Conclusions

AD and PD exemplify the urgent translational challenge of neurodegeneration: despite decades of mechanistic insight, therapeutic progress has largely stalled at symptomatic management. The convergence of protein aggregation, mitochondrial failure, oxidative stress, disrupted proteostasis, and circadian misalignment underscores the need for fundamentally new strategies that move beyond conventional pharmacology and invasive neuromodulation.

Magneto-proteins introduce a conceptual shift in how neuronal processes may be interrogated and controlled. By endowing biologically active proteins with magnetic field sensitivity, these systems enable remote, non-invasive, and spatiotemporally precise modulation of intracellular signalling networks. Among them, CRY-based magnetoreceptors-and particularly the CRY/MagR complex-stand out as uniquely positioned at the intersection of magnetic sensing, redox biology, and circadian regulation. This multifunctional integration directly overlaps with molecular pathways that define vulnerability in both AD and PD.

Evidence from experimental models indicates that CRY/MagR-mediated mechanisms can influence mitochondrial bioenergetics, ROS production, protein aggregation dynamics, autophagic flux, and circadian control of neuronal metabolism. In dopaminergic and cortical neurons, where energetic demand and oxidative burden are intrinsically high, even modest modulation of these pathways may exert outsized effects on disease trajectories. Although definitive validation in human systems is still lacking, the coherence between magnetoreceptor biology and neurodegenerative pathophysiology is difficult to ignore.

Moving forward, the field must prioritize rigorous mechanistic validation in mammalian models, quantitative assessment of magnetic field-protein interactions, and integration with gene delivery and precision neuromodulation technologies. If successfully translated, magneto-proteins could redefine non-invasive neuromodulation, not merely as a tool for symptom control, but as a platform for targeting core disease mechanisms in neurodegenerative disorders. Such a paradigm shift has the potential to reshape both our understanding and treatment of disorders that remain among the most intractable challenges in modern neuroscience.