Post H1N1 vaccination narcolepsy–cataplexy with decreased CSF beta-amyloid

Kallweit, Ulf; Hidalgo, Hildegard; Engel, Alice; Baumann, Christian R.; Dahmen, Norbert

doi:10.1016/j.sleep.2011.10.023

Cited by 15 publications

(8 citation statements)

References 4 publications

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“…Therefore, the positive correlation between CSF Aβ 42 and hypocretin-1 levels appears to be specific to the AD process. However, our results in NC contrasted with a previous case report of a hypocretin-deficient young girl with NC with low CSF Aβ 42 who had been vaccinated for pandemic H1N1 (Kallweit et al, 2012). Unexpectedly, we also found positive correlations between CSF Aβ 42 and tau and P-tau levels in patients with NC with no cognitive abnormalities, but no relationship was found with hypocretin-1.…”

Section: Discussioncontrasting

confidence: 99%

Hypocretin and brain Î²-amyloid peptide interactions in cognitive disorders and narcolepsy

Dauvilliers

Lehmann

Jaussent

et al. 2014

Front. Aging Neurosci.

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Objective: To examine relationships between cerebrospinal fluid (CSF) Alzheimer' disease (AD) biomarkers and hypocretin-1 levels in patients with cognitive abnormalities and hypocretin-deficient narcolepsy-cataplexy (NC), estimate diagnostic accuracy, and determine correlations with sleep disturbances.Background: Sleep disturbances are frequent in AD. Interactions between brain β-amyloid (Aβ) aggregation and a wake-related neurotransmitter hypocretin have been reported in a mouse model of AD.Methods: Ninety-one cognitive patients (37 AD, 16 mild cognitive impairment—MCI that converts to AD, 38 other dementias) and 15 elderly patients with NC were recruited. Patients were diagnosed blind to CSF results. CSF Aβ42, total tau, ptau181, and hypocretin-1 were measured. Sleep disturbances were assessed with questionnaires in 32 cognitive patients.Results: Lower CSF Aβ42 but higher tau and P-tau levels were found in AD and MCI compared to other dementias. CSF hypocretin-1 levels were higher in patients with MCI due to AD compared to other dementias, with a similar tendency for patients with advanced AD. CSF hypocretin-1 was significantly and independently associated with AD/MCI due to AD, with an OR of 2.70 after full adjustment, exceeding that for Aβ42. Aβ42 correlated positively with hypocretin-1 levels in advanced stage AD. No association was found between sleep disturbances and CSF biomarkers. No patients with NC achieved pathological cutoffs for Aβ42, with respectively one and four patients with NC above tau and P-tau cutoffs and no correlations between hypocretin-1 and other biomarkers.Conclusions: Our results suggest a pathophysiological relationship between Aβ42 and hypocretin-1 in the AD process, with higher CSF hypocretin-1 levels in early disease stages. Further longitudinal studies are needed to validate these biomarker interactions and to determine the cause-effect relationship and the role of wake/sleep behavior in amyloid plaque regulation.

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Section: Discussioncontrasting

confidence: 99%

Hypocretin and brain Î²-amyloid peptide interactions in cognitive disorders and narcolepsy

Dauvilliers

Lehmann

Jaussent

et al. 2014

Front. Aging Neurosci.

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“…Upper airway Streptococcus pyogenes infections and influenza‐A H1N1 infections and vaccinations have been considered as possible autoimmune triggers in genetically predisposed subjects (Kornum et al ., ). Recently, low cerebrospinal fluid (CSF) beta‐amyloid 1–42 (A β 1–42 ) levels have been described in a case of NC post‐H1N1 vaccination and also in an unpublished case of NC lacking previous history of vaccination/infection (Kallweit et al ., ). It has been hypothesized that the low A β 1–42 CSF levels encountered in genetically recognizable patients could be related to post‐infectious immunological processes.…”

Section: Introductionmentioning

confidence: 97%

CSF beta‐amyloid levels are altered in narcolepsy: a link with the inflammatory hypothesis?

Liguori

Placidi

Albanese

et al. 2014

Journal of Sleep Research

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SUMMARYNarcolepsy is characterized by hypocretin deficiency due to the loss of hypothalamic orexinergic neurons, and is associated with both the human leucocyte antigen DQB1*06:02 and the T cell receptor polymorphism. The above relationship suggests autoimmune/inflammatory processes underlying the loss of orexinergic neurons in narcolepsy. To test the autoimmune/inflammatory hypothesis by means of cerebrospinal fluid (CSF) levels of beta-amyloid 1-42 and/or total tau proteins in a sample of narcoleptic patients, we analysed 16 narcoleptic patients and 16 healthy controls. Beta-amyloid 1-42 CSF levels were significantly lower in narcoleptic patients compared with healthy controls. We also documented pathologically low levels of CSF beta-amyloid 1-42 (<500 pg mL À1 ) in six of 16 narcoleptic patients (37.5%). We hypothesize that the significant decrease of the CSF beta-amyloid 1-42 levels in narcoleptic patients may support both the inflammatory/autoimmune hypothesis as the basis of the pathogenesis of narcolepsy and the prevalence of an 'amyloidogenic' pathway caused by the deficiency of the alpha-secretases enzymes.

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“…Finally, the increased levels of specific cytokines (TNF and IL-6 among others) further support the evidence of an inflammatory and immune response in patients with narcolepsy since the very early phases of the disease [ 73 ]. The reduction of CSF ß-amyloid 42 levels in patients with narcolepsy near to disease onset has been also associated with the brain inflammatory response [ 74 – 76 ]. Moreover, other proofs of the activation of the immune system have been documented in patients with NT1, also with long-lasting disease [ 77 ].…”

Section: Narcolepsymentioning

confidence: 99%

COVID-19: dealing with a potential risk factor for chronic neurological disorders

Schirinzi

Landi²,

Liguori

2020

J Neurol

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SARS-CoV2 infection is responsible for a complex clinical syndrome, named Coronavirus Disease 2019 (COVID-19), whose main consequences are severe pneumonia and acute respiratory distress syndrome. Occurrence of acute and subacute neurological manifestations (encephalitis, stroke, headache, seizures, Guillain-Barrè syndrome) is increasingly reported in patients with COVID-19. Moreover, SARS-CoV2 immunopathology and tissue colonization in the gut and the central nervous system, and the systemic inflammatory response during COVID-19 may potentially trigger chronic autoimmune and neurodegenerative disorders. Specifically, Parkinson's disease, multiple sclerosis and narcolepsy present several pathogenic mechanisms that can be hypothetically initiated by SARS-CoV2 infection in susceptible individuals. In this short narrative review, we summarize the clinical evidence supporting the rationale for investigating SARS-CoV2 infection as risk factor for these neurological disorders, and suggest the opportunity to perform in the future SARS-CoV2 serology when diagnosing these disorders.

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Post H1N1 vaccination narcolepsy–cataplexy with decreased CSF beta-amyloid

Cited by 15 publications

References 4 publications

Hypocretin and brain Î²-amyloid peptide interactions in cognitive disorders and narcolepsy

Hypocretin and brain Î²-amyloid peptide interactions in cognitive disorders and narcolepsy

CSF beta‐amyloid levels are altered in narcolepsy: a link with the inflammatory hypothesis?

COVID-19: dealing with a potential risk factor for chronic neurological disorders

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