Preventing activity of the kinase tumor progression locus 2 modulates microglial activation, reduces T-cell brain infiltration, and is neuroprotective in disease models.

The combination of deep learning with whole-brain computational models reveals the low-dimensional representation of neurodegenerative diseases, which emerges from a highly multidimensional brain, providing valuable insight into pathological states' diagnostic, prognosis, and treatment response.

Promoting a Warburg-like shift in astrocytic metabolism through reduced mitochondrial electron transport accommodates the energetic burden caused by brain trauma without overwhelming cellular respiration and redox to salvage dopaminergic neurons.

Computational-driven, imaging-based topological profiles of neurodegeneration differ substantially in different neurodegenerative conditions, suggesting distinct modes of dependence of the pathological spread on the underlying connectivity.

Major cell types across various brain regions distinctively associate with tissue loss in 13 neurodegenerative conditions.

An effective and reversible mouse glaucoma model that replicates the secondary glaucoma in human patients caused by silicone oil after retina surgeries presents significant neurodegeneration, and is suitable for neuroprotectants selection.

In C. elegans, presenilin functions, independent of its gamma-secretase proteolytic activity, to regulate mitochondrial metabolism by controlling ER-mitochondrial calcium transfer and, even in the absence of Abeta signaling, loss of this activity leads to neurodegeneration.

A plant virus, Tomato yellow leaf curl virus, manipulates the host preference of the vector insect whitefly to promote its transmission by inducing caspase-dependent apoptotic neurodegeneration in vector's brain.

Inducing neuronal mitochondrial activity during central nervous system inflammation counteracts inflammation-induced neuronal electron transport chain deficiency and calcium toxicity, thereby protecting against neuronal loss in a multiple sclerosis mouse model.

Transportomic analysis of the changes underlying neurodegeneration reveals the importance of Kif5a for neuronal survival and highlights the need to restore specific anterograde cargo transport to for regeneration.