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Increased levels of Aβ, pTau and activated GSK3β are implicated in the development of axonal trafficking dysfunction in AD (Vicario-Orri et al., 2015).
Similarly, the biology underpinning TNFR1 dysfunction in TRAPS is also far from straightforward, with multiple models of trafficking dysfunction having been linked to various respective TNFR mutations.
Altogether therefore, we propose that mitochondrial trafficking dysfunction may contribute to risk of mental illness in individuals carrying deleterious variants or mutations affecting DISC1 expression and/or function.
Therefore, as AP-1 and NF-κB are simultaneously activated in IL-1 or TNF-stimulated PBMC, as well endothelial cells from TRAPS patients, TNFR1 trafficking dysfunction is likely to involve coordinated stimulation of both NF-κB and AP-1.
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They are caused by axonal degeneration, which might involve mechanisms including impaired cellular membrane trafficking and mitochondrial dysfunction.
Taken together, these findings link hereditary forms of CP and implicate abnormalities of components of the dynamic cytoskeleton, process outgrowth, and protein trafficking with neuromotor dysfunction.
The concept of phenotypic screens can be extended to include other toxicologically relevant end points by using additional fluorescent or other markers to probe other pathophysiological processes including steatosis, phospholipidosis, apoptosis, endoplasmic reticulum (ER) stress, protein trafficking and transport dysfunctions.
In this same study, in the entire cohort, we found that BC was associated with a decrease in heart rate variability, suggesting traffic-particle associated autraffic-particle associatedtz et autonomicess).
As aberrant endosomal trafficking and synaptic dysfunctions have both been described as early stage events in various neurodegenerative diseases, including AD (Pimplikar et al, 2010), we searched for regulators of internalization/trafficking of TLN, and explored how they affect its role in spine morphogenesis.
Disorder of the synaptic AMPARs trafficking contributes to cognitive dysfunction in Alzheimer׳s disease (AD).
Genetic evidence has revealed a direct link between epilepsy and GABAARs dysfunction, including trafficking alteration.
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