Certaines complications cognitives peuvent être atténuées, mais cela dépend de la gravité et du traitement.
RéversibilitéComplicationsNeurogranine
#5
Comment gérer les complications liées à la neurogranine ?
La gestion inclut des traitements médicaux, des thérapies cognitives et un soutien psychologique.
GestionThérapies cognitivesNeurogranine
Facteurs de risque
5
#1
Quels sont les facteurs de risque pour des niveaux élevés de neurogranine ?
L'âge avancé, les antécédents familiaux de démence et les maladies cardiovasculaires sont des facteurs de risque.
Facteurs de risqueDémenceMaladies cardiovasculaires
#2
Le mode de vie influence-t-il la neurogranine ?
Oui, un mode de vie sédentaire et une mauvaise alimentation peuvent augmenter les niveaux de neurogranine.
Mode de vieNeurogranineAlimentation
#3
Le stress est-il un facteur de risque ?
Oui, le stress chronique peut contribuer à des niveaux élevés de neurogranine et à des troubles cognitifs.
StressNeurogranineTroubles cognitifs
#4
Les maladies métaboliques affectent-elles la neurogranine ?
Oui, des maladies comme le diabète peuvent influencer les niveaux de neurogranine et la santé cognitive.
Maladies métaboliquesDiabèteNeurogranine
#5
L'hérédité joue-t-elle un rôle dans la neurogranine ?
Oui, des antécédents familiaux de troubles cognitifs peuvent augmenter le risque de niveaux élevés de neurogranine.
HéréditéNeurogranineTroubles cognitifs
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"@type": "Question",
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"@type": "Question",
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"position": 8,
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"@type": "Question",
"name": "Les troubles de la mémoire sont-ils liés à la neurogranine ?",
"position": 9,
"acceptedAnswer": {
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"@type": "Question",
"name": "La neurogranine influence-t-elle la concentration ?",
"position": 10,
"acceptedAnswer": {
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"text": "Des niveaux anormaux de neurogranine peuvent affecter la concentration et les fonctions exécutives."
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"@type": "Question",
"name": "Peut-on prévenir l'augmentation de la neurogranine ?",
"position": 11,
"acceptedAnswer": {
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"text": "Des modes de vie sains, comme l'exercice et une bonne alimentation, peuvent aider à prévenir l'augmentation."
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"position": 12,
"acceptedAnswer": {
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"text": "Oui, un engagement intellectuel peut réduire le risque de troubles cognitifs liés à la neurogranine."
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"@type": "Question",
"name": "Le stress influence-t-il la neurogranine ?",
"position": 13,
"acceptedAnswer": {
"@type": "Answer",
"text": "Le stress chronique peut affecter les niveaux de neurogranine et la santé cognitive."
}
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"@type": "Question",
"name": "Y a-t-il des aliments bénéfiques pour la neurogranine ?",
"position": 14,
"acceptedAnswer": {
"@type": "Answer",
"text": "Une alimentation riche en oméga-3 et antioxydants peut soutenir la santé cérébrale et la neurogranine."
}
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"@type": "Question",
"name": "L'exercice physique aide-t-il la neurogranine ?",
"position": 15,
"acceptedAnswer": {
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"text": "Oui, l'exercice régulier est bénéfique pour la santé cérébrale et peut influencer positivement la neurogranine."
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"@type": "Question",
"name": "Y a-t-il des traitements ciblant la neurogranine ?",
"position": 16,
"acceptedAnswer": {
"@type": "Answer",
"text": "Actuellement, il n'existe pas de traitements spécifiques ciblant la neurogranine."
}
},
{
"@type": "Question",
"name": "Comment la neurogranine influence-t-elle les traitements ?",
"position": 17,
"acceptedAnswer": {
"@type": "Answer",
"text": "La neurogranine peut servir de biomarqueur pour évaluer l'efficacité des traitements neurodégénératifs."
}
},
{
"@type": "Question",
"name": "Les médicaments peuvent-ils affecter la neurogranine ?",
"position": 18,
"acceptedAnswer": {
"@type": "Answer",
"text": "Certains médicaments pour les troubles cognitifs peuvent influencer les niveaux de neurogranine."
}
},
{
"@type": "Question",
"name": "Des thérapies non médicamenteuses aident-elles ?",
"position": 19,
"acceptedAnswer": {
"@type": "Answer",
"text": "Des thérapies cognitives peuvent améliorer les symptômes, mais leur impact sur la neurogranine est encore à étudier."
}
},
{
"@type": "Question",
"name": "La neurogranine est-elle impliquée dans la recherche de traitements ?",
"position": 20,
"acceptedAnswer": {
"@type": "Answer",
"text": "Oui, la neurogranine est un sujet de recherche pour développer de nouveaux traitements pour la démence."
