California Study Identifies New Source of Brain Bleeds
Because of the continuing study of long COVID-19, the topic of brain bleeds has emerged and their connection to the prolonged disease. A study in Sweden documented the link between long Covid and dementia, and one of the residual effects of the ailment is brain bleeds. The Swedish study found a link with the APOE4 genotype to a higher probability of post-Covid-related brain bleeds to accumulation of data suggesting the Covid-19-related protein may collect, accumulate and possibly inflame the brain. This can lead to Alzheimer’s and dementia. However, a new study could change the thinking on what causes brain bleeds.
California Study
In a study out of the University of California, Irvine scientists point out that the “interactions between aged red blood cells and brain capillaries” can cause microbleeds in brain tissue. It has always been assumed injured blood vessels caused brain bleeds. This study sheds new light on another possibility and these findings could lead to the potential to develop new therapies.
“Cerebral microhemorrhages (CMH) are associated with stroke, cognitive decline, and normal aging. Our previous study shows that the interaction between oxidatively stressed red blood cells (RBC) and cerebral endothelium may underlie CMH development. CMH are common findings in hypertension, cerebral amyloid angiopathy, Alzheimer’s disease, chronic kidney disease, cerebrovascular disease, and normal aging. Age is the most significant independent risk factor for CMB, with increasing CMB prevalence among older populations. CMB are associated with increased risk of ischemic and hemorrhagic stroke, cognitive decline, and dementia, making them increasingly clinically relevant for aging populations.” CMH is known to occur as a result of a brain vessel wall disruption and the forcing out of red blood cells (RBC) into the tissue of the brain. “In addition, disruption in brain iron homeostasis and the release of iron following ischemic damage can produce CMH.”
The researchers were able to watch the process where red blood cells stall in brain capillaries and see how the hemorrhage happens. “We have previously explored this issue in cell culture systems, but our current study is significant in expanding our understanding of the mechanism by which cerebral microbleeds develop,” said co-corresponding author Dr. Mark Fisher, professor of neurology in UCI’s School of Medicine. “Our findings may have profound clinical implications, as we identified a link between red blood cell damage and cerebral hemorrhages that occurs at the capillary level.”
Method
In laboratories, male mice were used in the experiment with the researchers exposing the subjects’ red blood cells to a chemical called tert-butyl hydroperoxide that caused oxidative stress. The cells were then marked with a fluorescent label and injected into mice. Using two different methods, the researchers observed the red blood cells getting stuck in the brain capillaries and then being cleared out in a process called endothelial erythrophagocytosis. As they moved out of the capillaries, microglia inflammatory cells engulfed the red blood cells, which led to the formation of a brain hemorrhage.
“It has always been assumed that in order for cerebral hemorrhage to occur, blood vessels need to be injured or disrupted. We found that increased red blood cell interactions with the brain capillaries represent an alternative source of development,” said co-corresponding author Xiangmin Xu, UCI professor of anatomy & neurobiology and director of the campus’s Center for Neural Circuit Mapping. “We need to examine in detail the regulation of brain capillary clearance and also analyze how that process may be related to insufficient blood supply and ischemic stroke, which is the most common form of stroke, to help advance the development of targeted treatments.”
Source: TS News
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