I wish they would at least compare and contrast their findings to the earlier one here:
from January 2013.
Kruppel-like Factor 2 Protects Against Ischemic Stroke by Regulating Endothelial Blood Brain Barrier Function
the new one here;
http://www.medicalnewstoday.com/releases/260812.php
While the effects of acute
stroke
have been widely studied, brain damage during the subacute phase of
stroke has been a neglected area of research. Now, a new study by the
University of South Florida reports that within a week of a stroke
caused by a blood clot in one side of the brain, the opposite side of
the brain shows signs of microvascular injury.
Stroke is a leading cause of death and disability in the United States, and increases the risk for
dementia.
"Approximately 80 percent of strokes are ischemic strokes, in which the
blood supply to the brain is restricted, causing a shortage of oxygen,"
said study lead author Svitlana Garbuzova-Davis, PhD, associate
professor in the USF Department of Neurosurgery and Brain Repair.
"Minutes after ischemic stroke, there are serious effects within the
brain at both the molecular and cellular levels. One understudied aspect
has been the effect of ischemic stroke on the competence of the
blood-brain barrier and subsequent related events in remote brain
areas."
Using a rat model, researchers at USF Health investigated the subacute
phase of ischemic stroke and found deficits in the microvascular
integrity in the brain hemisphere opposite to where the initial stroke
injury occured.
The study was published in the journal
PLOS One.
The USF team found that "diachisis," a term used to describe certain
brain deficits remote from primary insult, can occur during the subacute
phase of ischemic stroke. The research discovered diachisis is closely
related to a breakdown of the blood-brain barrier, which separates
circulating blood from brain tissue.
In the subacute phase of an ischemic stroke, when the stroke-induced
disturbances in the brain occur in remote brain microvessels, several
areas of the brain are affected by a variety of injuries, including
neuronal swelling and diminished myelin in brain structures. The
researchers suggest that recognizing the significance of microvascular
damage could make the blood-brain barrier (BBB) a therapeutic "target"
for future neuroprotective strategies for stroke patients.
The mechanisms of BBB permeability at different phases of stroke are
poorly understood. While there have been investigations of BBB integrity
and processes in ischemic stroke, the researchers said, most
examinations have been limited to the phase immediately after stroke,
known as acute stroke. Their interest was in determining microvascular
integrity in the brain hemisphere opposite to an initial stroke injury
at the subacute phase.
Accordingly, this study using rats with surgically-simulated strokes was
designed to investigate the effect of ischemic stroke on the BBB in the
subacute phase, and the effects of a compromised BBB upon various brain
regions, some distant from the stroke site.
"The aim of this study was to characterize subacute diachisis in rats
modeled with ischemic stroke," said co-author Cesar Borlongan, PhD,
professor and vice chairman for research in the Department of
Neurosurgery and Brain Repair and director of the USF Center for Aging
and Brain Repair. "Our specific focus was on analyzing the condition of
the BBB and the processes in the areas of the brain not directly
affected by ischemia. BBB competence in subacute diachisis is uncertain
and needed to be studied."
Their findings suggest that damage to the BBB, and subsequent vascular
leakage as the BBB becomes more permeable, plays a major role in
subacute diachisis.
The increasing BBB permeability hours after the simulated stroke, and
finding that the BBB "remained open" seven days post-stroke, were
significant findings, said Dr. Garbuzova-Davis, who is also a researcher
in USF Center for Aging and Brain Repair. "Since increased BBB
permeability is often associated with brain swelling, BBB leakage may be
a serious and life-threatening complication of ischemic stroke."
Another significant aspect was the finding that autophagy -- a mechanism
involving cell degradation of unnecessary or dysfunctional cellular
components --plays a role in the subacute phase of ischemia. Study
results showed that accumulation of numerous autophagosomes within
endothelial cells in microvessels of both initially damaged and
non-injured brain areas might be closely associated with BBB damage.
Autophagy is a complex but normal process usually aimed at
"self-removing" damaged cell components to promote cell survival. It was
unclear, however, whether the role of autophagy in subacute
post-ischemia was promoting cell survival or cell death.
More than 30 percent of patients who survive strokes develop dementia within two years, the researchers noted.
"Although dementia is complex, vascular damage in post-stroke patients
is a significant risk factor, depending on the severity, volume and site
of the stroke," said study co-author Dr. Paul Sanberg, USF senior vice
president for research and innovation. "Ischemic stroke might initiate
neurodegenerative dementia, particularly in the aging population."
The researchers conclude that repair of the BBB following ischemic
stroke could potentially prevent further degradation of surviving
neurons.
"Recognizing that the BBB is a therapeutic target is important for developing neuroprotective strategies," they said
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