Calbindin D-28K and parvalbumin immunoreactivity in the frontal cortex in patients with frontal lobe dementia of non-Alzheimer type associated with amyotrophic lateral sclerosis

The morphology and distribution of local-circuit neurons (interneurons) were examined, by calbindin D-28k and parvalbumin immunocytochemistry, in the frontal cortex (area 8) in two patients with frontal lobe dementia of non-Alzheimer type associated with classical amyotrophic lateral sclerosis (ALS)...

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Detalles Bibliográficos
Autores: Ferrer, Isidro (Ferrer Abizanda), Tuñón, Teresa, Serrano Piñol, M. Teresa, Casas, Rosaura, Alcántara Horrillo, Soledad, Zújar, M. J., Rivera, R. M.
Tipo de recurso: artículo
Fecha de publicación:1993
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/25546
Acceso en línea:https://hdl.handle.net/2445/25546
Access Level:acceso abierto
Palabra clave:Esclerosi lateral amiotròfica
Lòbul frontal
Demència
Amyotrophic lateral sclerosis
Frontal lobe
Dementia
Descripción
Sumario:The morphology and distribution of local-circuit neurons (interneurons) were examined, by calbindin D-28k and parvalbumin immunocytochemistry, in the frontal cortex (area 8) in two patients with frontal lobe dementia of non-Alzheimer type associated with classical amyotrophic lateral sclerosis (ALS), and in seven normal cases. The density of calbindin D-28k immunoreactive cells was dramatically reduced in ALS patients, but the density of parvalbumin-immunoreactive neurons was preserved. Decreased density of calbindin D-28k-immunoreactive neurons, which are mainly located in the upper cortical layers, may interfere with the normal processing of cortico-cortical connections, whereas integrity of parvalbumin-immunoreactive cells may be associated with the preservation of the major inhibitory intracortical circuits in patients with frontal lobe dementia.