Brain–heart coupling in Parkinson’s disease: from autonomic dysfunction to network physiology
- 1Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy
Abstract
Cardiovascular autonomic dysfunction is a well-established feature of Parkinson’s disease (PD), yet the brain and cardiovascular system are still largely investigated as separate physiological domains. This separation may overlook an important dimension of PD pathophysiology: the dynamic communication between them. Here, we examine emerging evidence that brain–heart coupling itself is altered in PD. A focused PubMed search identified studies directly relating neural activity to cardiac dynamics, complemented by relevant physiological and autonomic literature. Despite a small and heterogeneous evidence base, electrophysiological, neuroimaging, and dynamic network studies suggest disrupted central–cardiac coordination. Alterations are detectable in early and de novo PD, relate to dysautonomia, and appear sensitive to dopaminergic state. Emerging evidence for impaired cardiac interoception further suggests that dysfunction may extend from descending autonomic control to ascending heart-to-brain processing. Importantly, cross-system measures can reveal abnormalities that remain not captured by neural or cardiovascular signals alone. Their clinical potential is promising but remains to be established through larger, standardized, and longitudinal studies. At present, brain–heart coupling is best viewed as a physiological framework with emerging translational relevance rather than as a validated biomarker. By revealing interactions that remain hidden when neural and cardiovascular systems are examined separately, brain–heart coupling may uncover a distinct dimension of PD pathophysiology and provide a bridge from integrative physiology to disease phenotyping and future clinical stratification.
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BibTeX
@article{pagliaro2026brainheart,
title = {{Brain–heart coupling in Parkinson’s disease: from autonomic dysfunction to network physiology}},
author = {Pasquale Pagliaro},
journal = {Frontiers in Physiology},
year = {2026},
month = oct,
doi = {10.3389/fphys.2026.1974885},
url = {https://doi.org/10.3389/fphys.2026.1974885},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Brain–heart coupling in Parkinson’s disease: from autonomic dysfunction to network physiology
AU - Pasquale Pagliaro
PY - 2026
DA - 2026/10/22
JO - Frontiers in Physiology
DO - 10.3389/fphys.2026.1974885
UR - https://doi.org/10.3389/fphys.2026.1974885
AB - Cardiovascular autonomic dysfunction is a well-established feature of Parkinson’s disease (PD), yet the brain and cardiovascular system are still largely investigated as separate physiological domains. This separation may overlook an important dimension of PD pathophysiology: the dynamic communication between them. Here, we examine emerging evidence that brain–heart coupling itself is altered in PD. A focused PubMed search identified studies directly relating neural activity to cardiac dynamics, complemented by relevant physiological and autonomic literature. Despite a small and heterogeneous evidence base, electrophysiological, neuroimaging, and dynamic network studies suggest disrupted central–cardiac coordination. Alterations are detectable in early and de novo PD, relate to dysautonomia, and appear sensitive to dopaminergic state. Emerging evidence for impaired cardiac interoception further suggests that dysfunction may extend from descending autonomic control to ascending heart-to-brain processing. Importantly, cross-system measures can reveal abnormalities that remain not captured by neural or cardiovascular signals alone. Their clinical potential is promising but remains to be established through larger, standardized, and longitudinal studies. At present, brain–heart coupling is best viewed as a physiological framework with emerging translational relevance rather than as a validated biomarker. By revealing interactions that remain hidden when neural and cardiovascular systems are examined separately, brain–heart coupling may uncover a distinct dimension of PD pathophysiology and provide a bridge from integrative physiology to disease phenotyping and future clinical stratification.
SN - 1664-042X
ER -