Topic: memory impairment

In mouse models of Down syndrome (DS), cognitive deficits such as memory impairment are believed to be caused by overinhibition. However, recent studies indicate that the overexpression of Grik1, a gene mainly expressed at interneurons in the hippocampus, could be a key driver of memory deficits in individuals with DS due to a bidirectional alteration of synaptic inhibition on CA1 pyramidal cells (Valbuena et al, Nature Comms. 2019, 10:4991). Remarkably, normalizing Grik1 dosage in the Ts2Cje mouse model of DS specifically restores spatial memory and reverses the bidirectional alterations to C

Anti-NMDAR encephalitis (NMDARe) is a disorder mediated by antibodies against the GluN1 subunit of NMDAR. Patients develop severe neuropsychiatric symptoms that usually improve with immunotherapy, although very slowly. To better understand the neuro-immunobiology of the disease and how different treatments might work, we aimed to develop an animal model that reproduced most of the symptoms and their protracted clinical course. Eight-week-old female mice (C57BL/6J) were immunized (days 1 and 28) with GluN1356-385 peptide or saline with AddaVax adjuvant and Pertussis Toxin. After developing symp

Deep brain stimulation (DBS) of the fornix is currently being trialled in the treatment of memory impairment, including in Alzheimer’s disease. Commonly, DBS is delivered continuously at 130Hz, but the effect on memory performance of such stimulation has been mixed. Clinicians have suggested that delivering stimulation timed to ongoing neural activity may enhance the efficacy of DBS. Theta oscillations in the hippocampus, which have been hypothesised to support learning and memory, may provide a read out of memory relevant neural activity. Supporting this, optogenetic stimulation of the hippoc