Amyloid‐β in mitochondrial disease: mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processing

Abstract There is increasing evidence that common molecular pathways in neurons are closely linked with mitochondrial function and that mitochondrial dysfunction is connected to various forms of neurodegenerative diseases. For instance, mitochondria are involved in amyloid‐β (Aβ) deposition in Alzhe...

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Main Authors: Veronika Boczonadi, Rita Horvath
Format: Article
Language:English
Published: Springer Nature 2016-01-01
Series:EMBO Molecular Medicine
Online Access:https://doi.org/10.15252/emmm.201506050
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author Veronika Boczonadi
Rita Horvath
author_facet Veronika Boczonadi
Rita Horvath
author_sort Veronika Boczonadi
collection DOAJ
description Abstract There is increasing evidence that common molecular pathways in neurons are closely linked with mitochondrial function and that mitochondrial dysfunction is connected to various forms of neurodegenerative diseases. For instance, mitochondria are involved in amyloid‐β (Aβ) deposition in Alzheimer's disease, although the exact molecular pathways remain largely unknown. Brunetti et al (2015) in this issue of EMBO Molecular Medicine provide a novel link between Aβ accumulation and mitochondria. A pathogenic mutation in a Norwegian family in the mitochondrial metallopeptidase PITRM1 is found to underlie a novel mitochondrial neurodegenerative phenotype associated with Aβ accumulation.
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institution Kabale University
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language English
publishDate 2016-01-01
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spelling doaj-art-a30b22eb8e684a94b2a93e4cd96f19312025-08-20T04:02:55ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842016-01-018317317510.15252/emmm.201506050Amyloid‐β in mitochondrial disease: mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processingVeronika Boczonadi0Rita Horvath1Institute of Genetic Medicine, Wellcome Trust Centre for Mitochondrial Research, Newcastle UniversityInstitute of Genetic Medicine, Wellcome Trust Centre for Mitochondrial Research, Newcastle UniversityAbstract There is increasing evidence that common molecular pathways in neurons are closely linked with mitochondrial function and that mitochondrial dysfunction is connected to various forms of neurodegenerative diseases. For instance, mitochondria are involved in amyloid‐β (Aβ) deposition in Alzheimer's disease, although the exact molecular pathways remain largely unknown. Brunetti et al (2015) in this issue of EMBO Molecular Medicine provide a novel link between Aβ accumulation and mitochondria. A pathogenic mutation in a Norwegian family in the mitochondrial metallopeptidase PITRM1 is found to underlie a novel mitochondrial neurodegenerative phenotype associated with Aβ accumulation.https://doi.org/10.15252/emmm.201506050
spellingShingle Veronika Boczonadi
Rita Horvath
Amyloid‐β in mitochondrial disease: mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processing
EMBO Molecular Medicine
title Amyloid‐β in mitochondrial disease: mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processing
title_full Amyloid‐β in mitochondrial disease: mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processing
title_fullStr Amyloid‐β in mitochondrial disease: mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processing
title_full_unstemmed Amyloid‐β in mitochondrial disease: mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processing
title_short Amyloid‐β in mitochondrial disease: mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processing
title_sort amyloid β in mitochondrial disease mutation in a human metallopeptidase links amyloidotic neurodegeneration with mitochondrial processing
url https://doi.org/10.15252/emmm.201506050
work_keys_str_mv AT veronikaboczonadi amyloidbinmitochondrialdiseasemutationinahumanmetallopeptidaselinksamyloidoticneurodegenerationwithmitochondrialprocessing
AT ritahorvath amyloidbinmitochondrialdiseasemutationinahumanmetallopeptidaselinksamyloidoticneurodegenerationwithmitochondrialprocessing