Luteolin and neurodegenerative disease modulation: linking molecular mechanisms, neurotransmission, and pharmacokinetics.
TL;DR
This review presents an integrated summary of how luteolin orchestrates interconnected signaling networks, with receptor-level neuromodulation and neuroimmune regulation to preserve neuronal integrity in Alzheimer's disease, Parkinson's disease, and related disorders.
Abstract
Neurodegenerative disorders arise from the convergence of oxidative stress, neuroinflammation, synaptic dysfunction, mitochondrial failure, and dysregulated cell death, highlighting the need for therapeutic agents capable of coordinated, multi-target modulation. Luteolin (3',4',5,7-tetrahydroxyflavone), a dietary flavonoid widely present in edible and medicinal plants, has emerged as a promising neuroactive compound with pleiotropic biological actions. Rather than focusing on isolated outcomes, this review presents an integrated summary of how luteolin orchestrates interconnected signaling networks, with receptor-level neuromodulation and neuroimmune regulation to preserve neuronal integrity. Particular emphasis is placed on pathway convergence, cross-talk, and system-level neuroprotection across models of Alzheimer's disease, Parkinson's disease, and related disorders. In parallel, pharmacokinetic behavior, metabolite activity, and emerging delivery strategies are examined in relation to mechanistic efficacy. By linking molecular signaling, neurotransmission and therapeutic feasibility within a unified framework, this review offers a refined perspective on role of luteolin in neurodegenerative disease modulation.