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3 augustus 2026: Bron: Nature d.d. november 2025
Wanneer patiënten met de ziekte van Alzheimer - dementie gedurende korte sessies van 30 minuten per dag intermitterende hypercapnie – gecontroleerde blootstelling aan lage CO2-niveaus in aan-uit-cycli – krijgen toegediend via een zuurstofmasker dan blijkt het glymfatische systeem van de hersenen te worden geactiveerd.
Op die manier zorgen de CO2-pulsen ervoor dat bloedvaten in de hersenen verwijden en vernauwen, wat fungeert als een pomp die de vloeistofstroom door het hersenweefsel stimuleert. Daardoor worden giftige eiwitten zoals alfa-synucleïne, amyloïde bèta en gefosforyleerd tau die verband houden met de ziekte van Alzheimer - dementie en de ziekte van Parkinson afgevoerd. In feite worden de hersenen via deze korte pulsen van CO2 dus als het ware schoongemaakt.
Het glymfatische systeem functioneert als de afvoerroute voor afvalstoffen in de hersenen. Het is het meest actief tijdens de diepe slaap en is vaak verstoord bij neurodegeneratieve aandoeningen. Onderzoekers gebruikten maskers die afwisselend pulsen CO2-verrijkte lucht aan de deelnemers gaven. Ze observeerden een verbeterde verwijdering van gefosforyleerd tau uit de hersenen en verhoogde niveaus van amyloïde bèta in de bloedbaan, wat erop wijst dat de eiwitten werden afgevoerd. "Deze verwijding en vernauwing werkt in feite als een pomp die afvalstoffen uit de hersenen verwijdert", aldus prof. dr. Ryman, hoofd van het onderzoeksteam in de berichtgeving over de presentatie.
De studiepresentatie van afgelopen maand heb ik nog niet kunnen vinden maar wel de publicatie in Nature die gratis is in te zien of te downloaden. Ik vermoed dat het dezelfde studie is.
- Article
- Open access
- Published:
The influence of intermittent hypercapnia on cerebrospinal fluid flow and clearance in Parkinson’s disease and healthy older adults
npj Parkinson's Disease volume 11, Article number: 334 (2025)
Abstract
A failure of the glymphatic pathway to clear brain byproducts implicated in neurodegeneration may contribute to the pathophysiology of Parkinson’s disease. The glymphatic pathway relies on vasomotion (rhythmic constriction and dilation of blood vessels) to drive cerebrospinal fluid through the interstitial space and clear waste from the brain. The current study demonstrated that intermittent hypercapnia, exposure to low levels of CO2 in ON-OFF cycles, elicited vasomotion-induced cerebrospinal fluid inflow in both healthy controls and individuals with Parkinson’s disease. The magnitude of the vasomotion-induced cerebrospinal fluid inflow in patients with Parkinson’s disease was reduced relative to healthy controls. However, intermittent hypercapnia, administered in three 10-minute sessions totaling approximately 30 minutes, increased the appearance of total α-synuclein, neurofilament light, glial fibrillary acidic protein, amyloid β1-42, amyloid β1-40, and phosphorylated tau 217 in the plasma of both healthy controls and individuals with Parkinson’s disease. This suggests that intermittent hypercapnia can be used to clear potentially toxic brain byproducts from the brain, highlighting its potential use as a disease modifying treatment.
-
Coughlin, D. G., Hurtig, H. I. & Irwin, D. J. Pathological influences on clinical heterogeneity in Lewy body diseases. Mov. Disord. 35, 5–19 (2020).
-
Hirsch, E. C. & Hunot, S. Neuroinflammation in Parkinson’s disease: a target for neuroprotection?. Lancet Neurol. 8, 382–397 (2009).
-
Calabresi, P. et al. Alpha-synuclein in Parkinson’s disease and other synucleinopathies: from overt neurodegeneration back to early synaptic dysfunction. Cell Death Dis. 14, 176 (2023).
-
Massey, A. et al. Glymphatic System Dysfunction and Sleep Disturbance May contribute to the pathogenesis and progression of Parkinson’s Disease. Int. J. Mol. Sci. 23, 12928 (2022).
-
Sundaram, S. et al. Establishing a framework for neuropathological correlates and glymphatic system functioning in Parkinson’s disease. Neurosci. Biobehav. Rev. 103, 305–315 (2019).
-
Ryman, S. G. et al. Abnormal cerebrovascular activity, perfusion and glymphatic clearance in Lewy body diseases. Mov. Disord. 39, 1258–1268 (2024).
-
Iliff, J. J. et al. Cerebral arterial pulsation drives paravascular CSF–interstitial fluid exchange in the murine brain. J. Neurosci. 33, 18190–18199 (2013).
