Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Accumulation of TAR DNA-binding protein 43 (TDP43) in the neuronal cytoplasm and its loss from the nucleus are characteristic features of several neurodegenerative diseases. Tziortzouda, Van Den Bosch and Hirth describe three intrinsic mechanisms that control TDP43 levels and localization and are altered to drive pathology.
In this Review, Denoth-Lippuner and Jessberger present recent insights into adult hippocampal neurogenesis in rodents — from stem cell activation to the integration of newborn neurons into pre-existing circuits — and describe how newborn neurons affect brain function.
Inactivation of the gene encoding fragile X mental retardation protein (FMRP) drives the impairments in brain development and function that underlie fragile X syndrome. Richter and Zhao illustrate how innovative genetic and molecular biology tools have enhanced our understanding of both FMRP’s function and the causes of fragile X syndrome pathophysiology.
Flexibility is critical for the optimal adaptation of thoughts and actions under changing circumstances. In this Review, Uddin summarizes research that has identified cognitive processes and neural systems supporting flexibility and discusses ways to improve flexibility across the lifespan.
A substantial burden of neurological disease is related to mutations in three sodium channel genes: SCN1A, SCN2A and SCN8A. In this Review, Meisler and colleagues discuss the neurological disorders associated with these mutations and also the therapeutic opportunities that are being investigated as a result of these recent mechanistic insights.
The role of the default mode network (DMN) is unclear. In this Perspective, Yeshurun, Nguyen and Hasson review evidence that the DMN integrates extrinsic inputs with intrinsic information over long timescales, enabling it to represent meaning in a way that can be shared between individuals.
Lewy bodies, which are α-synuclein-rich intracellular inclusions, are pathological hallmarks of several neurodegenerative diseases, notably Parkinson disease. In this Review, Fares, Jagannath and Lashuel examine the biochemical, structural and morphological features of Lewy bodies as well as how α-synuclein pathology may form and spread.
The molecular basis of trans-synaptic signalling by Neurexins plays an important role in synapse organization. In this Review, Scheiffele and colleagues link cell type-specific alternative splicing to the combinatorial action of Neurexin isoforms, and provide a mechanistic framework for Neurexin functions in synapse organization.
