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. Issue 3 (March 1993)

• Record Type: Journal Article
• Authors: Ferrer, I; Tuñón, T; Serrano, M T; Casas, R; Alcántara, S; Zújar, M J; Rivera, R M
• Is Part Of: Journal of neurology, neurosurgery and psychiatry. Volume 56:Issue 3(1993)
• Page Start: 257
• Page End: 261
• Publication Date: 1993-03
• Subjects: Neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; Psychiatry -- Periodicals; 616.8
• DOI: 10.1136/jnnp.56.3.257
• Languages: English
• ISSNs: 0022-3050

Abstract

Abstract : 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.