-
Goodman, J. R. & Iliff, J. J. Vasomotor influences on glymphatic-lymphatic coupling and solute trafficking in the central nervous system. J. Cereb. Blood Flow. Metab. 40, 1724–1734 (2020).
-
Cui, H. et al. Decreased AQP4 expression aggravates ɑ-synuclein pathology in Parkinson’s disease mice, possibly via impaired glymphatic clearance. J. Mol. Neurosci. 71, 1–14 (2021).
-
Zhang, Y. et al. Interaction between the glymphatic system and α-synuclein in Parkinson’s disease. Mol. Neurobiol. 60, 2209–2222 (2023).
-
Shen, T. et al. The role of brain perivascular space burden in early-stage Parkinson’s disease. NPJ Parkinson’s Dis. 7, 12 (2021).
-
He, P. et al. The Association of the glymphatic function with Parkinson’s disease symptoms: neuroimaging evidence from longitudinal and cross-sectional studies. Ann. Neurol. 94, 672–683 (2023).
-
Lee, D. A., Lee, H. & Park, K. M. Glymphatic dysfunction in isolated REM sleep behavior disorder. Acta Neurol. Scand. 145, 464–470 (2022).
-
Bae, Y. J. et al. Altered brain glymphatic flow at diffusion-tensor MRI in rapid eye movement sleep behavior disorder. Radiology 307, e221848 (2023).
-
Park, Y. W. et al. Magnetic resonance imaging–visible perivascular spaces in basal ganglia predict cognitive decline in Parkinson’s disease. Mov. Disord. 34, 1672–1679 (2019).
-
Wood, K. H. et al. Diffusion tensor imaging-along the perivascular-space index is associated with disease progression in Parkinson’s disease. Mov. Disord. 39, 1504–1513 (2024).
-
Lin, C.-H. et al. Blood NfL: a biomarker for disease severity and progression in Parkinson disease. Neurology 93, e1104–e1111 (2019).
-
Aamodt, W. W. et al. Neurofilament light chain as a biomarker for cognitive decline in Parkinson disease. Mov. Disord. 36, 2945–2950 (2021).
-
Pilotto, A. et al. Plasma NfL, GFAP, amyloid, and p-tau species as Prognostic biomarkers in Parkinson’s disease. J. Neurol. 271, 7537–7546 (2024).
-
Batzu, L. et al. Plasma p-tau181, neurofilament light chain and association with cognition in Parkinson’s disease. npj Parkinson’s Dis. 8, 154 (2022).
-
Chen, N.-C. et al. Plasma Levels of α-Synuclein, Aβ-40 and T-tau as Biomarkers to Predict Cognitive Impairment in Parkinson’s Disease. Front. Aging Neurosci. 12, 112 (2020).
-
Benveniste, H. et al. The glymphatic system and waste clearance with brain aging: a review. Gerontology 65, 106–119 (2019).
-
van Veluw, S. J. et al. Vasomotion as a driving force for paravascular clearance in the awake mouse brain. Neuron 105, 549–561 (2020).
-
Hauglund, N. L. et al. Norepinephrine-mediated slow vasomotion drives glymphatic clearance during sleep. Cell 188, 606–622 (2025).
-
Mestre, H. et al. Flow of cerebrospinal fluid is driven by arterial pulsations and is reduced in hypertension. Nat. Commun. 9, 4878 (2018).
-
Helakari, H. et al. Human NREM sleep promotes brain-wide vasomotor and respiratory pulsations. J. Neurosci. 42, 2503–2515 (2022).
-
Murdock, M. H. et al. Multisensory gamma stimulation promotes glymphatic clearance of amyloid. Nature 627, 149–156 (2024).
-
Holstein-Rønsbo, S. et al. Glymphatic influx and clearance are accelerated by neurovascular coupling. Nat. Neurosci. 1, 12 (2023).
-
Ryman, S. G. et al. Reduced and Delayed Cerebrovascular Reactivity in Patients with Parkinson’s Disease. Mov. Disord. 38, 1260–1272 (2023).
-
van der Horn, H. J. et al. Parkinson’s disease cerebrovascular reactivity pattern: a feasibility study. J. Cerebral Blood Flow Metab. 44, 1774–1786 (2024).
-
Fultz, N. E. et al. Coupled electrophysiological, hemodynamic, and cerebrospinal fluid oscillations in human sleep. Science 366, 628–631 (2019).
-
Yang, H.-C. et al. Coupling between cerebrovascular oscillations and CSF flow fluctuations during wakefulness: an fMRI study. J. Cereb. Blood Flow. Metab. 42, 1091–1103 (2022).
