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Glucocorticoids, which are released in response to stress, modulate the consolidation, retrieval and extinction of memories. In this Review, de Quervainet al. suggest that, in fear-related disorders such as post-traumatic stress disorder, targeting glucocorticoid signalling to attenuate fear memories has therapeutic potential.
Following injection into the brain, different strains of tau aggregates induce different presentations of tau neuropathology in a mouse model of tauopathy.
The cognitive abnormalities observed in Alzheimer disease (AD) may be linked to alterations in oscillatory rhythmic activity and neuronal network hypersynchrony. Palop and Mucke review these links and explore how countering these network abnormalities and interneuron dysfunction may hold therapeutic potential for AD.
Viral entry into the CNS and infection of neural cells pose a specific challenge for the immune system: how to eradicate the invading pathogen without disrupting neuronal circuits. Rall and colleagues outline the host immune response to CNS viral infection and consider the possible consequences of non-lytic viral clearance in the brain.
The properties and location of synaptic integrins put them in an ideal position to transduce signals from the extracellular matrix to intracellular signalling pathways. Park and Goda, here, describe the mechanisms underlying integrin-mediated synapse regulation and its contributions to development, plasticity and disease.
This study suggests that brain-derived neurotrophic factor (BDNF) is released from dendritic spines in response to activity and acts in an autocrine manner to mediate structural plasticity of the spine from which it was released.
Mirror neurons transform sensory representations of others' behaviour into the observers' motor or visceromotor representations of that behaviour. In this Review, Giacomo Rizzolatti and Corrado Sinigaglia describe how the mirror mechanism is also likely to be involved in both action and emotion processing.
A loss of cholinergic inputs to the hippocampus in a mouse model of Alzheimer disease leads to memory deficits by affecting interneurons in the oriens lacunosum moleculare.