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Whether cell cycle re-entry is part of the normal life-cycle of a healthy neuron, or is restricted to diseased neuronal states, remains unclear [ 3, 5, 6].
This image shows minimal tissue scarring (green and red stains) and healthy neuron growth (purple) surrounding an implant.
The top image shows a healthy neuron, and the bottom one shows a neuron of an injured mouse given an experimental therapy.
Image of a healthy neuron.
Plaques linked to beta amyloid peptide inflame brain tissue, interfere with healthy neuron transmission, and are indicated in nerve degeneration.
A more complex anatomical model is required to explain how axonal degeneration passes from a diseased to a healthy neuron.
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The treatment involves interventions such as exercise, drugs, or nutrients that alter the neuronal microenviroment so that healthy neurons maintain their selective advantage and the brain doesn't shift from normal to pathological aging.
We observed a significant loss of healthy neurons because of a trans-neuronal degeneration mechanism in the chimeric mice.
Finally, using neurons from two distinct mutant mouse strains whose axons are highly resistant to neurodegeneration (Wld(S) and Sarm1, we found that the three different fibrils were secreted by axons after anterograde transport, in the absence of axonal lysis, indicating that trans-neuronal spread can occur in intact healthy neurons.
The requirement for both S100A4 and neuronal activity may be a way for TNTs to distinguish healthy neurons from others.
How is constitutive autophagy regulated in healthy neurons?
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com