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Open AccessJournal ArticleDOI

Anaesthetic neurotoxicity and neuroplasticity: an expert group report and statement based on the BJA Salzburg Seminar

TLDR
mounting evidence from preclinical studies reveals general anaesthetics to be powerful modulators of neuronal development and function, which could contribute to detrimental behavioural outcomes, however, definitive clinical data remain elusive.
Abstract
Although previously considered entirely reversible, general anaesthesia is now being viewed as a potentially significant risk to cognitive performance at both extremes of age. A large body of preclinical as well as some retrospective clinical evidence suggest that exposure to general anaesthesia could be detrimental to cognitive development in young subjects, and might also contribute to accelerated cognitive decline in the elderly. A group of experts in anaesthetic neuropharmacology and neurotoxicity convened in Salzburg, Austria for the BJA Salzburg Seminar on Anaesthetic Neurotoxicity and Neuroplasticity. This focused workshop was sponsored by the British Journal of Anaesthesia to review and critically assess currently available evidence from animal and human studies, and to consider the direction of future research. It was concluded that mounting evidence from preclinical studies reveals general anaesthetics to be powerful modulators of neuronal development and function, which could contribute to detrimental behavioural outcomes. However, definitive clinical data remain elusive. Since general anaesthesia often cannot be avoided regardless of patient age, it is important to understand the complex mechanisms and effects involved in anaesthesia-induced neurotoxicity, and to develop strategies for avoiding or limiting potential brain injury through evidence-based approaches.

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Dissertation

General Anaesthetic Modulation of Memory-Related Gene Expression in the Cerebral Cortex

TL;DR: This paper aims to provide a history of the field and some of the mechanisms that led to the current state of knowledge and practices in this area.

The stress peptide PACAP-38 protects neurons against ketamine-induced apoptosis in developing rat retina

TL;DR: It is demonstrated PACAP-38 could protect neurons from ketamine-induced apoptosis in early developmental rat retina, and PACAP’s anti-apoptotic effects could be partly antagonized by adenylate cyclase (AC) and protein kinase A (PKA) inhibitors, respectively, and mostly counteracted by extracellular signal-regulated kinase (ERK1/2) inhibitor.
Journal ArticleDOI

Multimodal monitoring (MMM) in the perioperative period

David Green
- 14 Jun 2016 - 
TL;DR: This paper concentrates on three classes of nonor minimally invasive monitors which have become additionally available in the last 10 to 15 years and if used in combination their potential impact on improving outcome following surgery in high risk patients.
References
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TL;DR: It is shown that C1q, the initiating protein in the classical complement cascade, is expressed by postnatal neurons in response to immature astrocytes and is localized to synapses throughout the postnatal CNS and retina, supporting a model in which unwanted synapses are tagged by complement for elimination and suggesting that complement-mediated synapse elimination may become aberrantly reactivated in neurodegenerative disease.
Journal ArticleDOI

Comparative aspects of the brain growth spurt

TL;DR: The brain in all species appears to grow through a sigmoid trajectory when its weight is plotted against its age, but the timing of the brain growth spurt is different in relation to birth in different species, so this must be one of the major factors to be taken into account when any attempt is made to extrapolate results obtained in one species to any other.
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Journal ArticleDOI

Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model

TL;DR: Reducing endogenous tau levels prevented behavioral deficits in transgenic mice expressing human amyloid precursor protein, without altering their high Aβ levels, and protected both transgenic and nontransgenic mice against excitotoxicity.
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