Swiss Archives of Neurology, Psychiatry and Psychotherapy

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Open AccessCase Report

Neuroimmunology: facts and clinical enigmas

by A. Steck and B. Steck

Swiss Arch. Neurol. Psychiatry Psychother. 1998, 149(4), 184-188; https://doi.org/10.4414/sanp.1998.01049 - 1 Jan 1998

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Abstract

We review here the evidence reminding us that the immune system and the brain have a close relationship that until recently has remained hidden. We begin with some of the facts concerning brain immune system interactions looking at the anatomical barriers and the [...] Read more.

We review here the evidence reminding us that the immune system and the brain have a close relationship that until recently has remained hidden. We begin with some of the facts concerning brain immune system interactions looking at the anatomical barriers and the mediators of immune and nervous system functions. We analyze the immunological events as well as some of the poorly understood symptoms of a devastating autoimmune disease of the brain such as multiple sclerosis. Finally, we consider the clinical enigmas where there is evidence that in stress situations the brain can influence the immune system through modification of the hypothalamic-pituitary-adrenal axis (HPA), a key player in stress responses. Full article

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Open AccessArticle

Amyotrophic lateral sclerosis Ig recognize CNS epitopes when passively transferred to mouse

by M. Schluep, B. Roth-Wicky and F. Regli

Swiss Arch. Neurol. Psychiatry Psychother. 1998, 149(4), 178-183; https://doi.org/10.4414/sanp.1998.01048 - 1 Jan 1998

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Abstract

Pathogenesis of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease, is unknown and several hypotheses are still under investigation. In order to test the occurrence of an autoimmune phenomenon in ALS (and in acquired lower motor neuron disease (LMND)), we (i) tested ALS/LMND sera [...] Read more.

Pathogenesis of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease, is unknown and several hypotheses are still under investigation. In order to test the occurrence of an autoimmune phenomenon in ALS (and in acquired lower motor neuron disease (LMND)), we (i) tested ALS/LMND sera on mouse central nervous system tissue sections, and (ii) passively immunized mice with ALS/LMND immunoglobulins (Ig). In in vitro and passive transfer studies, ALS/ LMND Ig (but not control Ig) labelled both neurons and astrocytes in the brain, brainstem, spinal cord and cerebellum of mice. These results emphasize the potential contribution of ALS/ LMND Ig to neuronal death process, and the role that astrocytes, that have the capacity to take part actively to immune responses, may play in this disorder Full article

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Open AccessArticle

Early onset Alzheimer’s disease in a large Swiss family

by G. Leuba Gfeller, K. Saini, P. Schwed, L. Lannfelt and A. Savioz

Swiss Arch. Neurol. Psychiatry Psychother. 1998, 149(4), 170-177; https://doi.org/10.4414/sanp.1998.01047 - 1 Jan 1998

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Abstract

Among the risk factors influencing the pathogenesis of Alzheimer’s disease (AD), genetic factors play a major role. The genes for early onset familial Alzheimer’s disease (FAD) include the ßamyloid protein precursor (APP) on chromosome 21, as well as the genes for presenilins 1 [...] Read more.

Among the risk factors influencing the pathogenesis of Alzheimer’s disease (AD), genetic factors play a major role. The genes for early onset familial Alzheimer’s disease (FAD) include the ßamyloid protein precursor (APP) on chromosome 21, as well as the genes for presenilins 1 and 2 on chromosomes 14 and 1. On the other hand, the E4 allele of the apolipoprotein E gene is considered as a risk factor for late onset FAD and sporadic AD, and decreases onset age in FAD with an APP mutation.We are studying a Swiss family with an early onset AD, for which we have built up the pedigree based on 10 generations. We have identified numerous AD cases in 3 generations with a necropsy confirmation of the clinical diagnosis. The clinical features of the affected members are those of classical AD with a duration of the disease from 5 to 20 years. Several members presented epileptic characteristics, even before the onset of the disease. The brain pathology is almost similar to that of sporadic AD, but with a heavier degeneration of pyramidal neurons and fibres in the subiculum and hippocampal regions. The massive cortical degeneration involves primary sensory areas such as the visual cortex. Subcortical regions are affected as well. Partial genetic analysis has been performed on DNA from six necropsy cases and demonstrated the presence of the ApoE4 allele in all the six cases.The pathogenic mutations previously described in the APP and presenilin 2 genes were not detected. Screening for possible mutations in the presenilin 1 gene is now underway. Full article

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Open AccessArticle

Gènes, mutations et maladies: nouveaux liens entre recherche fondamentale, industrie et clinique

by Stefan Catsicas

Swiss Arch. Neurol. Psychiatry Psychother. 1998, 149(4), 163-169; https://doi.org/10.4414/sanp.1998.01044 - 1 Jan 1998

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Abstract

Notre connaissance du génome humain augmente chaque année avec un rythme exponentiel. Parallèlement à ces progrès, la biologie moléculaire et la bioinformatique permettent d’identifier des mutations qui sont responsables de maladies importantes. Cette nouvelle information est d’une importance capitale pour la recherche biomédicale. [...] Read more.