}
},
{
"@type": "Question",
"name": "Quelles complications sont liées à des niveaux élevés de neurogranine ?",
"position": 21,
"acceptedAnswer": {
"@type": "Answer",
"text": "Des niveaux élevés peuvent être associés à des troubles cognitifs sévères et à la démence."
}
},
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"@type": "Question",
"name": "La neurogranine est-elle liée à d'autres maladies ?",
"position": 22,
"acceptedAnswer": {
"@type": "Answer",
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}
},
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"@type": "Question",
"name": "Des complications psychologiques sont-elles possibles ?",
"position": 23,
"acceptedAnswer": {
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}
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"@type": "Question",
"name": "Les complications sont-elles réversibles ?",
"position": 24,
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}
},
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"@type": "Question",
"name": "Comment gérer les complications liées à la neurogranine ?",
"position": 25,
"acceptedAnswer": {
"@type": "Answer",
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"@type": "Question",
"name": "Quels sont les facteurs de risque pour des niveaux élevés de neurogranine ?",
"position": 26,
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"text": "L'âge avancé, les antécédents familiaux de démence et les maladies cardiovasculaires sont des facteurs de risque."
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{
"@type": "Question",
"name": "Le mode de vie influence-t-il la neurogranine ?",
"position": 27,
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{
"@type": "Question",
"name": "Le stress est-il un facteur de risque ?",
"position": 28,
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}
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"@type": "Question",
"name": "Les maladies métaboliques affectent-elles la neurogranine ?",
"position": 29,
"acceptedAnswer": {
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}
},
{
"@type": "Question",
"name": "L'hérédité joue-t-elle un rôle dans la neurogranine ?",
"position": 30,
"acceptedAnswer": {
"@type": "Answer",
"text": "Oui, des antécédents familiaux de troubles cognitifs peuvent augmenter le risque de niveaux élevés de neurogranine."
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]
}
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK.
UK Dementia Research Institute at UCL, London, UK.
Department of Pharmacology, Toxicology, and Neuroscience, Louisiana State University Health Sciences Center, Shreveport, LA, 71130, USA. Electronic address: hnam@lsuhsc.edu.
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Laboratory Medicine, University of Palermo, Palermo, Italy.
Current AT(N) stratification for Alzheimer's disease (AD) accounts for complex combinations of amyloid (A), tau proteinopathy (T) and neurodegeneration (N) signatures. Understanding the transition bet...
This is an observational study, CSF levels of Tau, pTau181, pTau217, Aβ38/40/42, sAPPα/β, BACE1 and neurogranin were measured in the BALTAZAR cohort of cognitively impaired patients and in the Alzheim...
As expected, CSF Aβ42 decreased progressively with the AD continuum going from the A-T-N- to the A + T + N + profile. On the other hand, Tau and pTau181 increased progressively with the disease. The f...
The early transition to an A + phenotype (A + T-N-) primarily impacts synaptic function. The appearance of T + and then N + is associated with a significant and progressive increase in pathological Al...
CSF biomarkers have immense diagnostic and prognostic potential for Alzheimer disease (AD). However, AD is still diagnosed relatively late in the disease process, sometimes even years after the initia...
We enrolled participants with available neurogranin and BACE1 measurements in CSF from the DELCODE (DZNE-Longitudinal Cognitive Impairment and Dementia, Germany) cohort. The longitudinal change of Pre...
A total of 530 participants (mean age: 70.76 ± 6.01 years, 48.7% female) were analyzed in the study. The rate of cognitive decline was faster in individuals with SCD with higher neurogranin and neurog...
Our findings suggest that CSF neurogranin and BACE1 begin to change in the preclinical stage of AD and they are associated with clinical progression in individuals with SCD....
There is initial evidence suggesting that biomarker neurogranin (Ng) may distinguish Alzheimer's disease (AD) from other neurodegenerative diseases. Therefore, we assessed (a) the discriminant ability...
Participants with subjective cognitive decline (SCD) (n = 33), amnestic mild cognitive impairment (aMCI) due to AD (n = 109), AD dementia (n = 67), MCI due to FTLD (n = 25), and FTLD dementia (n = 29)...
Ng levels were higher in aMCI-AD patients compared to MCI-FTLD (F[1, 134] = 15.16, p < .001), and in AD-dementia compared to FTLD-dementia (F[1, 96] = 4.60, p = .029). Additionally, Ng levels were hig...
In this first study to-date to assess MCI and dementia due to AD or FTLD within one study, elevated CSF Ng appears to be an early biomarker of AD-related impairment, but its role as a biomarker appear...
