NDLI: A20 in Multiple Sclerosis and Parkinson’s Disease: Clue to a Common Dysregulation of Anti-Inflammatory Pathways?

Content Provider	Springer Nature Link
Author	Perga, Simona Martire, Serena Montarolo, Francesca Navone, Nicole D. Calvo, Andrea Fuda, Giuseppe Marchet, Alberto Leotta, Daniela Chiò, Adriano Bertolotto, Antonio
Copyright Year	2017
Abstract	Chronic inflammation significantly contributes to the pathogenesis of several neurodegenerative disorders. In physiological conditions, a chronic inflammatory state is prevented through the termination of the acute inflammatory response once the triggering insult is eliminated. Several mechanisms regulate the resolution of inflammation. Among these, a potent inhibitor of the pro-inflammatory NF-kB signaling known as A20 has emerged as a key player. Recent studies have shown reduced blood levels of A20 in the patients of diverse chronic inflammatory diseases. Similar results have also been demonstrated in patients of multiple sclerosis (MS), a neurodegenerative disease characterized by persisting inflammation. In the present study, we investigate whether other similar neurodegenerative disorders such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) also demonstrate deregulated levels of A20 expression as compared to healthy controls (HC) and treatment-naive MS patients. Our results confirm previous data that the A20 expression is reduced in whole blood of MS patients as compared to HC. Additionally, we demonstrate that significantly diminished A20 expression is also evident in PD patients. The dysregulation of the A20 pathway could then contribute to the persistence of inflammation in these disorders. It would thus be interesting to investigate further whether such commonly deregulated pathways between different inflammatory diseases could represent novel targets for therapy.
Starting Page	1
Ending Page	7
Page Count	7
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	32
Issue Number	1
e-ISSN	14763524
Language	English
Publisher	Springer US
Publisher Date	2017-03-23
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	A20/TNFAIP3 NF-kB Systemic chronic inflammation Multiple sclerosis Alzheimer’s diseases Parkinson diseases Amyotrophic lateral sclerosis Neurosciences Neurology Neurochemistry Pharmacology/Toxicology Neurobiology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

The Kynurenine Pathway and Inflammation in Amyotrophic Lateral Sclerosis

BMAA and Neurodegenerative Illness

The Potential Role of BMAA in Neurodegeneration

Prospects for redox-based therapy in neurodegenerative diseases

Causes and Consequences of MicroRNA Dysregulation in Neurodegenerative Diseases

Melatonin Antioxidative Defense: Therapeutical Implications for Aging and Neurodegenerative Processes

Pathway Analysis of Two Amyotrophic Lateral Sclerosis GWAS Highlights Shared Genetic Signals with Alzheimer’s Disease and Parkinson’s Disease

Concurrent multiple sclerosis and amyotrophic lateral sclerosis: where inflammation and neurodegeneration meet?

Doxycycline Suppresses Microglial Activation by Inhibiting the p38 MAPK and NF-kB Signaling Pathways

A20 in Multiple Sclerosis and Parkinson’s Disease: Clue to a Common Dysregulation of Anti-Inflammatory Pathways?

Similar Documents

The Kynurenine Pathway and Inflammation in Amyotrophic Lateral Sclerosis

BMAA and Neurodegenerative Illness

The Potential Role of BMAA in Neurodegeneration

Prospects for redox-based therapy in neurodegenerative diseases

Causes and Consequences of MicroRNA Dysregulation in Neurodegenerative Diseases

Melatonin Antioxidative Defense: Therapeutical Implications for Aging and Neurodegenerative Processes

Pathway Analysis of Two Amyotrophic Lateral Sclerosis GWAS Highlights Shared Genetic Signals with Alzheimer’s Disease and Parkinson’s Disease

Concurrent multiple sclerosis and amyotrophic lateral sclerosis: where inflammation and neurodegeneration meet?

Doxycycline Suppresses Microglial Activation by Inhibiting the p38 MAPK and NF-kB Signaling Pathways

A20 in Multiple Sclerosis and Parkinson’s Disease: Clue to a Common Dysregulation of Anti-Inflammatory Pathways?