What the f*cking hell will it take to complete the testing and creation of a translational stroke protocol based on this? Or will everybody assume this is somebody else's problem and nothing will get done for 50 years because our stroke associations will not take it upon themselves to solve this to improve stroke survivors lives? I'm looking at the boards of directors to push this forward.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=145573&CultureCode=en
A new study published in the prestigious publication The EMBO Journal
shows that the mitochondrial protein Mfn2 may be a future therapeutic
target for neuronal death reduction in the late phases of an ischemic
stroke. The study has been coordinated by Dr Francesc Soriano, Ramón y
Cajal researcher at the Department of Cell Biology of the University of
Barcelona (UB) and member of the Research Group Celltec UB.
The study, funded by the Fundació La Marató de TV3, is part of the
PhD thesis developed by Àlex Martorell Riera (UB), first author of the
article. Experts Antonio Zorzano and Manuel Palacín, from the Department
of Biochemistry and Molecular Biology of UB and the Institute for
Research in Biomedicine (IRB Barcelona), and Jesús Pérez Clausell and
Manuel Reina, from the Department of Cell Biology of UB, also
collaborated in the study.
When blood flow is blocked in the brain
According to the World Health Organization (WHO), strokes are the
second leading cause of death in the world. A stroke occurs when a blood
vessel is blocked interrupting blood flow in the brain. Ictus damage is
progressive: it begins some minutes after the attack. Recommended
treatment consists in restoring blood flow to the brain, but it must be
done during the first four hours after the stroke.
According to researcher Francesc Soriano, “one of the main causes of
brain death in ictus events is glutamate increase; glutamate is the main
excitatory neurotransmitter in the central nervous system. Glutamate
extracellular concentrations remain low due to the activity of membrane
transporters, which require energy to work”.
When blood flow is blocked, energy levels are reduced in the affected
area. This phenomenon leads glutamate transporters to work inversely,
so glutamate is expelled to the extracellular space. Glutamate activates
its receptors —particularly, the N-methyl-D-aspartate receptor (NMDA)—
on neurons’ surface, a process that triggers an excessive flux of
calcium, the activation of a series of reactions and neuronal death, in a
process known as excitotoxicity. “Many of these excitotoxic cascades
—points out Soriano— converge on the mitochondrion, an organelle which
plays a major role not only in energy production, but also in
apoptosis”.
New therapeutic strategies against ischemic ictus
Specifically, Mfn2 is a mitochondrial protein involved in the
regulation of organelles’ morphology and function. The team led by Dr
Francesc Soriano has just discovered that the reduction in Mfn2 protein
levels occurs four hours after the initiation of the excitotoxic process
in in vitro and in vivo animal models.
In vivo experiments proved that if Mfn2 reduction is stopped, delayed
excitotoxic cell death is blocked. The research team from the
Department of Cell Biology of UB found that the Mfn2 reduction is
triggered by a genetic transcription mechanism (DNA is transcribed into
RNA molecules). UB experts also discovered that MEF2 is the
transcription factor involved in this process. Authors affirm that these
findings are essential to find a strategy to reverse Mfn2 reduction.
Currently, the team led by Dr Francesc Soriano are researching on
brain damage in excitotoxic conditions in animal models where the gene
Mfn2 has been removed. The main objective is to design therapeutic
strategic in order to reduce damage.
http://www.ub.edu
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