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Author: Rung-Chi Li, Touro University College
of Osteopathic Medicine California, Class of 2013
Introduction: Accumulating evidence has linked
stroke and Alzheimer's disease (AD) and shown that each exacerbates
the severity of the other. Recent studies suggest that vascular
effects (such as vascular reactivity and inflammation) may play an
important role in AD pathophysiological progression. The original
concept that AD is a purely neurologically driven disorder has been
questioned based on this strong connection between AD and stroke.
It is challenging to completely separate the vascular and
neurological system and independently to investigate the importance
of each system in the AD pathology. We proposed here to use an
acute brain slice preparation to directly examine neuronal synaptic
properties under controlled conditions, by removing the need for
the vascular system for delivery of oxygen and glucose. This method
avoids the possible effects of amyloid on vascular dysfunction.
Therefore, using oxygen glucose deprivation we can investigate
whether ischemic neuronal damage in a triple transgenic mouse model
of AD is due to intrinsic neuronal sensitivity to ischemia or has
contributions from vascular dysfunction.
Methods: Ischemic damage was modeled using
oxygen-glucose deprivation (OGD; an in vitro global cerebral
ischemia model) in brain slices from mice with an APP/PS1/tau
triple gene mutation, an aggressive model of AD. These mice develop
amyloid plaques at about 2-3 months of age, and behavioral memory
deficits are developed by 6 months of age.
Results: Our results have demonstrated a
significantly higher maximum recovery rate after OGD for 7.5
minutes in 3.5 month-old AD mice compared to the wild-type cohorts.
More interestingly, 8 month-old AD mice group subjected to 5
minutes OGD insult showed a similar trend, compared to age-matched
wild-type cohorts. In contrast, we did not observe any difference
between WT and AD 8-month-old mice for 7.5 minutes OGD. These
results suggest that the hippocampal slices from transgenic mice
show less sensitivity to OGD, indicating that the sensitivity seen
in AD mice subject to vascular-occlusion models of ischemia may be
due primarily to vascular factors rather than intrinsic neuronal
Conclusion: The observed changes in
electrophysiological responses to OGD may reflect compensatory
mechanisms in response to disease state similar to those seen in
classic models of ischemic preconditioning. Such compensations may
confer direct neuronal protection against stressors such as
ischemia without improving vascular deficiencies that might lead to
chronic hypoperfusion of AD brains. The current findings provide a
new understanding of the close relationship between neuronal and
vascular contributions to AD.
January 2013 Issue of IMpact