“Killing the Blues”: A role for cellular suicide (apoptosis) in depression and the antidepressant response?

Apoptosis or programmed cell death is a critical regulator of tissue homeostasis and emerging evidence is focused on the role of apoptosis mechanisms in the central nervous system. Generally, apoptosis is necessary to prevent cancerous growths. However, excessive apoptosis in post-mitotic cells such as neurons leads to neurodegeneration. Chronic stress, which can precipitate depression, has been shown to increase the susceptibility of certain populations of neurons to cell death while antidepressant treatment, in general, shows the ability to oppose these effects and promote neuroprotection. Here, we discuss the major players in cell death pathways, the physiological implications of chronic stress and depression, chronic stress models in animals which result in cell death and the different classes of antidepressants and mood stabilizers that have been shown to prevent cell death. We discuss the cellular effects of antidepressants and possible modes of action in preventing apoptosis. Investigations on the role of apoptosis in mediating the molecular, physiological and behavioural effects of antidepressants may help gain a better mechanistic insight into drug action and allow refinement of current therapeutics in order to target these pathways in a specific manner.     

Intracranial hematomas: imaging by high-field MR

Twenty intracranial hematomas between 1 day and over 1 year old were imaged using magnetic resonance at 1.5 T, with T1- and T2-weighted spin-echo pulse sequences. Characteristic intensity patterns were observed in the evolution of the hematomas, which could be staged as acute (less than 1 week old), subacute (greater than 1 week and less than 1 month old), or chronic (greater than 1 month old). Acute hematomas were characterized by central hypointensity on T2-weighted images (WIs). Subacute hematomas had peripheral hyperintensity on T1-WIs and then on T2-WIs. This hyperintensity proceeded to fill in the hematoma in the chronic stage. In subacute and chronic hematomas, there was hypointensity on T2-WIs in the immediately adjacent part of the brain. On T2-WIs of acute and subacute hematomas, the nearby white matter was characterized by hyperintensity, consistent with edema. A different mechanism is proposed for each of the three characteristic intensity patterns. Two of these mechanisms increase in proportion to the square of the magnetic field magnitude.