ArticleAlzheimer's & dementia (New York, N. Y.)
What is new in delirium: A vascular etiology outlook.
Article in Alzheimer's & dementia (New York, N. Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Emerging studies have highlighted the vascular contributions to cognitive impairment and dementia (VCID), especially in the context of neurodegenerative disorders that cause cognitive decline (i.e., Alzheimer's disease and related dementias [ADRD]). More recent research on perioperative neurocognitive disorders, including postoperative delirium, is describing a potential role of neurovascular dysfunction in the pathogenesis of these common complications for many older adults. These findings support an expanded conceptual framework in which delirium is not simply a transient disorder of neuronal function but may represent an acute neurovascular phenotype that links systemic inflammation, blood-brain barrier injury, and VCID. Delirium is characterized by acute and fluctuating disturbances in attention, awareness, and cognition. It is a common, costly, neurologic complication in patients, especially critically ill patients, patients with chronic metabolic disorders, or older adults. In older adults, delirium is among the most consequential complications of hospitalization. A 2025 national cohort of > 5.5 million older adults undergoing major non-cardiac surgery found that postoperative delirium was associated with markedly higher odds of death or major complications, and 30-day mortality. These contemporary data reinforce a shift in framing: delirium should be treated as acute brain failure and as a quality target for perioperative and critical care systems, not merely as a temporary behavioral syndrome. In addition to the acute negative impacts, delirium significantly escalates the risk of persistent cognitive decline, presaging the potential onset of neurodegenerative disorders. Despite substantial research into delirium epidemiology, prevention, and control, its management is complicated by the elusive nature of its pathophysiological mechanisms. Here, we propose a vascular etiology outlook for delirium, with emphasis on the neurovascular unit as a key interface in determining the onset of this complication and potentially jump-starting permanent brain dysfunction and ADRD.
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