http://stroke.ahajournals.org/content/early/2013/11/06/STROKEAHA.113.001269.short
- Eng H. Lo, PhD
+ Author Affiliations
- Correspondence to Eng H. Lo, PhD, Massachusetts General Hospital, Harvard Medical School, MGH E 149-2401, 13th St, Charlestown, MA 02129. E-mail Lo@helix.mgh.harvard.edu
Abstract
The pathophysiology of stroke is
complex. Adaptive and maladaptive signalling occurs between multiple
cell types in the brain.
There is crosstalk between central and systemic
responses. And there are overlapping pathways during initial injury and
subsequent
repair. These numerous feed-forward and
feed-back interactions have made it difficult to translate experimental
discoveries
into clinical applications. An emerging
hypothesis in biomedical research now suggests that contrary to a
traditional model,
translation may not be efficiently obtained
without a rigorous understanding of mechanisms. Hence, to optimize
diagnostics
and therapeutics for stroke patients, it is
necessary to identify and define causal mechanisms. Mirroring the
multi-compartment
interactions in stroke pathophysiology,
bench-to-bedside, and bedside-back-to-bench advances in stroke may be
best achieved
with inter-disciplinary collaborations between
basic research, neuroimaging, and broadly based clinical science.
Causation
can then be two-fold, ie, dissecting mechanisms
and targets, as well as developing future scientists who can blur the
boundaries
between basic, translational, and clinical
research. In systems theory, a critical goal is to distinguish causation
from correlation.
In stroke research, causation may perhaps be
found through a collaborative search for mechanisms.
No comments:
Post a Comment