Abstract:
:Compelling evidence links amyloid beta (Aβ) peptide accumulation in the brains of Alzheimer's disease (AD) patients with the emergence of learning and memory deficits, yet a clear understanding of the events that drive this synaptic pathology are lacking. We present evidence that neurons exposed to Aβ are unable to form new synapses, resulting in learning deficits in vivo. We demonstrate the Nogo receptor family (NgR1-3) acts as Aβ receptors mediating an inhibition of synapse assembly, plasticity, and learning. Live imaging studies reveal Aβ activates NgRs on the dendritic shaft of neurons, triggering an inhibition of calcium signaling. We define T-type calcium channels as a target of Aβ-NgR signaling, mediating Aβ's inhibitory effects on calcium, synapse assembly, plasticity, and learning. These studies highlight deficits in new synapse assembly as a potential initiator of cognitive pathology in AD, and pinpoint calcium dysregulation mediated by NgRs and T-type channels as key components. VIDEO ABSTRACT.
journal_name
Neuronjournal_title
Neuronauthors
Zhao Y,Sivaji S,Chiang MC,Ali H,Zukowski M,Ali S,Kennedy B,Sklyar A,Cheng A,Guo Z,Reed AK,Kodali R,Borowski J,Frost G,Beukema P,Wills ZPdoi
10.1016/j.neuron.2017.09.041subject
Has Abstractpub_date
2017-10-11 00:00:00pages
355-372.e6issue
2eissn
0896-6273issn
1097-4199pii
S0896-6273(17)30910-8journal_volume
96pub_type
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