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Chunk #2 — INTRODUCTION

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Neurons derived from patients with bipolar disorder divide into intrinsically different sub-populations of neurons, predicting the patients' responsiveness to lithium.
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The reported neuropathology of BD includes reductions in neuronal and glial density in the prefrontal cortex, anterior cingulate cortex and hippocampus,30–33 although other studies of the anterior cingulate cortex have found no difference in neuronal and glial density.34 Genes and pathways associated with neurotransmitters have been shown to be altered in BD patients,35 along with changes in the levels of several neuromodulators and neurotransmitters.36,37 Alterations in the excitatory/inhibitory ratio have also been demonstrated,38,39 and mitochondrial cytopathies and dysfunction have been associated with BD.40,41