Literature DB >> 9113203

Follow-up study of subunit c of mitochondrial ATP synthase (SCMAS) in Batten disease and in unrelated lysosomal disorders.

M Elleder1, J Sokolová, M Hrebícek.   

Abstract

Immunohistochemical and biochemical studies of subunit c of mitochondrial ATP synthase (SCMAS) storage were carried out in neuronal ceroid lipofuscinosis (NCL) and in a series of unrelated inherited and acquired lysosomal disorders. In the NCL group, represented by the late infantile, early juvenile and juvenile types, SCMAS storage was generalized neurovisceral, with considerable difference in the visceral storage pattern between the types. In late infantile NCL the SCMAS storage was intensive and corresponded to the generalized, autofluorescent, uniformly curvilinear material, irrespective of the cell type affected. In both early juvenile and juvenile NCLs the SCMAS storage was strong and almost uniform in brain neurons, but did not correlate entirely with the visceral autofluorescent storage pool, being undetectable in autofluorescent storage deposits in a constant set of tissues. In the adult (Kufs) type, the brain neurons were stained with various intensity. In infantile NCL, SCMAS storage was restricted to some of the persisting neurons. In a series of inherited lysosomal enzymopathies and acquired lysosomal disorders, excessive SCMAS accumulation was found only in secondary neuronal lipopigments. It occurred as an early and more uniform phenomenon in mucopolysaccharidosis types I, II, IIIA and in polysulphatase deficiency, or as a delayed varied phenomenon in protracted variants of mucolipidosis I, Niemann-Pick types A and C, and GM2 and GM1 gangliosidoses. Neuronal ageing led to an irregular increase in immunodetectable SCMAS epitope in some neuronal lipofuscin granules. There was no evidence of significant SCMAS lysosomal accumulation in non-neural cells in the whole group, regardless of whether lipofuscin or ceroid accumulation occurred or not. The neuronal SCMAS storage is thus nosologically a common unspecific phenomenon, which is especially amplified in NCL. The specificity of the NCL storage process is shown by the fact that even lysosomes of non-neuronal cells in NCL accumulate SCMAS.

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Year:  1997        PMID: 9113203     DOI: 10.1007/s004010050629

Source DB:  PubMed          Journal:  Acta Neuropathol        ISSN: 0001-6322            Impact factor:   17.088


  31 in total

Review 1.  Correlations between genotype, ultrastructural morphology and clinical phenotype in the neuronal ceroid lipofuscinoses.

Authors:  Sara E Mole; Ruth E Williams; Hans H Goebel
Journal:  Neurogenetics       Date:  2005-09-28       Impact factor: 2.660

2.  Monitoring autophagy in lysosomal storage disorders.

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4.  Cathepsin D deficiency induces lysosomal storage with ceroid lipofuscin in mouse CNS neurons.

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Journal:  J Neurosci       Date:  2000-09-15       Impact factor: 6.167

5.  Lysosomal membrane permeability stimulates protein aggregate formation in neurons of a lysosomal disease.

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6.  Murine cathepsin F deficiency causes neuronal lipofuscinosis and late-onset neurological disease.

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7.  Neuromelanin organelles are specialized autolysosomes that accumulate undegraded proteins and lipids in aging human brain and are likely involved in Parkinson's disease.

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Journal:  NPJ Parkinsons Dis       Date:  2018-06-05

8.  A critical tryptophan and Ca2+ in activation and catalysis of TPPI, the enzyme deficient in classic late-infantile neuronal ceroid lipofuscinosis.

Authors:  Salomon Kuizon; Kathleen DiMaiuta; Marius Walus; Edmund C Jenkins; Marisol Kuizon; Elizabeth Kida; Adam A Golabek; Daniel O Espinoza; Raju K Pullarkat; Mohammed A Junaid
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9.  Progranulin Gene Therapy Improves Lysosomal Dysfunction and Microglial Pathology Associated with Frontotemporal Dementia and Neuronal Ceroid Lipofuscinosis.

Authors:  Andrew E Arrant; Vincent C Onyilo; Daniel E Unger; Erik D Roberson
Journal:  J Neurosci       Date:  2018-01-29       Impact factor: 6.167

Review 10.  Oxidative stress and autophagy in the regulation of lysosome-dependent neuron death.

Authors:  Violetta N Pivtoraiko; Sara L Stone; Kevin A Roth; John J Shacka
Journal:  Antioxid Redox Signal       Date:  2009-03       Impact factor: 8.401

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