ArticleDer Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft2010
[NCL in animal models].
Article in Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- A mixed breed dog with neuronal ceroid lipofuscinosis is homozygous for a CLN5 nonsense mutation previously identified in Border Collies and Australian Cattle Dogs.Molecular genetics and metabolism · 2019Article
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1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Neuronal ceroid lipofuscinoses (NCL) are severe neurodegenerative diseases leading to early death. They belong to the group of lysosomal storage diseases. Epileptic seizures, dementia and motor deficits are frequent symptoms which are to be found prior to a total dismantling of personality and death. At present 10 subtypes of NCL can be distinguished from which the genetic defect is known in eight. The encoded proteins are soluble or membrane proteins whose function is still unclear in most cases. The investigation of the pathology and pathophysiology of NCL is highly dependent on animal models. Mouse models existing for all forms with a known genetic defect play a prominent role. Unfortunately, the retinal phenotype of some mouse models is milder than in humans rendering the appreciation of a positive therapeutic effect more difficult. Because of the severity of NCL, therapy strategies only established in a mouse model will be transferred to humans very quickly.
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