In vivo studies reveal that mitochondrial Complex I deficiencies induce iron misregulation and liver iron overload that may contribute to neurodegeneration in mitochondrial disease mice, and that iron restriction is effective in reducing disease progression.

Perceived and unperceived visual stimuli that are contrast matched to produce similar BOLD responses in V1 elicit clearly distinct changes in the neurochemical profile, implying a perception-related dissociation between neurometabolic and neurovascular response.

Enhanced Gq-signaling-mediated activation of forebrain excitatory neurons in postnatal life programs enhanced anxiety-, despair- and schizophrenia-like behavior, recapitulating key aspects of the behavioral consequences of early life adversity.

Combining techniques that track blood oxygenation and biochemicals during neuronal activity reveals how the brain computes perceived and unperceived stimuli.

Fast oscillations (30-150Hz), generated by internal brain mechanisms may be essential for the maintenance of healthy brain function.

Lactate is preferred to glucose as an energy substrate and exacerbates spiking activity in most neuron types of juvenile somatosensory cortex by closing ATP-sensitive potassium channels.

Dysfunctions of myelin peroxisomes cause a lysosomal storage-like disorder associated with alterations in glial and axonal membranes, which is the likely cause of nerve impairment in peroxisomal disorders.

A mouse model of retinal degeneration reveals a common mechanism for axonal degeneration and photoreceptor cell death and identifies SARM1 as a therapeutic candidate for retinopathies.

The capacity to sustain effort to obtain rewards over time depends on the levels of the antioxidant glutathione in the nucleus accumbens - a brain region critical for motivated behavior - and can be boosted with a nutritional intervention (N-acetylcysteine).