Cells rely on molecular scaffolds to allow different organelles to interact. New work from King's College London shows how this scaffolding disintegrates in neurodegenerative diseases like Alzheimer's disease and amyotrophic lateral sclerosis. By studying cultured neurons, the researchers could identify the proteins that help bring the mitochondria (the cell's powerhouse) and the endoplasmic reticulum (which stores calcium and makes proteins) together, as well as how this scaffolding loosened and ceased functioning in the presence of a mutation linked to amyotrophic lateral sclerosis and frontotemporal dementia. By adding levels of these scaffolding proteins to the cell, the scientists were able to re-establish the strong bonds between the mitochondria and endoplasmic reticulum. They have concluded in Nature Communications that these findings make a good potential therapeutic target.
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Molecular 'scaffold' could hold key to new dementia treatments | neuroscientistnews.com
Journal article: ER–mitochondria associations are regulated by the VAPB–PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43. Nature Communications, 2014. doi: 10.1038/ncomms4996
Image credit: dandeluca/Flickr
Neuroscience Research Techniques
Cells rely on molecular scaffolds to allow different organelles to interact. New work from King's College London shows how this scaffolding disintegrates in neurodegenerative diseases like Alzheimer's disease and amyotrophic lateral sclerosis. By studying cultured neurons, the researchers could identify the proteins that help bring the mitochondria (the cell's powerhouse) and the endoplasmic reticulum (which stores calcium and makes proteins) together, as well as how this scaffolding loosened and ceased functioning in the presence of a mutation linked to amyotrophic lateral sclerosis and frontotemporal dementia. By adding levels of these scaffolding proteins to the cell, the scientists were able to re-establish the strong bonds between the mitochondria and endoplasmic reticulum. They have concluded in Nature Communications that these findings make a good potential therapeutic target.
Read more:
Journal article: ER–mitochondria associations are regulated by the VAPB–PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43. Nature Communications, 2014. doi: 10.1038/ncomms4996
Image credit: dandeluca/Flickr
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