MRI is sensitive to the increase in axonal caliber due to pathology and was used to detect widespread increase in the average axonal caliber in multiple sclerosis brains with short disease duration only.

When oligodendrocytes lack expression of the low-abundant myelin protein CMTM5, central nervous system axons are myelinated normally but subsequently degenerate involving a Wallerian-like pathomechanism.

Ultrastructural and loss-of-function experiments show that oligodendrocyte-encoded Kir4.1 is located near active axonal structures, including within myelin inner tongue, and has critical functions to promote axonal activity and preserve integrity.

Tau deposition in the aging brain follows patterns of functional connectivity that correspond to specific neural memory networks, and this relationship is strengthened in the presence of amyloid-β.

Mild myelin disruption leads to early axonal pathology, a novel pathological response in neural stem cells, regionally increased oligodendrocytes and altered behavior.

Loss of myelin integrity in the mouse forebrain perturbs executive functions, assessed by tests requiring normal motor performance.

The projections from discrete areas to motor cortex increase over disease course in motoneuron disease model with selective spatial and temporal patterns.

Brain-Age delta is a non-invasive marker of biological brain aging that is sensitive to the presence of risk factors and altered biomarkers of Alzheimer's disease in non-demented individuals.

Amyloid-β oligomers associated with Alzheimer’s disease interact with dynein motors to impair retrograde transport of autophagic vesicles in neurons.

Reducing Akt-mediated huntingtin phosphorylation decreases APP accumulation at the synapse by reducing its anterograde axonal transport and ameliorates learning and memory in a mouse model of familial Alzheimer disease.