TWEAK regulates proliferation and differentiation of adult neural progenitor cells.

The cytokine TWEAK is expressed in the brain and is induced in cerebral ischemia and other brain disorders. TWEAK regulates proliferation and differentiation of progenitor cells but its effect on adult neural progenitor cells is still unknown. Therefore, we investigated the proliferation of neural progenitor cells from the subventricular zone of adult mice in response to TWEAK treatment.

Low hemoglobin is associated with poor functional outcome after non-traumatic, supratentorial intracerebral hemorrhage.

Introduction: The impact of anemia on functional outcome and mortality in patients suffering from non-traumatic intracerebral hemorrhage (ICH) has not been investigated. Here, we assessed the relationship between hemoglobin (HB) levels and clinical outcome after ICH.

Methods: One hundred and ninety six patients suffering from supratentorial, non-traumatic ICH were extracted from our local stroke database (June 2004 to June 2006).

Transcriptional regulation of neurogenesis: potential mechanisms in cerebral ischemia.

Recent data provides evidence that new neurons are born in cerebral ischemia. Although ultimate evidence for their functional importance is lacking, correlational data suggest that they contribute to recovery. Therefore, the underlying mechanisms of neurogenesis are interesting as a basis for pharmacological enhancement of the phenomenon.

Crosstalk between nitric oxide and zinc pathways to neuronal cell death involving mitochondrial dysfunction and p38-activated K+ channels.

Nitric oxide (NO) and zinc (Zn2+) are implicated in the pathogenesis of cerebral ischemia and neurodegenerative diseases. However, their relationship and the molecular mechanism of their neurotoxic effects remain unclear. Here we show that addition of exogenous NO or NMDA (to increase endogenous NO) leads to peroxynitrite (ONOO-) formation and consequent Zn2+ release from intracellular stores in cerebrocortical neurons.

Glutamate activates NF-kappaB through calpain in neurons.

Glutamate induces gene transcription in numerous physiological and pathological conditions. Among the glutamate-responsive transcription factors, NF-kappaB has been mainly implicated in neuronal survival and death. Recent data also suggest a role of NF-kappaB in neural development and memory formation.

Dominant-interfering forms of MEF2 generated by caspase cleavage contribute to NMDA-induced neuronal apoptosis.

Myocyte enhancer factor-2 (MEF2) transcription factors are activated by p38 mitogen-activated protein kinase during neuronal and myogenic differentiation. Recent work has shown that stimulation of this pathway is antiapoptotic during development but proapoptotic in mature neurons exposed to excitotoxic or other stress. We now report that excitotoxic (N-methyl-D-aspartate) insults to mature cerebrocortical neurons activate caspase-3, -7, in turn cleaving MEF2A, C, and D isoforms.