X-Message-Number: 27063
Date: Fri, 16 Sep 2005 21:03:48 +0200
From: Eugen Leitl <>

Subject: [: [GRG] Heart attacks, stroke & neuronal cell 
death]

----- Forwarded message from "Robert J. Bradbury" <> -----

From: "Robert J. Bradbury" <>
Date: Fri, 16 Sep 2005 10:13:38 -0700 (PDT)
To: Gerontology Research Group <>
Subject: [GRG] Heart attacks, stroke & neuronal cell death
Reply-To: Gerontology Research Group <>


It is worth observing that probably more than 50% of all deaths are
due to neuronal death after ischemic/hypoxic insult (e.g. the
ultimate cause of death from heart attacks and strokes).

This is also the cause of significant levels of disability (and
therefore medical expense) in those cases where the heart attacks
or strokes do not happen to be fatal.

We have relatively good means at this point for dissolving clots
preventing the blood from reaching neurons and for promoting clots
in the case of hemmorhagic stroke.  What we do not have a good
handle on is preventing the neuron death associated with the
ischemic/hypoxic insult.

PNAS has an article today [1], that begins to get a handle on this.
It appears that rapid (excitotoxic) component of neuron death regulated
by p35 and cdk5 while the delayed (apoptotic-like) component is regulated
by cyclinD1 and cdk4.

This is actually quite good news as it starts to give you targets which can
be impacted by drugs.  Given the severe negative consequences of neuronal
cell death and the transitory nature of any drug therapy (just long enough
to allow the neurons to return to a normal state) one would hope that the
development of drug therapies to manage these pathways would be quite rapid.

Robert

1. Juliet Rashidian, et al, PNAS, 10.1073/pnas.0500099102
"Multiple cyclin-dependent kinases signals are critical mediators of
ischemia/hypoxic neuronal death in vitro and in vivo"
http://www.pnas.org/cgi/content/abstract/0500099102v1?etoc

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Eugen* Leitl <a href="http://leitl.org">leitl</a>
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