Components that comprise our brain parenchymal and cerebrovascular structures provide
a homeostatic environment for proper neuronal function to ensure normal cognition.
Cerebral insults (e.g. ischaemia, microbleeds and infection) alter cellular structures
and physiologic processes within the neurovascular unit and contribute to cognitive
dysfunction. COVID-19 has posed significant complications during acute and convalescent
stages in multiple organ systems, including the brain. Cognitive impairment is a prevalent
complication in COVID-19 patients, irrespective of severity of acute SARS-CoV-2 infection.
Moreover, overwhelming evidence from in vitro, preclinical and clinical studies has
reported SARS-CoV-2-induced pathologies in components of the neurovascular unit that
are associated with cognitive impairment. Neurovascular unit disruption alters the
neurovascular coupling response, a critical mechanism that regulates cerebromicrovascular
blood flow to meet the energetic demands of locally active neurons. Normal cognitive
processing is achieved through the neurovascular coupling response and involves the
coordinated action of brain parenchymal cells (i.e. neurons and glia) and cerebrovascular
cell types (i.e. endothelia, smooth muscle cells and pericytes). However, current
work on COVID-19-induced cognitive impairment has yet to investigate disruption of
neurovascular coupling as a causal factor. Hence, in this review, we aim to describe
SARS-CoV-2's effects on the neurovascular unit and how they can impact neurovascular
coupling and contribute to cognitive decline in acute and convalescent stages of the
disease. Additionally, we explore potential therapeutic interventions to mitigate
COVID-19-induced cognitive impairment. Given the great impact of cognitive impairment
associated with COVID-19 on both individuals and public health, the necessity for
a coordinated effort from fundamental scientific research to clinical application
becomes imperative. This integrated endeavour is crucial for mitigating the cognitive
deficits induced by COVID-19 and its subsequent burden in this especially vulnerable
population.
