Obstructive sleep apnea may induce orexinergic system and cerebral β-amyloid metabolism dysregulation

is it a further proof for Alzheimer's disease risk?

Claudio Liguori, Nicola Biagio Mercuri, Marzia Nuccetelli, Francesca Izzi, Alberto Cordella, Sergio Bernardini, Fabio Placidi

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: Obstructive Sleep Apnea (OSA)is associated with pathological changes of cerebral β-amyloid dynamics. Orexin has been demonstrated interfering with β-amyloid metabolism in Alzheimer's Disease (AD)pathology. The present study investigated cerebrospinal-fluid (CSF)β-amyloid 40 (Aβ 40 ), β-amyloid 42 (Aβ 42 )and orexin levels in OSA patients compared to AD patients and controls. Methods: OSA and AD patients were included in this study and compared to a group of controls. Patients and controls underwent lumbar puncture for the assessment of CSF Aβ 40 , Aβ 42 , tau proteins, orexin levels, and polysomnography to measure nocturnal sleep architecture. Results: 20 OSA patients, 20 AD patients, and 15 controls were included in our study. OSA patients showed higher CSF orexin levels than AD patients and controls, and AD patients showed higher CSF orexin levels than controls. Moreover, CSF Aβ 40 and Aβ 42 were lower in OSA patients than controls, but higher in OSA patients compared to AD patients. However, AD patients showed lower CSF Aβ 42 levels but comparable CSF Aβ 40 levels than controls. Sleep macrostructure was similarly altered in OSA and AD patients compared to controls. Finally, the apnea-hypopnea index (AHI)was related to the ratio Aβ 42 /Aβ 40 and CSF orexin levels in OSA patients. Conclusion: This study proved the alteration of CSF orexin levels and β-amyloid isoforms 40 and 42 in OSA patients. We suppose that sleep disruption and intermittent hypoxia, the two core features of OSA, may induce orexinergic system and cerebral β-amyloid metabolism dysregulation. This evidence further supports the current hypothesis that OSA may possibly start AD neuropathological processes.

Original languageEnglish
Pages (from-to)171-176
Number of pages6
JournalSleep Medicine
Volume56
DOIs
Publication statusPublished - Apr 1 2019

Fingerprint

Obstructive Sleep Apnea
Amyloid
Alzheimer Disease
Cerebrospinal Fluid
Sleep
tau Proteins
Spinal Puncture
Polysomnography
Apnea

Keywords

  • Alzheimer's disease
  • Obstructive sleep apnea
  • Orexin
  • Sleep
  • β-Amyloid

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Obstructive sleep apnea may induce orexinergic system and cerebral β-amyloid metabolism dysregulation : is it a further proof for Alzheimer's disease risk? / Liguori, Claudio; Mercuri, Nicola Biagio; Nuccetelli, Marzia; Izzi, Francesca; Cordella, Alberto; Bernardini, Sergio; Placidi, Fabio.

In: Sleep Medicine, Vol. 56, 01.04.2019, p. 171-176.

Research output: Contribution to journalArticle

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abstract = "Background: Obstructive Sleep Apnea (OSA)is associated with pathological changes of cerebral β-amyloid dynamics. Orexin has been demonstrated interfering with β-amyloid metabolism in Alzheimer's Disease (AD)pathology. The present study investigated cerebrospinal-fluid (CSF)β-amyloid 40 (Aβ 40 ), β-amyloid 42 (Aβ 42 )and orexin levels in OSA patients compared to AD patients and controls. Methods: OSA and AD patients were included in this study and compared to a group of controls. Patients and controls underwent lumbar puncture for the assessment of CSF Aβ 40 , Aβ 42 , tau proteins, orexin levels, and polysomnography to measure nocturnal sleep architecture. Results: 20 OSA patients, 20 AD patients, and 15 controls were included in our study. OSA patients showed higher CSF orexin levels than AD patients and controls, and AD patients showed higher CSF orexin levels than controls. Moreover, CSF Aβ 40 and Aβ 42 were lower in OSA patients than controls, but higher in OSA patients compared to AD patients. However, AD patients showed lower CSF Aβ 42 levels but comparable CSF Aβ 40 levels than controls. Sleep macrostructure was similarly altered in OSA and AD patients compared to controls. Finally, the apnea-hypopnea index (AHI)was related to the ratio Aβ 42 /Aβ 40 and CSF orexin levels in OSA patients. Conclusion: This study proved the alteration of CSF orexin levels and β-amyloid isoforms 40 and 42 in OSA patients. We suppose that sleep disruption and intermittent hypoxia, the two core features of OSA, may induce orexinergic system and cerebral β-amyloid metabolism dysregulation. This evidence further supports the current hypothesis that OSA may possibly start AD neuropathological processes.",
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T2 - is it a further proof for Alzheimer's disease risk?