The levels of synaptic markers synaptosomal-associated protein 25 (SNAP-25) and neurogranin (Ng) have been shown to increase early in the cerebrospinal fluid (CSF) of patients with Creutzfeldt-Jakob d...
In this retrospective study, using commercially available immunoassays, we measured the levels of SNAP-25, Ng, 14-3-3, total-tau (t-tau), neurofilament light chain (NfL), and phospho-tau181 (p-tau) in...
CSF SNAP-25 and Ng levels were higher in CJD than in np-RPD (SNAP-25: 582, 95% CI 240-1250 vs. 115, 95% CI 78-157 pg/ml, p < 0.0001; Ng: 841, 95% CI 411-1473 vs. 390, 95% CI 260-766 pg/ml, p < 0.001)....
In the clinical setting, CSF SNAP-25 is a viable alternative to t-tau, 14-3-3, and the t-tau/p-tau ratio in discriminating the CJD subtypes from other RPDs. Additionally, SNAP-25 and, to a lesser exte...
In addition to amyloid and tau pathology in the central nervous system (CNS), inflammatory processes and synaptic dysfunction are highly important mechanisms involved in the development and progressio...
Our aim was to examine the correlation between biomarkers of neuronal and glial cell damage and severity of disease in patients with tick-borne encephalitis....
One hundred and fifteen patients with tick-borne encephalitis diagnosed in Lithuania and Sweden were prospectively included, and cerebrospinal fluid (CSF) and serum samples were obtained shortly after...
Cerebrospinal fluid and serum concentrations of GFAP and NfL correlated with disease severity, independent of age, and with the presence of nerve paralysis. The markers neurogranin, YKL-40, tau and S1...
Neuronal cell damage and astroglial cell activation with increased NfL and GFAP in CSF and serum were associated with a more severe disease, independent of age. Increased GFAP and NfL concentrations i...
Synapse loss is an early event that precedes neuronal death and symptom onset and is considered the best neuropathological correlate of cognitive decline in Alzheimer's disease (AD). Vesicle-associate...
We developed a digital immunoassay on the Single Molecule Array platform to quantify VAMP-2 in CSF and used existing immunoassays to quantify Ng, SNAP-25 and core CSF AD biomarkers. The clinical study...
The VAMP-2 assay had a good analytical performance (repeatability 8.9%, intermediate precision 10.3%). Assay antibodies detected native VAMP-2 protein in human brain homogenates. CSF concentrations of...
Our novel digital immunoassay accurately measures VAMP-2 changes in CSF, which reflect AD biomarkers and cognitive performance across multiple domains....
One goal of the Longitudinal Early Onset Alzheimer's Disease Study (LEADS) is to define the fluid biomarker characteristics of early-onset Alzheimer's disease (EOAD)....
Cerebrospinal fluid (CSF) concentrations of Aβ1-40, Aβ1-42, total tau (tTau), pTau181, VILIP-1, SNAP-25, neurogranin (Ng), neurofilament light chain (NfL), and YKL-40 were measured by immunoassay in 1...
Biomarkers were correlated with one another. Levels of CSF Aβ42/40, pTau181, tTau, SNAP-25, and Ng in EOAD differed significantly from cognitively normal and early-onset non-AD dementia; NfL, YKL-40, ...
This study provides a comprehensive analysis of CSF biomarkers in sporadic EOAD that can inform EOAD clinical trial design....
Patients with Lewy body disease (LBD) often show a co-occurring Alzheimer disease (AD) pathology. CSF biomarkers allow the detection in vivo of AD-related pathologic hallmarks included in the amyloid-...
We retrospectively measured CSF levels of AD core biomarkers (Aβ42/40 ratio, phosphorylated tau protein, and total tau protein) and of synaptic (β-synuclein, α-synuclein, synaptosomal-associated prote...
CSF β-synuclein, α-synuclein, SNAP-25, neurogranin, and NfL levels did not differ between LBD (n = 101, age 67.2 ± 7.8 years, 27.7% females) and controls (age 64.8 ± 8.6 years, 39.3% females) and were...
LBD/A+T+ and AD cases showed significantly increased CSF levels of synaptic and neuroaxonal biomarkers compared with LBD/A-T- and control subjects. Patients with LBD and AT(N)-based AD copathology sho...
This study provides Class II evidence that CSF levels of β-synuclein, α-synuclein, SNAP-25, neurogranin, and NfL are higher in patients with AD than in patients with LBD....
Diffuse axonal injury (DAI), one of the most common and devastating type of traumatic brain injury, is the result of the shear force on axons due to severe rotational acceleration and deceleration. Ne...