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Within the CNS, APOE4 — a risk factor for late-onset Alzheimer disease — is produced by a variety of cell types. Blumenfeld, Yip, Kim and Huang discuss recent scientific advances that have begun to unravel the cell type-specific roles of APOE4 and outline a corresponding cell type-specific APOE4 cascade model of Alzheimer disease.
Data-driven disease progression models are computational tools that infer long-term disease timelines from short-term biomarker data and may provide insights into disease processes. In this Review, Young, Oxtoby et al. provide an overview of such models, with a focus on how they have been used in the context of neurodegenerative diseases, notably Alzheimer disease.
Around 10% of individuals with frontotemporal lobar dementia have amyloid filament inclusions that lack tau and TDP-43 and were thought to contain the protein FUS, but are found instead to contain the FUS homologue TAF15.
Cytoplasmic mislocalization of TDP-43 in neurodegenerative disease affects mRNA maturation and protein levels of stathmin-2, leading to a reduction in axon diameter and tearing of outer myelin layers and thereby disrupting neuronal function.
A study in mice identifies formin 2 as a regulator of axon regeneration and a potential target for promoting nerve repair after peripheral nerve injury.
Synaptic engineering involves the synthetic insertion of new synapses between neurons in vivo. In this Perspective, Rabinowitch, Colón-Ramos and Krieg explore this emerging approach for studying neural circuits, describing the different methods that have been used and how they have been implemented.