AU - Liguori, Claudio

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AU - Nuccetelli, Marzia

AU - Izzi, Francesca

AU - Cordella, Alberto

AU - Bernardini, Sergio

AU - Placidi, Fabio

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N2 - Background: Obstructive Sleep Apnea (OSA)is associated with pathological changes of cerebral β-amyloid dynamics. Orexin has been demonstrated interfering with β-amyloid metabolism in Alzheimer's Disease (AD)pathology. The present study investigated cerebrospinal-fluid (CSF)β-amyloid 40 (Aβ 40 ), β-amyloid 42 (Aβ 42 )and orexin levels in OSA patients compared to AD patients and controls. Methods: OSA and AD patients were included in this study and compared to a group of controls. Patients and controls underwent lumbar puncture for the assessment of CSF Aβ 40 , Aβ 42 , tau proteins, orexin levels, and polysomnography to measure nocturnal sleep architecture. Results: 20 OSA patients, 20 AD patients, and 15 controls were included in our study. OSA patients showed higher CSF orexin levels than AD patients and controls, and AD patients showed higher CSF orexin levels than controls. Moreover, CSF Aβ 40 and Aβ 42 were lower in OSA patients than controls, but higher in OSA patients compared to AD patients. However, AD patients showed lower CSF Aβ 42 levels but comparable CSF Aβ 40 levels than controls. Sleep macrostructure was similarly altered in OSA and AD patients compared to controls. Finally, the apnea-hypopnea index (AHI)was related to the ratio Aβ 42 /Aβ 40 and CSF orexin levels in OSA patients. Conclusion: This study proved the alteration of CSF orexin levels and β-amyloid isoforms 40 and 42 in OSA patients. We suppose that sleep disruption and intermittent hypoxia, the two core features of OSA, may induce orexinergic system and cerebral β-amyloid metabolism dysregulation. This evidence further supports the current hypothesis that OSA may possibly start AD neuropathological processes.

AB - Background: Obstructive Sleep Apnea (OSA)is associated with pathological changes of cerebral β-amyloid dynamics. Orexin has been demonstrated interfering with β-amyloid metabolism in Alzheimer's Disease (AD)pathology. The present study investigated cerebrospinal-fluid (CSF)β-amyloid 40 (Aβ 40 ), β-amyloid 42 (Aβ 42 )and orexin levels in OSA patients compared to AD patients and controls. Methods: OSA and AD patients were included in this study and compared to a group of controls. Patients and controls underwent lumbar puncture for the assessment of CSF Aβ 40 , Aβ 42 , tau proteins, orexin levels, and polysomnography to measure nocturnal sleep architecture. Results: 20 OSA patients, 20 AD patients, and 15 controls were included in our study. OSA patients showed higher CSF orexin levels than AD patients and controls, and AD patients showed higher CSF orexin levels than controls. Moreover, CSF Aβ 40 and Aβ 42 were lower in OSA patients than controls, but higher in OSA patients compared to AD patients. However, AD patients showed lower CSF Aβ 42 levels but comparable CSF Aβ 40 levels than controls. Sleep macrostructure was similarly altered in OSA and AD patients compared to controls. Finally, the apnea-hypopnea index (AHI)was related to the ratio Aβ 42 /Aβ 40 and CSF orexin levels in OSA patients. Conclusion: This study proved the alteration of CSF orexin levels and β-amyloid isoforms 40 and 42 in OSA patients. We suppose that sleep disruption and intermittent hypoxia, the two core features of OSA, may induce orexinergic system and cerebral β-amyloid metabolism dysregulation. This evidence further supports the current hypothesis that OSA may possibly start AD neuropathological processes.

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