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Drug Target Insights

Synopsis: An open access, peer reviewed electronic journal that covers drug treatment targets.


Indexing: 6 major databases. Pubmed indexing for NIH-funded research.

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About this journal

ISSN: 1177-3928



Aims and scope:

Drug Target Insights covers current developments in all areas of the field of clinical therapeutics. The journal has two specific areas of focus:

  • On molecular drug targets, including disease-specific proteins, receptors, enzymes, and genes.
  • The journal seeks to elucidate the impact of new therapeutic agents on patient acceptability, preference, satisfaction and quality of life.

Drug Target Insights seeks to be the most up-to-date journal for those who need to be informed of the latest and most important developments in the field. The journal seeks to be the most reliable and up-to-date journal in this field by offering rapid and credible pre-production submission processing to authors. By publishing in open-access format, authors are able to communicate with the widest possible group of readers.

Editorial standards and procedures:

Submissions, excluding editorials, letters to the editor and dedications, will be peer reviewed by two reviewers.  Reviewers are required to provide fair, balanced and constructive reports.  

Under our Fairness in Peer Review Policy authors may appeal against reviewers' recommendations which are ill-founded, unobjective or unfair.  Appeals are considered by the Editor in Chief or Associate Editor.

Papers are not sent to peer reviewers following submission of a revised manuscript. Editorial decisions on re-submitted papers are based on the author's response to the initial peer review report.

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This journal is indexed by the following services:

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This journal has been awarded a SPARC Europe Seal. The Seal is an initiative of SPARC Europe (Scholarly Publishing and Academic Resources Coalition) and the Directory of Open Access Journals (DOAJ) which is awarded to journals applying a Creative Commons CC-BY copyright license and that make journal metadata accessible to DOAJ.  

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National Institutes of Health Public Access Policy compliant:

As of April 7 2008, the US NIH Public Access Policy requires that all peer reviewed articles resulting from research carried out with NIH funding be deposited in the Pubmed Central archive.

If you are an NIH employee or grantee Libertas Academica will ensure that you comply with the policy by depositing your paper at Pubmed Central on your behalf. 



 
 
 


Targeting Insulin-Like Growth Factor-1 Signaling into the Central Nervous System for Promoting Myelin Repair

Authors: Nadine Wilczak, Jacques De Keyser and Daniel Chesik
Publication Date: 18 Apr 2008
Drug Target Insights 2008:3 37-44

Nadine Wilczak, Jacques De Keyser and Daniel Chesik

Department of Neurology, University Medical Center Groningen, the Netherlands.

Abstract

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system (CNS). Without myelin, nerve impulses in the CNS are slowed or stopped, leading to a constellation of neurological symptoms. Demyelination also provides a permitting condition for irreversible axonal damage. Remyelination of MS lesions largely fails, although oligodendrocyte precursors and premyelinating oligodendrocytes (myelin forming cells) are present in many demyelinated plaques. Insulin-like growth factor (IGF)-1 is a growth factor that should provide the appropriate signals to promote repair of MS lesions, because it acts as a survival factor for cells of the oligodendrocyte lineage and stimulates myelin synthesis. In a pilot study on MS patients, no detectable remyelinating effects in the CNS were observed following subcutaneous administration of IGF-1. A number of reasons might explain a lack of beneficial effects: a) it is unlikely that subcutaneous administration of IGF-1 provides sufficient passage across the blood-brain-barrier and into the CNS, b) the biological actions of IGF-1 are tightly regulated by several insulin-like growth factor binding proteins (IGFBPs), which become upregulated in the demyelinated lesions and may prevent access of IGF-1 to its receptor, c) IGF-1 not only acts on oligodendrocytes, but also stimulates the proliferation of astrocytes, which form the glial scar that impedes repair processes. In this review, we will discuss strategies to enhance IGF-1 signaling in the CNS utilizing a) alternative routes of administration, b) IGF analogues that displace IGF-1 from regulatory IGFBPs and c) strategies to selectively target IGF-1 to oligodendrocytes.



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