Cognitive Impairment in Asthma: Emerging Evidence, Clinical Consequences, and Future Directions
- 1Department of Respiratory Therapy, College of Applied Medical Sciences, King Faisal University, Al-Ahsa 31982, Saudi Arabia
Abstract
Asthma is increasingly recognised as a systemic inflammatory disease with effects extending beyond the respiratory system. Emerging evidence suggests that cognitive impairment may represent an under-recognised extrapulmonary manifestation with important implications for disease management and long-term neurological health. This narrative review critically synthesises current evidence regarding the epidemiology, clinical consequences, and potential mechanisms linking asthma with cognitive dysfunction. Observational and longitudinal studies indicate that asthma is associated with an increased risk of cognitive impairment, cognitive decline, and dementia. However, substantial heterogeneity in study design, cognitive assessment, asthma phenotyping, and adjustment for confounding factors limits causal inference. Cognitive deficits predominantly involve attention, executive function, memory, and, less consistently, processing speed, potentially compromising medication adherence, inhaler technique, symptom perception, and self-management. Current evidence supports a multifactorial pathophysiological model in which chronic systemic inflammation, oxidative stress, intermittent hypoxaemia, sleep disturbance, corticosteroid exposure, and psychological comorbidity interact to promote endothelial dysfunction, blood–brain barrier disruption, microglial activation, neuroinflammation, mitochondrial dysfunction, and impaired synaptic plasticity. These mechanisms may be particularly relevant in children with early-onset asthma, older adults, and patients with severe or poorly controlled disease, although direct mechanistic evidence remains limited. Future research should prioritise well-phenotyped longitudinal cohorts that integrate comprehensive cognitive assessment with neuroimaging, inflammatory biomarkers, and objective measures of disease control to establish temporal relationships, identify high-risk populations, and determine whether cognitive dysfunction is a modifiable component of asthma burden. Recognition of cognition as a clinically relevant outcome may ultimately improve risk stratification and support more personalised, holistic approaches to asthma care.
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BibTeX
@article{mengash2026cognitive,
title = {{Cognitive Impairment in Asthma: Emerging Evidence, Clinical Consequences, and Future Directions}},
author = {Aminah Mengash and Rayan A. Siraj},
journal = {Journal of Clinical Medicine},
year = {2026},
month = oct,
doi = {10.3390/jcm15197761},
url = {https://www.mdpi.com/2077-0383/15/19/7761},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Cognitive Impairment in Asthma: Emerging Evidence, Clinical Consequences, and Future Directions
AU - Aminah Mengash
AU - Rayan A. Siraj
PY - 2026
DA - 2026/10/08
JO - Journal of Clinical Medicine
DO - 10.3390/jcm15197761
UR - https://www.mdpi.com/2077-0383/15/19/7761
AB - Asthma is increasingly recognised as a systemic inflammatory disease with effects extending beyond the respiratory system. Emerging evidence suggests that cognitive impairment may represent an under-recognised extrapulmonary manifestation with important implications for disease management and long-term neurological health. This narrative review critically synthesises current evidence regarding the epidemiology, clinical consequences, and potential mechanisms linking asthma with cognitive dysfunction. Observational and longitudinal studies indicate that asthma is associated with an increased risk of cognitive impairment, cognitive decline, and dementia. However, substantial heterogeneity in study design, cognitive assessment, asthma phenotyping, and adjustment for confounding factors limits causal inference. Cognitive deficits predominantly involve attention, executive function, memory, and, less consistently, processing speed, potentially compromising medication adherence, inhaler technique, symptom perception, and self-management. Current evidence supports a multifactorial pathophysiological model in which chronic systemic inflammation, oxidative stress, intermittent hypoxaemia, sleep disturbance, corticosteroid exposure, and psychological comorbidity interact to promote endothelial dysfunction, blood–brain barrier disruption, microglial activation, neuroinflammation, mitochondrial dysfunction, and impaired synaptic plasticity. These mechanisms may be particularly relevant in children with early-onset asthma, older adults, and patients with severe or poorly controlled disease, although direct mechanistic evidence remains limited. Future research should prioritise well-phenotyped longitudinal cohorts that integrate comprehensive cognitive assessment with neuroimaging, inflammatory biomarkers, and objective measures of disease control to establish temporal relationships, identify high-risk populations, and determine whether cognitive dysfunction is a modifiable component of asthma burden. Recognition of cognition as a clinically relevant outcome may ultimately improve risk stratification and support more personalised, holistic approaches to asthma care.
SN - 2077-0383
ER -