Identification and Cost of Potentially Avoidable Transfers to a Tertiary Care Neurosurgery Service: A Pilot Study.

Background: Thousands of neurosurgical emergencies are transferred yearly to tertiary care facilities to assume a higher level of care. Several studies have examined how neurosurgical transfers influence patient outcomes, but characteristics of potentially avoidable transfers have yet to be investigated.

Objective: To identify whether potentially avoidable transfers represent a significant portion of transfers to a tertiary neurosurgical facility.

Tau-mediated NMDA receptor impairment underlies dysfunction of a selectively vulnerable network in a mouse model of frontotemporal dementia.

Frontotemporal dementia (FTD) is a neurodegenerative behavioral disorder that selectively affects the salience network, including the ventral striatum and insula. Tau mutations cause FTD, but how mutant tau impairs the salience network is unknown. Here, we address this question using a mouse model expressing the entire human tau gene with an FTD-associated mutation (V337M).

An acetylcholinesterase inhibitor, eserine, induces long-term depression at CA3-CA1 synapses in the hippocampus of adult rats.

Studies in humans and rodents support a role for muscarinic ACh receptor (mAChR) and nicotinic AChR in learning and memory, and both regulate hippocampal synaptic plasticity using complex and often times opposing mechanisms. Acetylcholinesterase (AChE) inhibitors are commonly prescribed to enhance cholinergic signaling in Alzheimer's disease in hopes of rescuing cognitive function, caused, in part, by degeneration of cholinergic innervation to the hippocampus and cortex. Unfortunately, therapeutic efficacy is moderate and inconsistent, perhaps due to unanticipated mechanisms.

Dissociation of frontotemporal dementia-related deficits and neuroinflammation in progranulin haploinsufficient mice.

Frontotemporal dementia (FTD) is a neurodegenerative disease with hallmark deficits in social and emotional function. Heterozygous loss-of-function mutations in GRN, the progranulin gene, are a common genetic cause of the disorder, but the mechanisms by which progranulin haploinsufficiency causes neuronal dysfunction in FTD are unclear. Homozygous progranulin knock-out (Grn(-/-)) mice have been studied as a model of this disorder and show behavioral deficits and a neuroinflammatory phenotype with robust microglial activation.

Bidirectional axonal plasticity during reorganization of adult rat primary somatosensory cortex.

Cortical sensory maps contain discrete functional subregions that are separated by borders that restrict tangential activity flow. Interestingly, the functional organization of border regions remains labile in adults, changing in an activity-dependent manner. Here, we investigated if axon remodeling contributes to this reorganization.