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  1. Article ; Online: Long COVID: Does SARS-CoV-2 induce lingering brain lesions?

    Hugon, Jacques

    European journal of neurology

    2023  Volume 30, Issue 5, Page(s) 1165–1166

    Abstract: Hundreds of millions of COVID cases have been reported so far and long-term lingering clinical symptoms are frequent and are called long COVID. Neurological signs including cognitive complaints are often described in long Covid. In COVID patients, the ... ...

    Abstract Hundreds of millions of COVID cases have been reported so far and long-term lingering clinical symptoms are frequent and are called long COVID. Neurological signs including cognitive complaints are often described in long Covid. In COVID patients, the Sars-Cov-2 virus can reach the brain and could be responsible for cerebral anomalies observed in long COVID. Long-term careful clinical follow-up of these patients is necessary to detect early signs of neurodegeneration.
    MeSH term(s) Humans ; SARS-CoV-2 ; COVID-19/complications ; Post-Acute COVID-19 Syndrome ; Nervous System Diseases ; Brain/diagnostic imaging
    Language English
    Publishing date 2023-03-03
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 1280785-0
    ISSN 1468-1331 ; 1351-5101 ; 1471-0552
    ISSN (online) 1468-1331
    ISSN 1351-5101 ; 1471-0552
    DOI 10.1111/ene.15751
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    Zs.A 4738: Show issues Location:
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  2. Article ; Online: Rheumatoid arthritis and cognitive decline.

    Hugon, Jacques

    Joint bone spine

    2022  Volume 89, Issue 3, Page(s) 105346

    MeSH term(s) Arthritis, Rheumatoid/complications ; Arthritis, Rheumatoid/diagnosis ; Arthritis, Rheumatoid/drug therapy ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/etiology ; Humans
    Language English
    Publishing date 2022-01-20
    Publishing country France
    Document type Editorial
    ZDB-ID 2020487-5
    ISSN 1778-7254 ; 1297-319X
    ISSN (online) 1778-7254
    ISSN 1297-319X
    DOI 10.1016/j.jbspin.2022.105346
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    Zs.A 4590: Show issues Location:
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  3. Article ; Online: Author's response to the letter on the article: "Long-COVID: cognitive deficits (brain fog) and brain lesions in non-hospitalized patients".

    Hugon, Jacques

    Presse medicale (Paris, France : 1983)

    2022  Volume 51, Issue 2, Page(s) 104137

    MeSH term(s) Humans ; Post-Acute COVID-19 Syndrome ; COVID-19/complications ; Cognition Disorders/etiology ; Nervous System Diseases ; Brain/diagnostic imaging ; Cognition
    Language English
    Publishing date 2022-09-06
    Publishing country France
    Document type Letter
    ZDB-ID 120943-7
    ISSN 2213-0276 ; 0032-7867 ; 0755-4982 ; 0301-1518
    ISSN (online) 2213-0276
    ISSN 0032-7867 ; 0755-4982 ; 0301-1518
    DOI 10.1016/j.lpm.2022.104137
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  4. Article ; Online: Long-COVID: Cognitive deficits (brain fog) and brain lesions in non-hospitalized patients.

    Hugon, Jacques

    Presse medicale (Paris, France : 1983)

    2021  Volume 51, Issue 2, Page(s) 104090

    MeSH term(s) Humans ; Post-Acute COVID-19 Syndrome ; COVID-19/complications ; Cognition Disorders/etiology ; Nervous System Diseases ; Brain/diagnostic imaging ; Cognition
    Language English
    Publishing date 2021-10-28
    Publishing country France
    Document type Editorial
    ZDB-ID 120943-7
    ISSN 2213-0276 ; 0032-7867 ; 0755-4982 ; 0301-1518
    ISSN (online) 2213-0276
    ISSN 0032-7867 ; 0755-4982 ; 0301-1518
    DOI 10.1016/j.lpm.2021.104090
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  5. Article ; Online: Maladie d’Alzheimer : une maladie biologique ?

    Hugon, Jacques

    La Revue du praticien

    2020  Volume 70, Issue 2, Page(s) 152–155

    Abstract: Alzheimer's disease: a biological disorder? Alzheimer's disease often begins clinically with memory problems progressively followed by aphasia, apraxia, agnosia and behavioral disturbances. Recent studies of biological markers of cerebrospinal fluid or ... ...

    Title translation Alzheimer's disease: a biological disorder?
    Abstract Alzheimer's disease: a biological disorder? Alzheimer's disease often begins clinically with memory problems progressively followed by aphasia, apraxia, agnosia and behavioral disturbances. Recent studies of biological markers of cerebrospinal fluid or amyloid and tau PET imaging have shown that abnormalities can begin one to two decades before the onset of symptoms. This clinically silent phase is a biological phase where neurons fight the toxic effects of amyloid and tau accumulations as well as neuroinflammation. An ATN biological classification has been proposed (A: amyloid, T tau, N: neurodegeneration). The discovery of blood or other biomarkers should allow detection of this silent phase leading to the setup of therapeutic trials when brain lesions are minimal and neurons less affected, to be able to prevent the late cognitive decline of this disease.
    MeSH term(s) Alzheimer Disease ; Amyloid beta-Peptides ; Amyloidosis ; Biomarkers ; Cognitive Dysfunction ; Humans ; Positron-Emission Tomography ; tau Proteins
    Chemical Substances Amyloid beta-Peptides ; Biomarkers ; tau Proteins
    Language French
    Publishing date 2020-09-02
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 205365-2
    ISSN 2101-017X ; 0035-2640
    ISSN (online) 2101-017X
    ISSN 0035-2640
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  6. Article ; Online: The PKR/P38/RIPK1 Signaling Pathway as a Therapeutic Target in Alzheimer's Disease.

