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Narcolepsy Protect Against Alzheimer's Disease?

Not Applicable
Completed
Conditions
Amyloid Pathology
Narcolepsy
Interventions
Device: PET-scan18F-AV-45
Registration Number
NCT03378453
Lead Sponsor
University Hospital, Montpellier
Brief Summary

Links between orexin and amyloid processes have been underlined recently. During the Alzheimer's process an upregulation of the orexin mechanism has been observed. The pathophysiological mechanism of narcolepsy type 1 is linked to orexin deficiency. Thus, the investigators hypothesized that patients with narcolepsy may be protected from amyloid brain lesions, hallmarks of the Alzheimer's process. To test this hypothesis, the investigators analyzed the brain amyloid load measured by PET-scan amyloid brain imaging in patients with narcolepsy type 1 compared to controls without cognitive deficits.

Detailed Description

The lack of innovative treatments in Alzheimer' disease (AD) is due to the non-understanding of the pathological process. The investigators need to include the latest concept of the sleep-wake/circadian kinetics of proteins in the brain, the new theory of the wash-out of pathological proteins via the brain glymphatic system during sleep and act at an early stage. New pathways are opened to better understand proteinopathies' processes and to propose new therapeutics interventions. The variations of the production/clearance curves of amyloid in the cerebrospinal fluid (CSF) during circadian rhythms and sleep-wake cycles have been demonstrated in in vivo metabolism experimentations. Suprachiasmatic nucleus damages due to AD may induce circadian regulation dysfunction and secondary sleep/wake cycle alterations. Key sleep/wake cycle neuromediators (Orexin-A, melatonin) are involved in the regulation of brain amyloid levels. The influence of orexin-A signaling on Aβ metabolism in animals and humans was recently highlighted. In rats, orexin-A release shows a 24-h fluctuation similar to that of brain interstitial fluid Aβ. In transgenic mice that overexpress amyloid precursor protein (APP), brain interstitial fluid Aβ concentration increases during wakefulness and after orexin-A infusion. Conversely, it decreases during sleep and after infusion of an orexin-A receptor antagonist6. In transgenic mice that overexpress APP/presenilin1 (PS1), in which the orexin gene is knocked out, a reduction of Aβ pathology was found, possibly caused by changes in sleep time. Orexin-A is linked to Aβ42 in AD and an increase of CSF orexin-A is observed in AD vs. controls, possibly related to sleep deterioration and neurodegeneration.

The narcolepy with cataplexy type 1 is the only disease with a specific orexin deficiency. Montpellier team have previously underlined in 15 patients with narcolepsy type 1 a normal level of Aβ42 in the CSF. The clinical expertise of the narcolepsy center suggested that the frequency of AD in old narcoleptic patients is low. The hypothesis was that patients with narcolepsy type 1 may be protected from amyloid brain lesions, hallmarks of the Alzheimer's process. The objective was to determine whether the brain amyloid load by PET-scan18 F-AV-45 measured with a semi-quantitative analysis (mean cortical SuVr) is lower in patients with narcolepsy type 1 older than 65 years-old than in cognitively normal age- and gender-matched controls.

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
38
Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
CoSPET-scan18F-AV-45Cognitevement healthy controls
NarCoPET-scan18F-AV-45Narcolepsy type 1 over 65 years old
Primary Outcome Measures
NameTimeMethod
Mean of cortical SuVr based of the PET-scan18F-AV-45 imagingUpon study completion, an average of one year

Mean of cortical SuVr based of the PET-scan18F-AV-45 imaging

Secondary Outcome Measures
NameTimeMethod
Beck Depression Inventory (BDI)Upon study completion, an average of one year

Score as a number

CSF Tau proteinUpon study completion, an average of one year

pg/ml

Day-time sleep durationUpon study completion, an average of one year

Hours/day

CataplexyUpon study completion, an average of one year

Numbers/week

Epworth sleepiness scale (ESS)Upon study completion, an average of one year

Score as a number

Mean regional SuVr with PET-scan AV45Upon study completion, an average of one year
CSF Amyloid Aβ42Upon study completion, an average of one year

pg/ml

CSF Amyloid Aβ40Upon study completion, an average of one year

pg/ml

CSF Orexin concentrationUpon study completion, an average of one year

pg/ml

Night-time sleep durationUpon study completion, an average of one year

Hours/night

European Quality of Life Dimension (EQL-5)Upon study completion, an average of one year

Score as a number

Trial Locations

Locations (1)

Montpellier University Hospital, Gui de Chauliac

🇫🇷

Montpellier, France

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