Topic: Ts65Dn mice

Down syndrome (DS) patients who show mental retardation also present acquired anosmia, i.e., the loss of odor detection. At the present time, no viable treatment exists for cognitive and olfactory deficits in DS. Interestingly, the ability to reach puberty and become fertile is also affected in these patients. An intriguing candidate, whose absence could mediate most of these phenotypes, is the gonadotropin-releasing hormone (GnRH), the neurohormone controlling reproduction. However, whether GnRH plays a role in the age-related cognitive decline in DS is unknown.We showed in Ts65dn mice, a wel

Down syndrome (DS) is characterized by deficits in neuronal activity and connectivity, with unclear contributions from different cell types. Microglia, the brain's immune cells, shape neuronal circuits by influencing the number of synaptic connections, both excitatory and inhibitory. This study investigates the microglial involvement in DS-related connectivity deficits. Using in vivo mesoscale wide-field calcium imaging, we analyzed the cortical connectivity of Ts65Dn and euploid mice injected retroorbitally with a CAMKII-GCaMP7f viral vector, in response to a drug effective in blocking neuron

Down syndrome (DS) individuals are characterized by a variety of pathological phenotypes that manifest with wide variability in different tissues. In the central nervous system, the accelerated aging phenotype is associated with the risk of developing Alzheimer-like dementia. A central aspect of neurodegeneration is the close association between metabolic disorders and cognitive decline. Multiple studies have suggested a link between metabolic disorder and microRNAs (miR), small non-coding RNAs acting as post-transcriptional regulators of a plethora of genes. Among triplicated miRNAs on chromo