-
Nair, V. V. et al. Neurofluid coupling during sleep and wake states. Sleep. Med. 110, 44–53 (2023).
-
Han, F. et al. Decoupling of global brain activity and cerebrospinal fluid flow in Parkinson’s disease cognitive decline. Mov. Disord. 36, 2066–2076 (2021).
-
Wang, Z. et al. Reduced coupling of global brain function and cerebrospinal fluid dynamics in Parkinson’s disease. J. Cereb. Blood Flow Metab. 43, 1328–1339 (2023).
-
Wang, Y. et al. Cerebrovascular activity is a major factor in the cerebrospinal fluid flow dynamics. Neuroimage 258, 119362 (2022).
-
van der Voort, E. C et al. CO2 as an engine for neurofluid flow: Exploring the coupling between vascular reactivity, brain clearance, and changes in tissue properties. NMR Biomed. 37, e5126 (2024).
-
Carr, J. M., Caldwell, H. G. & Ainslie, P. N. Cerebral blood flow, cerebrovascular reactivity and their influence on ventilatory sensitivity. Exp. Physiol. 106, 1425–1448 (2021).
-
Hoiland, R. L., Fisher, J. A. & Ainslie, P. N. Regulation of the cerebral circulation by arterial carbon dioxide. Compr. Physiol. 9, 1101–1154 (2019).
-
van Der Voort, E. C. et al. CO2 as an engine for neurofluid flow: Exploring the coupling between vascular reactivity, brain clearance, and changes in tissue properties. NMR Biomed. 37, e5126 (2024).
-
Della Monica, C. et al. P-tau217 and other blood biomarkers of dementia: variation with time of day. Transl. Psychiatry 14, 373 (2024).
-
Iliff, J. J. et al. The glymphatic system clears amyloid beta and tau from brain to plasma in humans. medRxiv 2024–07 (2024).
-
Eide, P. K. et al. Plasma neurodegeneration biomarker concentrations associate with glymphatic and meningeal lymphatic measures in neurological disorders. Nat. Commun. 14, 2084 (2023).
-
Zheng, X., Yang, J., Hou, Y., Shi, X. & Liu, K. Prediction of clinical progression in nervous system diseases: plasma glial fibrillary acidic protein (GFAP). Eur. J. Med. Res. 29, 51 (2024).
-
Gafson, A. R. et al. Neurofilaments: neurobiological foundations for biomarker applications. Brain 143, 1975–1998 (2020).
-
Bates, D., Mächler, M., Bolker, B. & Walker, S. Fitting linear mixed-effects models using lme4. J. Stat. Softw. 67, 1–48 (2015).
-
Bhavani-Shankar, K., Moseley, H., Kumar, A. & Delph, Y. Capnometry and anaesthesia. Can. J. Anaesth. 39, 617–632 (1992).
-
Buongiorno, M. et al. Altered sleep and neurovascular dysfunction in alpha-synucleinopathies: the perfect storm for glymphatic failure. Front. Aging Neurosci. 15, 1251755 (2023).
-
Koep, J. L. et al. Autonomic control of cerebral blood flow: fundamental comparisons between peripheral and cerebrovascular circulations in humans. J. Physiol. 600, 15–39 (2022).
-
Lohela, T. J., Lilius, T. O. & Nedergaard, M. The glymphatic system: implications for drugs for central nervous system diseases. Nat. Rev. Drug Discov. 21, 763–779 (2022).
-
Lee, H. et al. The effect of body posture on brain glymphatic transport. J. Neurosci. 35, 11034–11044 (2015).
-
von Holstein-Rathlou, S., Petersen, N. C. & Nedergaard, M. Voluntary running enhances glymphatic influx in awake behaving, young mice. Neurosci. Lett. 662, 253–258 (2018).
-
He, X. et al. Voluntary exercise promotes glymphatic clearance of amyloid beta and reduces the activation of astrocytes and microglia in aged mice. Front. Mol. Neurosci. 10, 144 (2017).
-
Liu, X. et al. Polyunsaturated fatty acid supplement alleviates depression-incident cognitive dysfunction by protecting the cerebrovascular and glymphatic systems. Brain, Behav. Immun. 89, 357–370 (2020).
-
Ren, H. et al. Omega-3 polyunsaturated fatty acids promote amyloid-β clearance from the brain through mediating the function of the glymphatic system. FASEB J. 31, 282–293 (2017).
-
van Hattem, T. et al. Targeting sleep physiology to modulate glymphatic brain clearance. Physiology 40, 271–290 (2025).
-
Xie, L. et al. Sleep drives metabolite clearance from the adult brain. science 342, 373–377 (2013).
-
Hablitz, L. M. et al. Increased glymphatic influx is correlated with high EEG delta power and low heart rate in mice under anesthesia. Sci. Adv. 5, eaav5447 (2019).
