Canine cognitive dysfunction and the cerebellum: acetylcholinesterase reduction, neuronal and glial changes

摘要: The specific functional and pathological alterations observed in Alzheimer's disease are less severe the cerebellum than other brain areas, particularly entorhinal cortex hippocampus. Since dense core amyloid-beta plaque formation has been associated with an acetylcholinesterase heterogeneous nucleator action, we examined if imbalance was involved deposition. By using canine counterpart of senile dementia type, a promising model human aging early phases disease, investigated how cerebellar pathology density could be related cognitive dysfunction. As late affectation evidenced by its lack presence diffuse deposition throughout all cortical grey matter layers. highest optic corresponded to islands granular layer predominantly synaptic glomeruli somata Golgi cells. Its reduction correlated loss granule cells, whereas deficit only Purkinje Bergmann glia may correspond reactive response damage their neuronal partner. Regarding role mediation deposition, our data argue against interaction between these two proteins because correlates but not deficit. Finally, support use companion dogs breeds study disease.