I. Slassi

Centre Hospitalier Universitaire Hassan II, Fez, Fès-Boulemane, Morocco

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Publications (181)108.7 Total impact

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    ABSTRACT: IntroductionNeuromyelitis optica (NMO) has been traditionally described as the association of optic neuritis and longitudinally extensive transverse myelitis (LETM) [1]. Identification of aquaporin-4 antibody (AQP-4) has deeply changed the concept of this disease and allowed identification of cases beyond this classical phenotype [1]. Indeed, clinical and MRI analysis of larger cohorts in the last few years, allowed the description of various ≪ atypical ≫ clinical symptoms, as a syndrome of intractable hiccups nausea and vomiting (IHNV) [2] or more recently, painful tonic spasms (PTS) [3] and neuropathic pruritus (NP) [4].We report a case of LETM associated with AQP-4 antibodies, preceded by IHNV and NP and followed by PTS. To our knowledge, the association of these three unusual symptoms in the same patient has never previously been reported.Case reportA 45-year-old man was admitted in September 2010 after 9 weeks of severe vomiting and hiccups (resulting in a weight loss of 11 kg ...
    Acta neurologica Belgica 01/2015; · 0.60 Impact Factor
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    ABSTRACT: Introduction The diagnostic approach for Alzheimer's disease is based on the presence of cerebral atrophy combined with the score of the mini-examination of the mental state. In this context, this study was conducted to assess the correlation between imaging and neuropsychological testing for cases of early-onset and late-onset Alzheimer's disease. Aim of the study Analysis of the clinical and paraclinical aspects of Moroccan cases with Alzheimer's disease. Methods Seventeen sporadic cases and 8 family cases were seen at the memory clinic of the Neurology Department of the University of Casablanca Ibn Rochd Hospital. A family history was obtained through a clinical interview of the patient and a yes or no self-reporting questionnaire from the guardian or other family member. The disease was considered familial if at least one additional first degree relative suffered from early-onset AD-type dementia. All patients underwent standard somatic neurological examination, cognitive function assessment, brain imaging and laboratory tests. Written consent was obtained from the patients and their guardians prior to the study. Results In our study of 25 individuals, the observed mean age of AD patients was 64.52 ± 9.30 and we observed a slight female predominance (56% versus 44%). In addition, we found a prevalence of AD of approximately 20%, increasing with age, in the population below 60 years of age. Approximately half of our patients (48%) had a score lower than 10 and were affected by severe insanity, while 28% were affected by moderate severe insanity and 24% were light to moderately insane. Twenty-five patients underwent neuroimaging, 18 of whom were assessed by MRI, while 7 were assessed by CT. All patients had hippocampal atrophy, which progressed to affect others brain regions. The blood tests showed no abnormalities in the 25 enrolled AD cases. Discussion Age is undoubtedly the main risk factor for AD; this is also the true for our cases where advanced age was responsible for the exponential increase of the disease's frequency; it reached a peak in the age group of 60–69 years. The AD diagnosis approach is based on the presence of cerebral atrophy combined with the score of the mini-examination of the mental state (MMSE). In our study, in addition to the MMSE, depending on the level of education, the clinician used other tests that do not necessarily require a level of education such as the BEC96, visual short-term or digital memory assessment, work memory assessment, language assessment test (DO80) and apraxia. Neuropsychological examination of the cases with a score of less than 10 showed severe cognitive impairment. The cases presented memory and language impairments, aphasia, visual spatial disorientation, decreased autonomy, executive dysfunction and praxis deficits, all major causes of severe dementia. Neuroimaging revealed hippocampal and cortical atrophy. Correlated with the other studies that aimed to establish links between brain alterations and neuropsychological disorders, we can conclude that a higher level of atrophy reflects a decrease in neuropsychological performance.
