Abstract
The NCLs (neuronal ceroid lipofuscinosis) are forms of neurodegenerative disease that affect people of all ages and ethnicities but are most prevalent in children. Commonly known as Batten disease, this debilitating neurological disorder is comprised of 13 different subtypes that are categorized based on the particular gene that is mutated (CLN1-8, CLN10-14). The pathological mechanisms underlying the NCLs are not well understood due to our poor understanding of the functions of NCL proteins. Only one specific treatment (enzyme replacement therapy) is approved, which is for the treating the brain in CLN2 disease. Hence there remains a desperate need for further research into disease-modifying treatments. In this review, we present and evaluate the genes, proteins and studies performed in the social amoeba, nematode, fruit fly, zebrafish, mouse and large animals pertinent to NCL. In particular, we highlight the use of multicellular model organisms to study NCL protein function, pathology and pathomechanisms. Their use in testing novel therapeutic approaches is also presented. With this information, we highlight how future research in these systems may be able to provide new insight into NCL protein functions in human cells and aid in the development of new therapies.
Original language | English |
---|---|
Article number | 165614 |
Journal | Biochimica et Biophysica Acta - Molecular Basis of Disease |
Volume | 1866 |
Issue number | 9 |
DOIs | |
Publication status | Published - 1 Sept 2020 |
Externally published | Yes |
Bibliographical note
Funding Information:The Huber laboratory is supported by grants from the Canadian Institutes of Health Research (PJT165873) and the Natural Sciences and Engineering Research Council of Canada (RGPIN-2018-04855). The Hughes laboratory is supported by funding from the BDSRA and Charlotte and Gweneth Gray Foundation, USA, Neurological Foundation of New Zealand and Cure Kids New Zealand. WL is funded by an UK Medical Research Council Biomedical Catalyst: Developmental Pathway Funding Scheme grant. AM is supported by UK Medical Research Council grant MR/P012965/1. RIT is supported by UK Biotechnology and Biological Sciences Research Council grant BB/N008472/1. CR was supported by the European Union?s Horizon 2020 research and innovation programme under grant agreement No. 666918 (BATCure).
Funding Information:
The Huber laboratory is supported by grants from the Canadian Institutes of Health Research ( PJT165873 ) and the Natural Sciences and Engineering Research Council of Canada ( RGPIN-2018-04855 ). The Hughes laboratory is supported by funding from the BDSRA and Charlotte and Gweneth Gray Foundation, USA, Neurological Foundation of New Zealand and Cure Kids New Zealand. WL is funded by an UK Medical Research Council Biomedical Catalyst: Developmental Pathway Funding Scheme grant. AM is supported by UK Medical Research Council grant MR/P012965/1. RIT is supported by UK Biotechnology and Biological Sciences Research Council grant BB/N008472/1. CR was supported by the European Union ‘s Horizon 2020 research and innovation programme under grant agreement No. 666918 (BATCure).
Publisher Copyright:
© 2019 Elsevier B.V.
Keywords
- Batten disease
- Disease mechanism
- Experimental therapy
- Lysosomal storage disorder
- Model organism
- Neuronal ceroid lipofuscinosis
- Pathology
ASJC Scopus subject areas
- Molecular Medicine
- Molecular Biology