The relationship between parkin and protein aggregation in neurodegenerative diseases

The most prominent changes in neurodegenerative diseases are protein accumulation and inclusion formation. Several neurodegenerative diseases, including Alzheimer’s, the Synucleinopathies and Tauopathies share several overlapping clinical symptoms manifest in Parkinsonism, cognitive declin...

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Main Authors: Preeti J Khandelwal, Charbel Moussa
Format: Article
Language:English
Published: Frontiers Media S.A. 2010-06-01
Series:Frontiers in Psychiatry
Subjects:
tau
Online Access:http://journal.frontiersin.org/Journal/10.3389/fpsyt.2010.00015/full
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spelling doaj-8b2f8e2f83af434db4a94af0820d90102020-11-24T21:05:40ZengFrontiers Media S.A.Frontiers in Psychiatry1664-06402010-06-01110.3389/fpsyt.2010.000151633The relationship between parkin and protein aggregation in neurodegenerative diseasesPreeti J Khandelwal0Charbel Moussa1Charbel Moussa2Georgetown University Medical CenterGeorgetown University Medical CenterGeorgetown University Medical CenterThe most prominent changes in neurodegenerative diseases are protein accumulation and inclusion formation. Several neurodegenerative diseases, including Alzheimer’s, the Synucleinopathies and Tauopathies share several overlapping clinical symptoms manifest in Parkinsonism, cognitive decline and dementia. As degeneration progresses in the disease process, clinical symptoms suggest convergent pathological pathways. Biochemically, protein cleavage, ubiquitination and phosphorylation seem to play fundamental roles in protein aggregation, inclusion formation and inflammatory responses. In the following we provide a synopsis of the current knowledge about protein accumulation and astrogliosis as a common denominator in neurodegenerative diseases, and we propose insights into protein degradation and anti-inflammation. We review the E3-ubiquitin ligase and other possible functions of parkin as a suppressant of inflammatory signs and a strategy to clear amyloid proteins in neurodegenerative diseases.http://journal.frontiersin.org/Journal/10.3389/fpsyt.2010.00015/fullDementiaTauopathiestauTDP-43Aβα-Synuclein
collection DOAJ
language English
format Article
sources DOAJ
author Preeti J Khandelwal
Charbel Moussa
Charbel Moussa
spellingShingle Preeti J Khandelwal
Charbel Moussa
Charbel Moussa
The relationship between parkin and protein aggregation in neurodegenerative diseases
Frontiers in Psychiatry
Dementia
Tauopathies
tau
TDP-43
Aβ
α-Synuclein
author_facet Preeti J Khandelwal
Charbel Moussa
Charbel Moussa
author_sort Preeti J Khandelwal
title The relationship between parkin and protein aggregation in neurodegenerative diseases
title_short The relationship between parkin and protein aggregation in neurodegenerative diseases
title_full The relationship between parkin and protein aggregation in neurodegenerative diseases
title_fullStr The relationship between parkin and protein aggregation in neurodegenerative diseases
title_full_unstemmed The relationship between parkin and protein aggregation in neurodegenerative diseases
title_sort relationship between parkin and protein aggregation in neurodegenerative diseases
publisher Frontiers Media S.A.
series Frontiers in Psychiatry
issn 1664-0640
publishDate 2010-06-01
description The most prominent changes in neurodegenerative diseases are protein accumulation and inclusion formation. Several neurodegenerative diseases, including Alzheimer’s, the Synucleinopathies and Tauopathies share several overlapping clinical symptoms manifest in Parkinsonism, cognitive decline and dementia. As degeneration progresses in the disease process, clinical symptoms suggest convergent pathological pathways. Biochemically, protein cleavage, ubiquitination and phosphorylation seem to play fundamental roles in protein aggregation, inclusion formation and inflammatory responses. In the following we provide a synopsis of the current knowledge about protein accumulation and astrogliosis as a common denominator in neurodegenerative diseases, and we propose insights into protein degradation and anti-inflammation. We review the E3-ubiquitin ligase and other possible functions of parkin as a suppressant of inflammatory signs and a strategy to clear amyloid proteins in neurodegenerative diseases.
topic Dementia
Tauopathies
tau
TDP-43
Aβ
α-Synuclein
url http://journal.frontiersin.org/Journal/10.3389/fpsyt.2010.00015/full
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