Notre connaissance du génome humain augmente chaque année avec un rythme exponentiel. Parallèlement à ces progrès, la biologie moléculaire et la bioinformatique permettent d’identifier des mutations qui sont responsables de maladies importantes. Cette nouvelle information est d’une importance capitale pour la recherche biomédicale. En effet, le fait de savoir qu’une altération du génome est responsable – ou est l’une des causes – d’une maladie permet de cibler les approches thérapeutiques sur le mécanisme d’action du gène impliqué. Cette approche, dite «caractérisation génétique fonctionnelle» nécessite des compétences que l’on retrouve distribuée parmi les centres de recherche liniques, académiques et industriels. Full article

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Open AccessReview

The genetic basis of movement disorders

by E. M. Valentea, A. R. Bentivoglio and Alberto Albanesec

Swiss Arch. Neurol. Psychiatry Psychother. 1998, 149(4), 157-162; https://doi.org/10.4414/sanp.1998.01046 - 1 Jan 1998

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Abstract

Recent developments in molecular genetics have had a profound influence on the diagnosis and classification of inherited movement disorders. Parkinson’s disease occurs in familial aggregation and one gene has recently been mapped. Eight genes responsible for different inherited dystonia syndromes have been mapped, [...] Read more.

Recent developments in molecular genetics have had a profound influence on the diagnosis and classification of inherited movement disorders. Parkinson’s disease occurs in familial aggregation and one gene has recently been mapped. Eight genes responsible for different inherited dystonia syndromes have been mapped, and two of them have been identified. Essential tremor also occurs in familial aggregation and a first gene has recently been mapped. Huntington’s disease is caused by the expansion of an unstable trinucleotide repeat sequence. Molecular diagnosis can easily be performed, and the study of the effects of the repeat expansion on the function of the encoded protein will help in understanding the pathogenesis of the disease. Wilson’s disease is caused by a large number of different mutations in a copper-binding ATPase gene. The genetic basis of Gilles de la Tourette’s syndrome is still obscure.The available data indicate that movement disorders are in most cases genetically heterogeneous. Molecular genetics will provide new classifications for these rather common disorders. Full article

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Open AccessReview

Traitement des accidents ischémiques cérébraux en phase aiguë: bilan et perspectives

by F. Nicoli and J. Bogousslavsky

Swiss Arch. Neurol. Psychiatry Psychother. 1998, 149(4), 145-156; https://doi.org/10.4414/sanp.1998.01045 - 1 Jan 1998

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Abstract

La mise au point d’un traitement efficace des accidents vasculaires cérébraux ischémiques aigus (AICA) représente un problème important de santé publique. Des avancées significatives sont en train de se produire concernant les traitements thrombolytiques et neuroprotecteurs. Cette revue se propose de faire le [...] Read more.

La mise au point d’un traitement efficace des accidents vasculaires cérébraux ischémiques aigus (AICA) représente un problème important de santé publique. Des avancées significatives sont en train de se produire concernant les traitements thrombolytiques et neuroprotecteurs. Cette revue se propose de faire le point sur ces progrès thérapeutiques et d’évaluer quelles pourraient être les stratégies thérapeutiques futures des AICA. Cette mise au point est basée, en partie, sur une recherche par MEDLINE, des articles publiés entre 1993 et 1997, et dont le sujet principal concerne l’ischémie cérébrale, les traitements thrombolytiques et les médicaments neuroprotecteurs. L’utilisation d’un activateur du plasminogène tissulaire (rt-PA) chez des patients sélectionnés présentant un AICA datant de moins de 3 heures a récemment été approuvée, aux Etats-Unis, par la Federal Drug Administration. Mais, en Europe, ce traitement est encore en phase d’expérimentation clinique compte tenu des résultats contradictoires de l’essai européen ECASS évaluant cette molécule. Le traitement par streptokinase, quant à lui, s’est révélé non seulement inefficace mais aussi associé à un risque accru d’hémorragie cérébrale.Toutefois, ce dernier n’a pas été évalué avec un délai d’initiation du traitement aussi précoce que celui imposé concernant l’utilisation du rt-PA. L’efficacité de diverses stratégies neuroprotectrices a été démontrée dans des modèles animaux, mais ces résultats expérimentaux n’ont jamais pu être extrapolables à l’homme jusqu’à présent. Plusieurs médicaments neuroprotecteurs sont en cours d’évaluation dans le cadre d’essais thérapeutiques déjà avancés, dont certains pourraient démontrer un effet bénéfique clinique suffisant pour qu’ils soient approuvés comme traitement des AICA. Dans l’avenir, la combinaison des deux stratégies, thrombolytique et neuroprotectrice, sera utilisée pour essayer d’obtenir une récupération neurologique maximale. Mais, cela ne sera possible que par une sélection et une gestion thérapeutique rigoureuses des patients présentant un AICA. La rapidité d’intervention thérapeutique, en particulier, restera une condition sine qua non pour espérer atteindre cet objectif Full article

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Open AccessEditorial

Editorial: Quelques travaux des groupes lausannois

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 1998, 149(4), 144; https://doi.org/10.4414/sanp.1998.01043 - 1 Jan 1998

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Abstract

La communauté lausannoise des neurosciences continue de se développer aussi bien dans ses aspects liés à la recherche fondamentale que du côté clinique [...] Full article

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Open AccessArticle

Changements au niveau de la rédaction

by EMH Swiss Medical Publishers Ltd.

Swiss Arch. Neurol. Psychiatry Psychother. 1998, 149(4), 143; https://doi.org/10.4414/sanp.1998.01042 - 1 Jan 1998

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Abstract

Nous souhaitons informer nos lecteurs d’un certain nombre de changements qui sont intervenus au niveau de la rédaction [...] Full article

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Swiss Arch. Neurol. Psychiatry Psychother., Volume 149, Issue 4 (01 1998) – 8 articles , Pages 143-188

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