Literature DB >> 1381122

Changes in Ca(2+)-binding proteins in human neurodegenerative disorders.

C W Heizmann1, K Braun.   

Abstract

The cellular distribution of Ca(2+)-binding proteins has been extensively studied during the past decade. These proteins have proved to be useful neuronal markers for a variety of functional brain systems and their circuitries. Their major roles are assumed to be Ca2+ buffering and transport, and regulation of various enzyme systems. Since cellular degeneration is accompanied by impaired Ca2+ homeostasis, a protective role for Ca(2+)-binding proteins in certain neuron populations has been postulated. As massive neuronal degeneration takes place in several brain diseases of humans, such as Alzheimer's disease, Parkinson's disease and epilepsy, changes in the expression of Ca(2+)-binding proteins have therefore been studied during the course of these diseases. Although the data from these studies are inconsistent, the detection and quantification of Ca(2+)-binding proteins and the neuron populations in which they occur may nevertheless be useful to estimate, for example, the location and extent of brain damage in the various neurological disorders. If future studies advance our knowledge about the physiological functions of these proteins, the neuronal systems in which they are expressed may become important therapeutical targets for preventing neuronal death in an array of neurodegenerative diseases.

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Year:  1992        PMID: 1381122     DOI: 10.1016/0166-2236(92)90067-i

Source DB:  PubMed          Journal:  Trends Neurosci        ISSN: 0166-2236            Impact factor:   13.837


  67 in total

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Authors:  L D Brewer; V Thibault; K C Chen; M C Langub; P W Landfield; N M Porter
Journal:  J Neurosci       Date:  2001-01-01       Impact factor: 6.167

2.  Suppression of calbindin-D28k expression exacerbates SCA1 phenotype in a disease mouse model.

Authors:  Parminder J S Vig; Jinrong Wei; Qingmei Shao; Maripar E Lopez; Rebecca Halperin; Jill Gerber
Journal:  Cerebellum       Date:  2012-09       Impact factor: 3.847

3.  Mutational analysis of dendritic Ca2+ kinetics in rodent Purkinje cells: role of parvalbumin and calbindin D28k.

Authors:  Hartmut Schmidt; Klaus M Stiefel; Peter Racay; Beat Schwaller; Jens Eilers
Journal:  J Physiol       Date:  2003-06-17       Impact factor: 5.182

4.  Immunoreactivity for calretinin and calbindin in the vestibular nuclear complex of the monkey.

Authors:  Joan S Baizer; James F Baker
Journal:  Exp Brain Res       Date:  2005-12-21       Impact factor: 1.972

Review 5.  Circuits formultisensory integration and attentional modulation through the prefrontal cortex and the thalamic reticular nucleus in primates.

Authors:  Basilis Zikopoulos; Helen Barbas
Journal:  Rev Neurosci       Date:  2007       Impact factor: 4.353

6.  Ataxia and altered dendritic calcium signaling in mice carrying a targeted null mutation of the calbindin D28k gene.

Authors:  M S Airaksinen; J Eilers; O Garaschuk; H Thoenen; A Konnerth; M Meyer
Journal:  Proc Natl Acad Sci U S A       Date:  1997-02-18       Impact factor: 11.205

7.  Combinations of AMPA receptor subunit expression in individual cortical neurons correlate with expression of specific calcium-binding proteins.

Authors:  M Kondo; R Sumino; H Okado
Journal:  J Neurosci       Date:  1997-03-01       Impact factor: 6.167

8.  Progressive decline in avoidance learning paralleled by inflammatory neurodegeneration in transgenic mice expressing interleukin 6 in the brain.

Authors:  C J Heyser; E Masliah; A Samimi; I L Campbell; L H Gold
Journal:  Proc Natl Acad Sci U S A       Date:  1997-02-18       Impact factor: 11.205

9.  Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced by L-DOPA?

Authors:  Mariza Bortolanza; Fernando E Padovan-Neto; Roberta Cavalcanti-Kiwiatkoski; Maurício Dos Santos-Pereira; Miso Mitkovski; Rita Raisman-Vozari; Elaine Del-Bel
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2015-07-05       Impact factor: 6.237

10.  Resveratrol Directly Controls the Activity of Neuronal Ryanodine Receptors at the Single-Channel Level.

Authors:  Jacob G Kraus; Peter Koulen
Journal:  Mol Neurobiol       Date:  2019-08-02       Impact factor: 5.590

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