The Emerging Role of Altered Cerebellar Synaptic Processing in Alzheimer’s Disease

Frontiers in Aging Neuroscience

Ilaria Balbo¹  Eriola Hoxha¹  Fabio Zurlo²  Pellegrino Lippiello²  Maria Concetta Miniaci²  Rita Santamaria²  Filippo Tempia³ 

[1] Department of Neuroscience, University of Torino, Turin, Italy;Department of Pharmacy, School of Medicine, University of Naples Federico II, Naples, Italy;National Institute of Neuroscience (INN), Turin, Italy;Neuroscience Institute Cavalieri Ottolenghi (NICO), Turin, Italy;

关键词: cerebellum;    Alzheimer’s disease;    β-amyloid;    purkinje cell;    synaptic plasticity;    noradrenaline;   

DOI  :  10.3389/fnagi.2018.00396

来源: DOAJ

【 摘 要 】

The role of the cerebellum in Alzheimer’s disease (AD) has been neglected for a long time. Recent studies carried out using transgenic mouse models have demonstrated that amyloid-β (Aβ) is deposited in the cerebellum and affects synaptic transmission and plasticity, sometimes before plaque formation. A wide variability of motor phenotype has been observed in the different murine models of AD, without a consistent correlation with the extent of cerebellar histopathological changes or with cognitive deficits. The loss of noradrenergic drive may contribute to the impairment of cerebellar synaptic function and motor learning observed in these mice. Furthermore, cerebellar neurons, particularly granule cells, have been used as in vitro model of Aβ-induced neuronal damage. An unexpected conclusion is that the cerebellum, for a long time thought to be somehow protected from AD pathology, is actually considered as a region vulnerable to Aβ toxic damage, even at the early stage of the disease, with consequences on motor performance.

【 授权许可】

Unknown