Abstract
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Highlights
● Ischemic and hemorrhagic stroke differ by the temporal dynamics of cell-free DNA (cfDNA) accumulation.
● In hemorrhagic stroke, an initial increase in cfDNA, most likely reflects an extent of the tissue damage
● In ischemic patients, the apoptotic cfDNA increase in parallel with the damage caused by hypoxia and subsequent compensatory reperfusion.
● An optimal assessment windows with maximum differentiating power for stroke outcomes is 24-48 hours post-event for ischemic stroke, and as close as possible to the moment of hospital admission for hemorrhagic stroke.
Plain Language Summary
Acute cerebrovascular accidents are a prominent cause of death worldwide and are the leading cause of long-term disability. Stroke is a phenotypically, various disease. The outcome of acute cerebrovascular accidents is largely determined by the timeliness and adequacy of treatment, which is fundamentally different in patients with ischemic and hemorrhagic stroke. Cell-free DNA is released from apoptotic and necrotic cells, and its fragments circulate in the blood until cleared by DNA hydrolyzing enzymes. In plasma, cell-free DNA is represented by fragments of various sizes, with the most common fragment length corresponding to the nucleosome's size and reflecting its apoptotic origin. LmwDNA samples were isolated from plasma and cerebrospinal fluid by phenol deproteinization; they were analyzed by gradient polyacrylamide electrophoresis and were quantified by spectrophotometry. Two common types of stroke, ischemic and hemorrhagic, differ by the temporal dynamics of cell-free DNA accumulation. In hemorrhagic stroke, an initial increase in lmwDNA levels most likely reflects an extent of the tissue damage. In contrast, in ischemic patients, the lmwDNA levels increase in parallel with the damage caused by hypoxia and subsequent compensatory reperfusion. These time-course data specify optimal assessment windows with maximum differentiating power for stroke outcomes: 24-48 hours post-event for ischemic stroke, and as close as possible to the moment of hospital admission for hemorrhagic stroke. These data also indicate the role of apoptosis in the formation of ischemic focus.