    L Encéphale 12/2014; · 0.60 Impact Factor
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    ABSTRACT: Nitric oxide plays a major role in the regulation of cerebral blood flow and loss of its function leads to alteration of the vascular relaxation given its central role in the physiology of the vascular system. G894T eNOS polymorphism could have adverse effects on the expression and activity of endothelial nitric oxide synthase, which can result in functional impairment of the endothelium and contribute to the development of ischemic stroke in the different models of transmission. In this study, genotyping with PCR-RFLP and HRM (high resolution melting) methods were conducted on 165 ischemic stroke patients as well as 182 controls. The goal here was to compare genotyping with PCR-RLFP primer sequences of eNOS gene (size < 300 bp) to HRM. Our data suggests a statistically significant association between G894T eNOS polymorphism and ischemic stroke in recessive, dominant and additive models with P < 0.05 and odds ratio of 2.68 (1.08–6.70), 1.78 (1.16–2.73), and 1.71 (1.21–2.43) respectively. In sum, although the sample size is relatively small, it suggests that G894T eNOS polymorphism could be a potentially important genetic marker of ischemic stroke in the Moroccan population. Future studies should be conducted in this direction taking into consideration the functional activity of eNOS.
    Meta Gene. 12/2014; 2:349–357.
  • Feuillets de Radiologie 11/2014; · 0.05 Impact Factor
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    ABSTRACT: Testez si vous avez assimilé les points importants de cet article en répondant à ce questionnaire sous forme de QCM.
    Feuillets de Radiologie 11/2014; · 0.05 Impact Factor
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    La Presse Médicale 11/2014; · 1.17 Impact Factor
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    ABSTRACT: Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a ubiquitous enzyme that catalyzes the sixth step of glycolysis and thus, serves to break down glucose for energy production. Beyond the traditional aerobic metabolism of glucose, recent studies have highlighted additional roles played by GAPDH in non-metabolic processes, such as control of gene expression and redox post-translational modifications. Neuroproteomics have revealed high affinity interactions between GAPDH and Alzheimer's disease-associated proteins, including the β-amyloid, β-amyloid precursor protein and tau. This neuronal protein interaction may lead to impairment of the GAPDH glycolytic function in Alzheimer's disease and may be a forerunner of its participation in apoptosis. The present review examines the crucial implication of GAPDH in neurodegenerative processes and clarifies its role in apoptotic cell death.
    Pathologie Biologie 09/2014; · 1.07 Impact Factor
  • Feuillets de Radiologie 09/2014; · 0.05 Impact Factor
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    ABSTRACT: Multiple sclerosis (MS) is not uncommon in children. The aim of this study was to compare early onset MS (EOMS) with adult onset MS (AOMS).
    Revue Neurologique 08/2014; · 0.60 Impact Factor
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    ABSTRACT: The diagnostic approach for Alzheimer's disease is based on the presence of cerebral atrophy combined with the score of the mini-examination of the mental state. In this context, this study was conducted to assess the correlation between imaging and neuropsychological testing for cases of early-onset and late-onset Alzheimer's disease.
    L'Encephale. 08/2014;
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    ABSTRACT: Introduction: Several recent articles have highlighted the potential involvement of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in neurodegeneration by reporting the great GAPDH non-glycolytic activity specifically in brains of subjects with Alzheimer's disease (AD). In Morocco, to our knowledge, no proteomic study was carried out in this area. The aim of this original study is to: Elucidate the critical role of GAPDH in blood of Moroccan FAD cases carrying frameshift mutations in presenilin genes by interacting with Aβ amyloide aggregation. Methods: Activity assay of GAPDH, Western blot analysis, Dot Blotting and Electron microscopy (EM) were performed on blood of FAD cases carrying mutations in presenilin genes and healthy subjects. Brain specimens, Mutant tau transgenic mice were used as