-
Osorio-Forero, A. et al. Noradrenergic circuit control of non-REM sleep substates. Curr. Biol. 31, 5009–5023 (2021).
-
Antila, H. et al. A noradrenergic-hypothalamic neural substrate for stress-induced sleep disturbances. Proc. Natl. Acad. Sci. USA 119, e2123528119 (2022).
-
Ringstad, G. et al. Brain-wide glymphatic enhancement and clearance in humans assessed with MRI. JCI insight 3, e121537 (2018).
-
Eide, P. K. et al. Clinical application of intrathecal gadobutrol for assessment of cerebrospinal fluid tracer clearance to blood. JCI insight 6, e147063 (2021).
-
Louveau, A. et al. Understanding the functions and relationships of the glymphatic system and meningeal lymphatics. J. Clin. Investig. 127, 3210–3219 (2017).
-
Rasmussen, M. K., Mestre, H. & Nedergaard, M. Fluid transport in the brain. Physiol. Rev. 102, 1025–1151 (2022).
-
Proulx, S. T. Cerebrospinal fluid outflow: a review of the historical and contemporary evidence for arachnoid villi, perineural routes, and dural lymphatics. Cell. Mol. Life Sci. 78, 2429–2457 (2021).
-
van Osch, M. J. et al. Human brain clearance imaging: pathways taken by magnetic resonance imaging contrast agents after administration in cerebrospinal fluid and blood. NMR Biomed. 37, e5159 (2024).
-
Lau, K., Kotzur, R. & Richter, F. Blood–brain barrier alterations and their impact on Parkinson’s disease pathogenesis and therapy. Transl. Neurodegener. 13, 37 (2024).
-
Al-Bachari, S., Naish, J. H., Parker, G. J., Emsley, H. & Parkes, L. M. Blood-brain barrier leakage is increased in Parkinson’s disease. Front. Physiol. 11, 593026 (2020).
-
Liu, X. et al. Hypercapnia exacerbates the blood–brain barrier disruption via promoting HIF-1a nuclear translocation in the astrocytes of the hippocampus: implication in further cognitive impairment in hypoxemic adult rats. Neurochem. Res. 45, 1674–1689 (2020).
-
Zou, W. et al. Blocking meningeal lymphatic drainage aggravates Parkinson’s disease-like pathology in mice overexpressing mutated α-synuclein. Transl. Neurodegener. 8, 1–17 (2019).
-
Lee, H.-J., Bae, E.-J. & Lee, S.-J. Extracellular α-synuclein—a novel and crucial factor in Lewy body diseases. Nat. Rev. Neurol. 10, 92–98 (2014).
-
Abeliovich, A. & Gitler, A. D. Defects in trafficking bridge Parkinson’s disease pathology and genetics. Nature 539, 207–216 (2016).
-
Coppens, S., Lehmann, S., Hopley, C. & Hirtz, C. Neurofilament-light, a promising biomarker: analytical, metrological and clinical challenges. Int. J. Mol. Sci. 24, 11624 (2023).
-
Yang, Z. & Wang, K. K. Glial fibrillary acidic protein: from intermediate filament assembly and gliosis to neurobiomarker. Trends Neurosci. 38, 364–374 (2015).
-
Ryman, S. G. et al. Cognition at each stage of lewy body disease with co-occurring Alzheimer’s disease pathology. J. Alzheimer’s Dis. 1, 14 (2021).
-
Irwin, D. J. et al. Neuropathological and genetic correlates of survival and dementia onset in synucleinopathies: a retrospective analysis. Lancet Neurol. 16, 55–65 (2017).
-
Jellinger, K. A., Seppi, K., Wenning, G. K. & Poewe, W. Impact of coexistent Alzheimer pathology on the natural history of Parkinson’s disease. J. Neural Transm. 109, 329–339 (2002).
-
Verbree, J. et al. Assessment of middle cerebral artery diameter during hypocapnia and hypercapnia in humans using ultra-high-field MRI. J. Appl. Physiol. 117, 1084–1089 (2014).
-
Slessarev, M. et al. Prospective targeting and control of end-tidal CO2 and O2 concentrations. J. Physiol. 581, 1207–1219 (2007).
-
Fisher, J. A. The CO2 stimulus for cerebrovascular reactivity: fixing inspired concentrations vs. targeting end-tidal partial pressures. J. Cereb. Blood Flow. Metab. 36, 1004–1011 (2016).
-
Liu, P., Jill, B. & Lu, H. Cerebrovascular reactivity (CVR) MRI with CO2 challenge: a technical review. Neuroimage 187, 104–115 (2019).
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