From unmet need to biological hypothesis
Motor symptoms of Parkinson’s disease arise primarily from dopamine loss within the basal ganglia. However, many disabling symptoms — including sleep disruption, fatigue, mood changes, and cognitive impairment — are linked to dysfunction in broader neural networks.
Celeste is designed to engage retinal signaling pathways that influence circadian and distributed neural systems implicated in these symptoms.
Targeting the biology that underlies
non-motor disability
Celeste is designed to modulate intrinsic light-sensitive signaling pathways linked to circadian and neural network regulation.
The underlying hypothesis is that distributed network dysfunction—rather than dopamine deficiency alone—drives many non-motor symptoms that persist despite best-available motor therapy.
Retinal Entry Point
Intrinsically photosensitive retinal ganglion cells (ipRGCs) provide a non-invasive access point to neural networks governing circadian rhythm, mood, and cognition.
Optical Wavelength Delivery
Celeste delivers precisely characterized optical parameters designed to engage the retinohypothalamic pathway and influence downstream neural network activity.
Network Modulation
The therapeutic objective is to produce measurable effects in circadian and related neural systems—domains where dopaminergic therapies have limited impact.
THE GAP
Why motor therapies don’t reach non-motor symptoms
Dopamine replacement targets basal ganglia circuitry. Non-motor symptoms arise from broader network dysfunction—circadian, limbic, and cortical systems requiring a fundamentally different approach.
THE APPROACH
Light as a therapeutic signaling modality
Celeste engages the retinohypothalamic pathway through controlled optical delivery designed to influence circadian and limbic signaling networks.
PLATFORM POTENTIAL
Beyond Parkinson’s disease
The neural network hypothesis may extend to other neurodegenerative conditions characterized by circadian and network dysfunction.
Retinal Signaling as a Therapeutic Entry Point
Intrinsically photosensitive retinal ganglion cells (ipRGCs) provide a direct biological link between light exposure and central neural networks regulating circadian rhythm, sleep, mood, and cognition.
Celeste is designed to engage this pathway using precisely characterized optical parameters delivered through a non-invasive device
01
Sleep Disruption
Circadian rhythm disturbance is common in Parkinson’s disease and contributes significantly to non-motor symptom burden. Many patients experience fragmented sleep, altered sleep–wake timing, and reduced sleep efficiency. These disruptions affect daytime functioning and may exacerbate fatigue, mood instability, and fluctuations in overall neurologic performance.
02
Daytime Fatigue
Dopaminergic medications, while essential for motor management, may further alter daily rhythm patterns, contributing to irregular physiologic signaling across the 24-hour cycle.
03
Mood & Cognitive Effects
Circadian signaling pathways regulate neural networks involved in mood, cognition, and emotional stability. When these rhythms are disrupted, patients may experience depression, reduced mental clarity, and impaired cognitive performance. Targeting retinal signaling pathways offers a differentiated strategy aimed at restoring healthier neural timing.
Celeste: A Targeted Photo-Neuromodulation Platform
Celeste is a non-invasive, home-use therapeutic device designed to deliver controlled optical stimulation to retinal pathways linked to circadian and neural network regulation.
The platform is intended to influence distributed neural systems involved in non-motor symptoms of Parkinson’s disease.
Scientific Foundation
The scientific basis for Celeste draws from decades of research on circadian biology, retinal signaling, and neural network regulation. Intrinsically photosensitive retinal ganglion cells (ipRGCs) are known to influence central pathways governing sleep, mood, cognition, and autonomic regulation.
Celeste applies these insights through a targeted photo-neuromodulation approach designed for therapeutic investigation.
Celeste is being evaluated in a fully enrolled Phase 3 pivotal trial designed to assess its potential to improve symptoms associated with non-motor dysfunction in Parkinson’s disease.
Selected Scientific Articles
Circadian rhythms are the daily activity and sleep patterns regulated by the suprachiasmatic nucleus, and they have a profound effect on daily physiological function. These rhythms are reset daily in response to light.
Circadian system responds to specific wavelengths of light. Light at low intensities stimulate rods and cones, which activate melanopsin signaling, however sustained non-visual signaling occurs via 480nm excitement of the melanopsin photoreceptors, at higher irradiance than rods and cones.
Circadian rhythms are blunted in Parkinson’s and do not respond to normal light signals. Melanopsin cells are damaged in neurodegenerative diseases, resulting in blunted circadian profiles.
- La Morgia, C., et al. (2017). Retinal Ganglion Cells and Circadian Rhythms in Alzheimer’s Disease, Parkinson’s Disease, and Beyond. Frontiers in Neurology, 8, 162. Lax, P., Ortuño-Lizarán, I., Maneu, V., Vidal-Sanz, M., & Cuenca, N. (2019).
- Photosensitive melanopsin-containing retinal ganglion cells in health and disease: Implications for circadian rhythms. International journal of molecular sciences, 20(13), 3164.
- Evans JA, Davidson AJ. Health consequences of circadian disruption in humans and animal models. Prog Mol Biol Transl Sci. 2013;119:283-323. doi: 10.1016/B978-0-12-396971-2.00010-5. PMID: 23899601.
Additional evidence of damaged melanopsin signaling. Melanopsin signaling also controls the sustained pupillary light reflex which is damaged in neurodegeneration.
- Joyce, D. S., et al. (2018). Melanopsin-mediated pupil function is impaired in Parkinson’s disease. Scientific Reports, 8(1), 1–9.
- Chougule, P. S., Najjar, R. P., Finkelstein, M. T., Kandiah, N., & Milea, D. (2019). Light-induced pupillary responses in Alzheimer’s disease. Frontiers in neurology, 10, 360.