Examines theobromine's effects on dopaminergic neurons in Parkinson's disease, suggesting its potential as a neuroprotective agent.
The defining neuropathological features of Parkinson’s disease (PD) include the progressive loss of dopaminergic neurons in the substantia nigra, together with the intraneuronal accumulation of α-synuclein in the form of Lewy bodies. Theobromine has been shown to possess neuroprotective effects, preventing neuronal damage, enhancing motor memory and cognitive function in humans (Gao et al. 2022). Bhat et al. (2021) demonstrated the neuroprotective effects of theobromine in a rat model of transient global cerebral ischemia/reperfusion (tGCI/R). The study of Haj Ahmed et al. (2020) investigated the interaction between several methylxanthines and primary amine oxidase (PrAO)/ monoamine oxidase (MAO) in human subcutaneous adipose tissue (hScAT). Caffeine and theobromine produced a remarkable 50% inhibition of PrAO activity when incubated at 2.5 mM with hScAT. Due to its low side-effect profile and minimal toxicity at appropriate doses, theobromine and its derivatives are considered promising agents for the prevention of neurological disorders, offering potential applications in medicine.
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Kondeva-Burdina et al. (2026) studied this question.
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