Study | Model | Main findings |
Hamani et al 3 | 1 obese patient | Acute 130 Hz DBS induced old memories recall |
Laxton et al 2010 | 6 Patients with AD | Clinical trial phase I: forniceal DBS was safe and drove neural activity in the memory circuit, including the entorhinal and hippocampal areas, and activated the brain’s default mode network |
Smith et al 2012 | 6 Patients with AD | Increased connectivity after 1 year of DBS is observed. The persistent cortical metabolic increases after 1 year of DBS were associated with better clinical outcomes |
Sankar et al 2015 | Patients with AD | In addition to modulating neural circuit activity, forniceal DBS influenced the natural course of brain atrophy in a neurodegenerative disease |
Lozano et al 2016 | Patients with AD | Clinical trial phase II: no significant differences in the primary cognitive outcomes in the ‘on’ vs ‘off’ stimulation group at 12 months, but in patients >65 years old was associated with a trend towards both benefit on clinical outcomes |
Hescham et al 2015a | Rats | 1 hour of 100 Hz DBS increased c-Fos in CA1 and CA3 and led to ACh increase in hippocampus peaking 20 min after stimulus onset, and no change of glutamate |
Zhang et al 2015 | Rats with hippocampal AP 1–42 | 24-hour-long DBS facilitated hippocampus-dependent spatial memory 4 weeks later |
Hescham et al 2016 | Rats | Acute 100 Hz DBS improved performance in Morris Water Maze test |
Hescham et al 2013 | Rats, IP scopolamine | Forniceal DBS reversed the memory impairing effects of scopolamine. DBS efficacy was not sensitive to the frequency of stimulation, but rather to current levels |
Gondard et al 2015 | Rats | Forniceal DBS triggers hippocampal activity and rapidly modulates the expression of neurotrophic factors and markers of synaptic plasticity known to play key roles in memory processing |
ACh, acetylcholine; AD, Alzheimer's disease; AP 1-42, amyloid peptide 1-42; DBS, deep brain stimulation; IP, intraperitoneal.