    Hugon, Jacques / Paquet, Claire

    International journal of molecular sciences

    2021  Volume 22, Issue 6

    Abstract: Neuropathological lesions in Alzheimer's disease (AD) include amyloid plaques formed by the accumulation of amyloid peptides, neurofibrillary tangles made of hyperphosphorylated tau protein, synaptic and neuronal degenerations, and neuroinflammation. The ...

    Abstract Neuropathological lesions in Alzheimer's disease (AD) include amyloid plaques formed by the accumulation of amyloid peptides, neurofibrillary tangles made of hyperphosphorylated tau protein, synaptic and neuronal degenerations, and neuroinflammation. The cause of AD is unknown, but according to the amyloid hypothesis, amyloid oligomers could lead to the activation of kinases such as eukaryotic translation initiation factor 2-alpha kinase 2 (PKR), p38, and receptor-interacting serine/threonine-protein kinase 1 (RIPK1), which all belong to the same stress-activated pathway. Many toxic kinase activations have been described in AD patients and in experimental models. A p38 mitogen-activated protein kinase inhibitor was recently tested in clinical trials but with unsuccessful results. The complex PKR/P38/RIPK1 (PKR/dual specificity mitogen-activated protein kinase kinase 6 (MKK6)/P38/MAP kinase-activated protein kinase 2 (MK2)/RIPK1) is highly activated in AD brains and in the brains of AD transgenic animals. To delineate the implication of this pathway in AD, we carried out a search on PubMed including PKR/MKK6/p38/MK2/RIPK1, Alzheimer, and therapeutics. The involvement of this signaling pathway in the genesis of AD lesions, including Aβ accumulations and tau phosphorylation as well as cognitive decline, is demonstrated by the reports described in this review. A future combination strategy with kinase inhibitors should be envisaged to modulate the consequences for neurons and other brain cells linked to the abnormal activation of this pathway.
    MeSH term(s) Alzheimer Disease/drug therapy ; Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Animals ; Biomarkers ; Brain/metabolism ; Brain/pathology ; Combined Modality Therapy ; Disease Management ; Disease Susceptibility ; Drug Discovery ; Humans ; Molecular Targeted Therapy ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Signal Transduction/drug effects ; eIF-2 Kinase/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Biomarkers ; EIF2AK2 protein, human (EC 2.7.11.1) ; RIPK1 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2021-03-19
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22063136
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  7. Article ; Online: Stimulation cérébrale transcrânienne dans la maladie d’Alzheimer.

    Hugon, Jacques / Paquet, Claire

    La Revue du praticien

    2020  Volume 70, Issue 2, Page(s) 173–174

    Title translation Transcranial cerebral stimulation in Alzheimer's disease.
    MeSH term(s) Alzheimer Disease/therapy ; Humans
    Language French
    Publishing date 2020-09-02
    Publishing country France
    Document type Journal Article
    ZDB-ID 205365-2
    ISSN 2101-017X ; 0035-2640
    ISSN (online) 2101-017X
    ISSN 0035-2640
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  8. Article ; Online: Maladie d’Alzheimer : aspects précliniques et précoces : 10 messages clés.

    Hugon, Jacques / Ménard, Joël

    La Revue du praticien

    2020  Volume 70, Issue 2, Page(s) 177

    Title translation Alzheimer's disease: preclinical and early aspects : 10 key messages.
    MeSH term(s) Alzheimer Disease/diagnosis ; Alzheimer Disease/epidemiology ; Alzheimer Disease/therapy ; Disease Progression ; Humans ; Neuropsychological Tests
    Language French
    Publishing date 2020-09-02
    Publishing country France
    Document type Journal Article
    ZDB-ID 205365-2
    ISSN 2101-017X ; 0035-2640
    ISSN (online) 2101-017X
    ISSN 0035-2640
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  9. Article ; Online: Des connaissances qui s’accumulent et un objectif : agir précocement.

    Hugon, Jacques / Ménard, Joël

    La Revue du praticien

    2020  Volume 70, Issue 2, Page(s) 147–148

    Title translation Accumulating knowledge and one objective: to act early.
    MeSH term(s) Alzheimer Disease ; Humans
    Language French
    Publishing date 2020-09-02
    Publishing country France
    Document type Journal Article
    ZDB-ID 205365-2
    ISSN 2101-017X ; 0035-2640
    ISSN (online) 2101-017X
    ISSN 0035-2640
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  10. Article ; Online: Could ryanodine receptor dysfunction be linked to PKR brain accumulations in Alzheimer's disease?

    Hugon, Jacques / Paquet, Claire

    Medical hypotheses

    2018  Volume 113, Page(s) 45

    MeSH term(s) Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/metabolism ; Humans ; Neurons/metabolism ; Phosphorylation ; Ryanodine Receptor Calcium Release Channel/metabolism ; Signal Transduction ; eIF-2 Kinase/metabolism ; tau Proteins/metabolism
    Chemical Substances Amyloid beta-Peptides ; Ryanodine Receptor Calcium Release Channel ; tau Proteins ; EIF2AK2 protein, human (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1) ; CAMKK2 protein, human (EC 2.7.11.17) ; Calcium-Calmodulin-Dependent Protein Kinase Kinase (EC 2.7.11.17) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2018-02-19
    Publishing country United States
    Document type Letter
    ZDB-ID 193145-3
    ISSN 1532-2777 ; 0306-9877
    ISSN (online) 1532-2777
    ISSN 0306-9877
    DOI 10.1016/j.mehy.2018.02.012
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