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   <dc:title>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</dc:title>
   <dc:creator>Ferrer, Isidro (Ferrer Abizanda)</dc:creator>
   <dc:creator>Tuñón, Teresa</dc:creator>
   <dc:creator>Serrano Piñol, M. Teresa</dc:creator>
   <dc:creator>Casas, Rosaura</dc:creator>
   <dc:creator>Alcántara Horrillo, Soledad</dc:creator>
   <dc:creator>Zújar, M. J.</dc:creator>
   <dc:creator>Rivera, R. M.</dc:creator>
   <dc:subject>Esclerosi lateral amiotròfica</dc:subject>
   <dc:subject>Lòbul frontal</dc:subject>
   <dc:subject>Demència</dc:subject>
   <dc:subject>Amyotrophic lateral sclerosis</dc:subject>
   <dc:subject>Frontal lobe</dc:subject>
   <dc:subject>Dementia</dc:subject>
   <dc:description>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.</dc:description>
   <dc:date>2012-05-14T10:37:07Z</dc:date>
   <dc:date>2012-05-14T10:37:07Z</dc:date>
   <dc:date>1993</dc:date>
   <dc:type>info:eu-repo/semantics/article</dc:type>
   <dc:identifier>0022-3050</dc:identifier>
   <dc:identifier>https://hdl.handle.net/2445/25546</dc:identifier>
   <dc:identifier>92192</dc:identifier>
   <dc:identifier>8459241</dc:identifier>
   <dc:language>eng</dc:language>
   <dc:relation>Reproducció del document publicat a: http://dx.doi.org/10.1136/jnnp.56.3.257</dc:relation>
   <dc:relation>Journal of Neurology Neurosurgery and Psychiatry, 1993, num. 56, p. 257-261</dc:relation>
   <dc:relation>http://dx.doi.org/10.1136/jnnp.56.3.257</dc:relation>
   <dc:rights>(c) British Medical Journal, 1993</dc:rights>
   <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
   <dc:format>5 p.</dc:format>
   <dc:format>application/pdf</dc:format>
   <dc:publisher>BMJ Publishing Group</dc:publisher>
   <dc:source>Articles publicats en revistes (Patologia i Terapèutica Experimental)</dc:source>
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