The Canadian Journal of Neurological Sciences

نویسندگان

  • Cheryl Ezrin-Waters
  • L. Resch
چکیده

The nucleus basalis of Meynert has been studied extensively in the recent literature. Interest in this nucleus has resulted from the discovery that it is a major source of cortical cholinergic input and that there is neuronal loss in the nucleus basalis in some dementing illnesses. Consistent and severe involvement of the nucleus basalis of Meynert has been found in Alzheimer's disease and in the dementia accompanying Parkinson's disease. Occasional involvement is present in other dementing illnesses, such as progressive supranuclear palsy, Parkinsonism-Dementia complex of Guam, dementia pugilistica, Pick's disease, Korsakoff's syndrome, Down's Syndrome and CreutzfeldtJakob disease. Huntington's disease spares this nucleus. However, the role of the nucleus in cognitive function is as yet undetermined. Even its alteration with normal aging remains controversial. This review details the pathological studies of this region to date, with particular emphasis on the dementias. Its role in the dementias of Alzheimer's disease and Parkinson's disease is specifically addressed. RESUME: Le noyau basal de Meynert — Une revue Le noyau basal de Meynert (nbM) a ete intensement etudie dans la litterature recente. L'interet porte a ce noyau resulte du fait qu'il est l'origine principale des fibres cholinergiques a destination corticale et que c'est a ce niveau qu'il y a perte neuronale dans certaines maladies avec demence. Une atteinte constante et severe de ce noyau a ete trouvee dans la maladie d'Alzheimer et dans la demence accompagnant la maladie de Parkinson. On retrouve une atteinte occasionnelle dans plusieurs autres entites, comme le complexe Parkinson-demence du Guam, la demence pugilistique, la maladie de Pick, le syndrome de Korsakoff, le syndrome de Down et la maladie de Creutzfeldt-Jakob. Par contre le noyau est epargne dans la maladie de Huntington. On ne connait pas encore le role exact de ce noyau dans les fonctions cognitives. Meme les modifications inherentes au vieillissement sont controversies. La presente revue insiste sur les modifications neuropathologiques de cette region, surtout dans les demences et, particulierement, dans la demence accompagnant les maladies d'Alzheimer et de Parkinson. Can. J. Neurol. Sci. 1986; 13:8-14 Theodor Meynert, a teacher of neuroanatomy, neuropathology and psychiatry, believed that neuropsychiatric disease could be understood on the basis of structural changes in the brain. In this regard, he was particularly interested in the relationship between cortical and subcortical structures. He described a cluster of cells (a "ganglion") in the substantia innominata and named it the nucleus of the ansa lenticularis, but it was later renamed the nucleus basalis of Meynert (nbM) by Kolliker in 1896. Unfortunately, there has been much confusion (in the literature) with regard to terminology. The nbM has been called the nucleus of the ansa lenticularis, the preoptic magnocellular nucleus, the nucleus of the ansa peduncularis, the substantia innominata, the nucleus of the horizontal limb of the diagonal band, and nucleus of the septal plane. Interest in this nucleus was to remain dormant until the discovery of intracytoplasmic inclusions, called Lewy bodies, in 1913. These were felt to be pathognomonic for idiopathic Parkinson's disease, and this was a method by which idiopathic Parkinson's disease could be differentiated from post-encephalitic Parkinsonism where Lewy bodies were absent. Recently there has been a resurgence of interest in the nucleus basalis of Meynert since it was shown to be a major source of cortical cholinergic input. It has been studied extensively in senile dementia of the Alzheimer type (DAT) as well as other illnesses, such as Parkinson's and Huntington's diseases, in which dementia is a component. This article will review the anatomy, neurochemistry, function and the pathology of the nucleus basalis of Meynert. Its involvement in DAT as well as its possible role as a more general substrate for dementia will be specifically addressed.

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تاریخ انتشار 2015