controls. Results: The activity of GAPDH in FAD cases, was significantly decreased relative to healthy controls. Brain specimens of Mutant tau transgenic mice and AD case was unchanged relative to healthy controls. In contrast , the expression of GAPDH in blood of Mutant tau transgenic mice and FAD cases was decreased relative to controls. The Dot blotting examination showed an incresead Aβ accumulation in blood of FAD cases. EM examination showed a significant amyloid fibrils formation both in brain, also in blood of FAD cases. Conlusion: Our proteomic analysis, referring to others studies, report the involvement of GAPDH in AD that may influence the pathogenesis of neurodegenerative disease.
    4th International Conference on proteomics and Bioinformatics, August 04-06, 2014 Hilton-Chicago/Northbrook, Chicago, USA; 08/2014
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    ABSTRACT: Several articles have highlighted the potential involvement of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in neurodegeneration by showing a non-glycolytic activity of GAPDH specifically in the brains of subjects with Alzheimer's disease (AD). The novel aim of this study was to elucidate the critical role of GAPDH and its interaction with β-amyloid in the blood of Moroccan patients with familial AD (FAD) carrying presenilin mutations and in sporadic late onset AD (LOAD). Our results show a significant decrease in the activity of GAPDH in blood samples from patients with FAD as compared to sporadic cases and healthy controls. The expression level of GAPDH in brain specimens from mutant tau transgenic mice and patients with FAD was unchanged as compared to healthy controls. In contrast, the expression level of GAPDH in blood samples from mutant tau transgenic mice and patients with FAD was decreased as compared to sporadic cases and healthy controls. Moreover, there is an accumulation of β-amyloid aggregates in the blood samples of patients with FAD and an increase in amyloid fibrils in both the blood and brain samples of these patients. Our study adds new insight to previous ones by showing the involvement of GAPDH in AD, which may influence the pathogenesis of this neurodegenerative disease.
    Journal of Molecular Neuroscience 07/2014; · 2.76 Impact Factor
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    Presse medicale (Paris, France : 1983). 07/2014;
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    ABSTRACT: Alzheimer's disease (AD) is a progressive brain disorder that causes gradual and irreversible loss of higher brain functions and is the most common cause of dementia in the elderly,, as assessed by autopsy and clinical series. Furthermore, it has an annual incidence of approximately 3% in the 65-74 age group. This incidence rate doubles with every increment of 5 years above the age of 65. In Morocco, AD affects almost 30,000 individuals and this number will possibly increase to 75,000 by 2020 (projections of the World Health Organization (WHO)). Genetically, Alzheimer disease is caused by a mutation in one of at least 3 genes: presenilin 1 (PS1), presenilin 2 (PS2) and amyloid precursor protein(APP). Most cases are late onset and apparently sporadic, most likely as a result of a combination of environmental and non-dominant genetic factors. In Morocco, the genes predisposing individuals to Alzheimer's disease (AD) and predicting disease incidence remain elusive. The purpose of the present study was to evaluate the genetic contribution of mutations in the PS1 and PS2 genes to familial early-onset AD cases and sporadic late-onset AD cases. Seventeen sporadic late-onset AD cases and eight familial early-onset AD cases were seen at the memory clinic of the University of Casablanca Neurology Department. These patients underwent standard somatic neurological examination, cognitive function assessment, brain imaging and laboratory tests. Direct sequencing of each exon in PS1 and PS2 genes was performed on genomic DNA of AD patients. Further, we identified 1 novel frameshift mutation in the PS1 gene and 2 novel frameshift mutations in the PS2 gene. Our mutational analysis reports a correlation between clinical symptoms and genetic factors in our cases of Early Onset Alzheimer's Disease (EOAD). These putative mutations cosegregate with affected family members suggesting a direct mutagenic effect.
    Neuroscience 04/2014; · 3.33 Impact Factor
  • Feuillets de Radiologie 04/2014; · 0.05 Impact Factor
