ArticleCNS neuroscience & therapeutics2026
Chronic Smoking Impairs Glymphatic Transport and Cognitive Function in Adolescent Mice Through Cardiac, Vascular, and Perivascular Aquaporin-4 Mechanisms.
Article in CNS neuroscience & therapeutics, 2026. 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
aimsSmoking significantly impairs cognitive function and is a major risk factor for dementia, particularly when initiated during adolescence, a critical period for brain development. The glymphatic system, which is thought to participate in metabolic waste clearance, has been implicated in maintaining cognitive health. This study investigates the effects of chronic smoking on glymphatic transport and its underlying mechanisms.
methodsGlymphatic transport was assessed using immunofluorescence and two-photon microscopy, while phosphorylated tau accumulation in the dentate gyrus (DG) was examined via immunohistochemical staining. Synaptogenesis and neurogenesis in the hippocampal DG were analyzed using synaptophysin, PSD-95, doublecortin, and standard histological techniques. Cognitive function was measured through the Morris water maze (MWM) test and novel object recognition (NOR) tests, with cardiac function assessed by echocardiography.
resultsThe findings indicate that chronic smoking leads to a duration-dependent disruption of glymphatic transport, resulting in the accumulation of phosphorylated tau in the hippocampal DG, reduced synaptogenesis and neurogenesis, and subsequent cognitive decline.
conclusionThis glymphatic dysfunction may be associated with impaired cardiac ejection, diminished arterial pulsatility, and loss of perivascular aquaporin-4 (AQP4), collectively contributing to smoking-related cognitive impairment.
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