Impaired wound healing in Parkinson's disease: a hypothesis on altered epidermal growth factor (EGF) and N-methyl-D-aspartate (NMDA) signaling in keratinocytes.

Abstract

Parkinson's Disease (PD) is a neurodegenerative disorder characterized by the depletion of dopaminergic neurons in the substantia nigra, leading to hallmark motor symptoms such as bradykinesia, tremor, and rigidity. While the focus of PD has been on motor changes, dermatological changes are also commonly seen and may even precede the neurological symptoms. Individuals with PD may exhibit impaired wound healing, potentially due to dysregulated mechanisms involving epidermal growth factor (EGF) and N-methyl-D-aspartate (NMDA) in keratinocytes. This paper hypothesizes that the potential for impaired wound healing in PD patients is linked to reduced EGFR activity and altered NMDAR subunit expression in keratinocytes, in contrast to the upregulated wound healing seen in conditions like psoriasis, which demonstrates elevated EGFR and changes in NMDAR subunit activity. Furthermore, a potential co-interaction between EGF and NMDA in keratinocytes may further contribute to impaired wound healing. Investigating these signaling mechanisms can improve understanding and management of associated dermatological symptoms. We propose additional studies to quantify differences in rates of wound healing between PD patients and age-matched controls in effort to explore therapeutic targets for enhancing wounding healing in the context of PD.