Frontal cortical circuit alterations and cognitive deficits identified in mouse genetic models are reversed by chemogenetic or optogenetic stimulation of the mesocortical dopamine circuit in an adolescent period.

Repression of the G protein-coupled chemokine receptor CCR5 enhances MAPK/CREB signaling, long-term potentiation, somatosensory cortical plasticity, and learning and memory, while CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits.

Lrp4 mutant mice display profound deficits in cognitive tasks that assess learning and memory with disruptions in the subcellular organization of synaptic inputs and synaptic plasticity in the hippocampus.

Children with autism often 'tune out' the voices in their environment and new results show that impaired processing of voices in the brain's reward system may underlie this social behavior.

While semantic symptoms in fronto-temporal dementia patients were mainly dependent on short-range white-matter fibre disruption, long-range white-matter fibres damage was the major contributor to executive dysfunction, highlighting the importance of controlling for risk factors associated with deep white-matter disease.

Social and cognitive functions require normal activity during development of the posterior cerebellum.

Lesions to the anterior-medio-dorsal thalamus cause widespread behavioral impairments across multiple cognitive domains, suggesting that thalamic hubs are critical for interconnecting diverse cognitive processes.

High-definition anodal transcranial stimulation alleviated cognitive deficits, affected dopaminergic neurotransmission factors, increased expression of several neurotrophic factors involving brain-derived neurotrophic factor (BDNF), and activated hippocampal neurogenesis.

A neural precursor cell defect precedes widespread inflammation, amyloid plaque pathology, and cognitive deficit in Alzheimer's disease, which can be reversed by inhibiting USP16.

Whole-brain radiotherapy, but not glioma growth in distal region from the hippocampus, results in impaired recognition memory, which can be prevented by CSF-1R inhibitor-mediated microglia depletion.