Exocrine Gland Dysfunction in Parkinson's Disease: Pathophysiology, Clinical Manifestations, and Therapeutic Perspectives-A Narrative Review.
Narrative review synthesizing evidence that exocrine gland dysfunction in Parkinson's disease reflects central and peripheral autonomic and glandular alpha-synuclein pathology, can precede motor symptoms, and surveys diagnostic methods and management approaches.
What the AI sees
Narrative review synthesizing evidence that exocrine gland dysfunction in Parkinson's disease reflects central and peripheral autonomic and glandular alpha-synuclein pathology, can precede motor symptoms, and surveys diagnostic methods and management approaches.
Research significance
Identifies accessible peripheral exocrine tissues as potential prodromal biomarkers and windows into autonomic alpha-synuclein pathology that could aid early diagnosis and patient stratification, offering translational value despite limited direct novel molecular targets for drug development.
Source abstract
BACKGROUND: Non-motor symptoms, especially autonomic dysfunction, are major contributors to disability and decreased quality of life in Parkinson's disease (PD). Despite being common and having a wide range of clinical facets, exocrine gland dysfunction is still not well recognized and managed. OBJECTIVE: The aim of this narrative review is to present a thorough and integrative synthesis of exocrine gland dysfunction in PD, including an overview of its underlying mechanisms, clinical manifestations, diagnostic techniques, and treatment approaches. METHODS: We critically reviewed the literature addressing autonomic regulation of exocrine glands, α-synuclein pathology in central and peripheral autonomic networks, and clinical studies of glandular dysfunction across salivary, lacrimal, sebaceous, nasal, sweat, gastric, and pancreatic systems in PD. RESULTS: Exocrine dysfunction in PD is multifaceted and potentially linked to degeneration within central autonomic control regions, peripheral autonomic nerves, and even glandular tissues themselves, often compounded by iatrogenic medication effects. Importantly, certain disturbances may precede motor features, underscoring their potential as prodromal markers. Clinically, such dysfunctions significantly impair different aspects of health and well-being overall. Multidisciplinary approach is needed for management, striking a balance between symptom relief and consideration of treatment-related tradeoffs. CONCLUSIONS: Exocrine gland dysfunction represents a prevalent, intricate, and clinically significant range of non-motor symptoms in PD, indicative of extensive autonomic involvement. Early detection may enhance quality of life and symptom management while also offering insights into disease mechanisms, the discovery of biomarkers and therapeutic interventions.