Amyloid beta 42 peptide (Abeta42) accumulation is a key characteristic of Alzheimer's disease (AD) and causes synaptic dysfunctions. To date, the effects of Abeta42 accumulation on GABAergic synapses are poorly understood Our findings suggest that, similarly to what observed on glutamatergic synapses, Abeta42 modifies GABAergic synapses by targeting ryanodine receptors and causing calcium dysregulation The GABAergic impairments can be restored by the RyR-calstabin interaction stabilizer S107 Based on our research, RyRs stabilization may represent a novel pharmaceutical strategy for preventing or delaying of AD.
The RyR-calstabin interaction stabilizer S107 protects hippocampal neurons from GABAergic synaptic alterations induced by Abeta42 oligomers
Hidisoglu, Enis;Chiantia, Giuseppe;Franchino, Claudio;Tomagra, Giulia;Giustetto, Maurizio;Carbone, Emilio;Carabelli, Valentina;Marcantoni, Andrea
Last
2022-01-01
Abstract
Amyloid beta 42 peptide (Abeta42) accumulation is a key characteristic of Alzheimer's disease (AD) and causes synaptic dysfunctions. To date, the effects of Abeta42 accumulation on GABAergic synapses are poorly understood Our findings suggest that, similarly to what observed on glutamatergic synapses, Abeta42 modifies GABAergic synapses by targeting ryanodine receptors and causing calcium dysregulation The GABAergic impairments can be restored by the RyR-calstabin interaction stabilizer S107 Based on our research, RyRs stabilization may represent a novel pharmaceutical strategy for preventing or delaying of AD.
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