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    ABSTRACT: In Morocco, Alzheimer's disease (AD) affects almost 30,000 individuals, and this number could increase to 75,000 by 2020. To our knowledge, the genes predisposing individuals to AD and predicting disease incidence remain elusive. In this study, we aimed to evaluate the genetic contribution of mutations in the amyloid precursor protein (APP) gene exons 16 and 17 to familial and sporadic AD cases. Seventeen sporadic cases and eight family cases were seen at the memory clinic of the University of Casablanca Neurology Department. These patients underwent standard somatic neurological examination, cognitive function assessment, brain imaging, and laboratory tests. Direct sequencing of exons 16 and 17 of the APP gene was performed on genomic DNA of AD patients. In this original Moroccan study, we identified seven novel frameshift mutations in exons 16 and 17 of the APP gene. Interestingly, only one novel splice mutation was detected in a family case. There is a strong correlation between clinical symptoms and genetic factors in Moroccan patients with a family history of AD. Therefore, mutations in APP gene exons 16 and 17 may eventually become genetic markers for AD predisposition.
    Journal of Molecular Neuroscience 03/2014; · 2.76 Impact Factor
  • Feuillets de Radiologie 03/2014; · 0.05 Impact Factor
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    ABSTRACT: Introduction Multiple sclerosis (MS) is not uncommon in children. The aim of this study was to compare early onset MS (EOMS) with adult onset MS (AOMS). Methods A retrospective study including MS cases between 1997 and 2010. EOMS was defined by age at MS onset < 18 years. Data were collected using the EDMUS database (European Database of Multiple Sclerosis) including: sex, age at onset, disease duration, EDSS, score after relapse. The MSSS and the Progression Index were calculated. Patients with disease duration less than one year were excluded. MS symptoms at onset and at further relapses were also noted. These parameters were compared between the EOMS and the AOMS groups. Results Two hundred fifty-nine cases were included including 31 EOMS (11.96%). The mean follow-up was 96 months. The relapsing-remittent form was significantly more frequent in the pediatric group (94% vs 79%). Mean EDSS and MSSS scores and the percentage of fast progressors (MSSS > 5) were lower in the EOMS group. Analysis of neurological symptoms at the first MS attack and further neurological events showed a lower frequency of gait disturbances, motor symptoms and bladder symptoms in the EOMS group compared with the AOMS group. The 10-year mean EDSS score was 1.9 for EOMS and 4.1 for AOMS, after 25 years it was 4.5, and 7.27 respectively. Conclusion This study highlights the relative frequency of EOMS in our MS population. However, different severity scores showed less disability progression in EOMS patients compared with AOMS patient; irreversible disability was reached at an early age.
    Revue Neurologique 01/2014; · 0.60 Impact Factor
  • Research. 01/2014; 1.
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    ABSTRACT: Alzheimer's disease is a degenerative brain disorder, which concerns memory, cognition and behavior pattern. Its etiology is unknown, it is characterized by typical histological lesions: senile plaques and neuro-fibrillary tangles. Alzheimer's disease is a multifactorial pathology, characterized by interactions between genetic and environmental factors. Genetic factors concern first of all the exceptional monogenic forms, characterized by early onset (< 60 years), autosomal dominant forms. Mutations of the genes coding for amyloid-ß precursor protein or preselinins 1 and 2 are involved. The much more frequent sporadic forms also have genetic factors, the best studied being the apolipoprotein E4 coding allele and some more recent genotypes which will be mentioned. No causal, only symptomatic treatments are available.
    Pathologie Biologie 12/2013; · 1.07 Impact Factor

Publication Stats

151 Citations
108.70 Total Impact Points

Institutions

  • 2014
    • Centre Hospitalier Universitaire Hassan II
      Fez, Fès-Boulemane, Morocco
  • 2010–2014
    • Faculté de Medecine et de Pharmacie de Casablanca
      Anfa, Grand Casablanca, Morocco
  • 2009–2014
    • Université Hassan II Casablanca
      Anfa, Grand Casablanca, Morocco
  • 2008–2013
    • Centre Hospitalier Universitaire IBN Rochd
      Anfa, Grand Casablanca, Morocco