PMID: 35384934.)) ---- Ou-Yang MH, Xu F, Liao MC, Davis J, Robinson JK, Van Nostrand WE. N-terminal region of myelin basic protein reduces fibrillar amyloid-β deposition in Tg-[[5xFAD mice]]. Neurobiol Aging. 2015 Feb;36(2):801-11. doi: 10.1016/j.neurobiolaging.2014.10.006. Epub 2014 Oct 13. PMID: 25457550; PMCID: PMC4315736.