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Cerebrovascular dysfunction is a pathological state characterized by the structural and functional impairment of the brain's vasculature, including the blood-brain barrier (BBB) and the neurovascular unit (NVU). It involves a breakdown in the mechanisms that regulate cerebral blood flow, such as neurovascular coupling and autoregulation, leading to chronic hypoperfusion and metabolic distress in neural tissues [1, 2]. This condition is a critical driver in the pathogenesis of stroke, Alzheimer's disease, and vascular cognitive impairment, where microvascular leaks and reduced vessel reactivity contribute to neurodegeneration [3]. While not a single molecular target, it represents a complex physiological process addressed by various pharmacological agents aimed at stabilizing endothelial function and maintaining perfusion [4]. Current therapeutic approaches focus on managing underlying risk factors like hypertension and dyslipidemia to mitigate further vascular damage [5].
Therapeutic interventions typically involve calcium channel blockade to prevent vasospasm, HMG-CoA reductase inhibition for endothelial stabilization, or ACE inhibition to manage perfusion pressure and reduce vascular inflammation [4, 5].
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