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.
The brain balances the segregation and integration of incoming information to facilitate flexible cognition and behaviour. In this Opinion article, Deco and colleagues argue that whole-brain computational modelling based on neuroimaging data can provide insights into these segregation and integration processes.
Research into the underlying pathology of c9FTD/ALS has been hampered by a lack of good mouse models, but a new study reports a mouse model that recapitulates both the cellular and the behavioural pathology associated with these disorders.
Interactions among semaphorin 6A, plexin A2 and plexin A4, and between contactin 4 and amyloid precursor protein, are crucial for the normal development of the circuits underlying vertical and horizontal optokinetic reflexes, respectively.
Disruption of actin polymerization in the frontal cortex, which causes abnormal dendritic spine structures, results in locomotor hyperactivity owing to dysregulation of a midbrain dopaminergic circuit.
The brain is increasingly thought to predict sensory inputs, based on previous experience. In this Opinion article, Barrett and Simmons integrate this active inference account with an anatomical model of corticocortical connections, and describe how such a system may unify allostatic control and interoception within an integrated neural architecture.
Recent methodological progress has greatly facilitated the determination of the connectivity and functional characterization of complex neural circuits. In this Review, Tovote, Fadok and Lüthi examine studies that have adopted circuit-based approaches to gain insight into how the brain governs fear and anxiety.
It is now emerging that the neuroinflammation that is associated with Alzheimer disease may have a key role in driving this disease. In this Review, Heppner, Ransohoff and Becher examine the contribution of the immune system to the pathogenesis of this disorder.
Dysfunction of autophagy — an intracellular degradation pathway for cytosolic material — has been implicated in the pathogenesis of various neurodegenerative diseases. Rubinsztein and colleagues review recent progress in this area, focusing on macroautophagy, and discuss how this process may be manipulated to protect against neurodegeneration.
Reelin induces transcriptional changes in neurons by increasing the formation of an intracellular fragment of its target receptor that interacts with specific enhancer regions in the nucleus.
