Journal
CELL DEATH & DISEASE
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41419-017-0022-7
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Funding
- Alzheimer's Research UK
- Alzheimer's Society
- Guy's & St Thomas' Charity
- Parkinson's UK
- MRC
- BBSRC
- MNDA
- Wellcome Trust
- Alzheimers Research UK [ARUK-PG2014-5, ART-PG2011-5, ARUK-PG2017B-3, ARUK-EG2013B-1] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BB/L019299/1] Funding Source: researchfish
- Medical Research Council [MR/R022666/1, G0501573] Funding Source: researchfish
- Motor Neurone Disease Association [Miller/Oct12/863-792] Funding Source: researchfish
- Parkinson's UK [G-1308] Funding Source: researchfish
- BBSRC [BB/L019299/1] Funding Source: UKRI
- MRC [G0501573, MR/R022666/1] Funding Source: UKRI
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Fronto-temporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are two related and incurable neurodegenerative diseases. Features of these diseases include pathological protein inclusions in affected neurons with TAR DNA-binding protein 43 (TDP-43), dipeptide repeat proteins derived from the C9ORF72 gene, and fused in sarcoma (FUS) representing major constituent proteins in these inclusions. Mutations in C9ORF72 and the genes encoding TDP-43 and FUS cause familial forms of FTD/ALS which provides evidence to link the pathology and genetics of these diseases. A large number of seemingly disparate physiological functions are damaged in FTD/ALS. However, many of these damaged functions are regulated by signalling between the endoplasmic reticulum and mitochondria, and this has stimulated investigations into the role of endoplasmic reticulum-mitochondria signalling in FTD/ALS disease processes. Here, we review progress on this topic.
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