Roles for the TGFß superfamily in the development and survival of midbrain dopaminergic neurons.

Typeset version

 

TY  - JOUR
  - Review Articles
  - Hegarty, S.V., Collins, L.M, Gavin, A.M., Roche, S.L., Wyatt, S.L., Sullivan, A.M., O'Keeffe, G.W.
  - 2014
  - October
  - Roles for the TGFß superfamily in the development and survival of midbrain dopaminergic neurons.
  - Author
  - Validated
  - 0
  - Scopus: 18 ()
  - The adult midbrain contains 75% of all dopaminergic neurons in the CNS. Within the midbrain, these neurons are divided into three anatomically and functionally distinct clusters termed A8, A9 and A10. The A9 group plays a functionally non-redundant role in the control of voluntary movement, which is highlighted by the motor syndrome that results from their progressive degeneration in the neurodegenerative disorder, Parkinson's disease. Despite 50 years of investigation, treatment for Parkinson's disease remains symptomatic, but an intensive research effort has proposed delivering neurotrophic factors to the brain to protect the remaining dopaminergic neurons, or using these neurotrophic factors to differentiate dopaminergic neurons from stem cell sources for cell transplantation. Most neurotrophic factors studied in this context have been members of the transforming growth factor ß (TGFß) superfamily. In recent years, an intensive research effort has focused on understanding the function of these proteins in midbrain dopaminergic neuron development and their role in the molecular architecture that regulates the development of this brain region, with the goal of applying this knowledge to develop novel therapies for Parkinson's disease. In this review, the current evidence showing that TGFß superfamily members play critical roles in the regulation of midbrain dopaminergic neuron induction, differentiation, target innervation and survival during embryonic and postnatal development is analysed, and the implications of these findings are discussed.
  - Molecular Neurobiology
  - 559
  - 573
  - 10.1007/s12035-014-8639-3
DA  - 2014/10
ER  - 
@article{V286292551,
   = {Review Articles},
   = {Hegarty,  S.V. and  Collins,  L.M and  Gavin,  A.M. and  Roche,  S.L. and  Wyatt,  S.L. and  Sullivan,  A.M. and  O'Keeffe,  G.W. },
   = {2014},
   = {October},
   = {Roles for the TGFß superfamily in the development and survival of midbrain dopaminergic neurons.},
   = {Author},
   = {Validated},
   = {0},
   = {Scopus: 18 ()},
   = {{The adult midbrain contains 75% of all dopaminergic neurons in the CNS. Within the midbrain, these neurons are divided into three anatomically and functionally distinct clusters termed A8, A9 and A10. The A9 group plays a functionally non-redundant role in the control of voluntary movement, which is highlighted by the motor syndrome that results from their progressive degeneration in the neurodegenerative disorder, Parkinson's disease. Despite 50 years of investigation, treatment for Parkinson's disease remains symptomatic, but an intensive research effort has proposed delivering neurotrophic factors to the brain to protect the remaining dopaminergic neurons, or using these neurotrophic factors to differentiate dopaminergic neurons from stem cell sources for cell transplantation. Most neurotrophic factors studied in this context have been members of the transforming growth factor ß (TGFß) superfamily. In recent years, an intensive research effort has focused on understanding the function of these proteins in midbrain dopaminergic neuron development and their role in the molecular architecture that regulates the development of this brain region, with the goal of applying this knowledge to develop novel therapies for Parkinson's disease. In this review, the current evidence showing that TGFß superfamily members play critical roles in the regulation of midbrain dopaminergic neuron induction, differentiation, target innervation and survival during embryonic and postnatal development is analysed, and the implications of these findings are discussed.}},
   = {{Molecular Neurobiology}},
  pages = {559--573},
   = {10.1007/s12035-014-8639-3},
  source = {IRIS}
}
OTHER_PUB_TYPEReview Articles
AUTHORSHegarty, S.V., Collins, L.M, Gavin, A.M., Roche, S.L., Wyatt, S.L., Sullivan, A.M., O'Keeffe, G.W.
YEAR2014
MONTHOctober
TITLERoles for the TGFß superfamily in the development and survival of midbrain dopaminergic neurons.
RESEARCHER_ROLEAuthor
STATUSValidated
PEER_REVIEW0
TIMES_CITEDScopus: 18 ()
SEARCH_KEYWORD
REFERENCE
ABSTRACTThe adult midbrain contains 75% of all dopaminergic neurons in the CNS. Within the midbrain, these neurons are divided into three anatomically and functionally distinct clusters termed A8, A9 and A10. The A9 group plays a functionally non-redundant role in the control of voluntary movement, which is highlighted by the motor syndrome that results from their progressive degeneration in the neurodegenerative disorder, Parkinson's disease. Despite 50 years of investigation, treatment for Parkinson's disease remains symptomatic, but an intensive research effort has proposed delivering neurotrophic factors to the brain to protect the remaining dopaminergic neurons, or using these neurotrophic factors to differentiate dopaminergic neurons from stem cell sources for cell transplantation. Most neurotrophic factors studied in this context have been members of the transforming growth factor ß (TGFß) superfamily. In recent years, an intensive research effort has focused on understanding the function of these proteins in midbrain dopaminergic neuron development and their role in the molecular architecture that regulates the development of this brain region, with the goal of applying this knowledge to develop novel therapies for Parkinson's disease. In this review, the current evidence showing that TGFß superfamily members play critical roles in the regulation of midbrain dopaminergic neuron induction, differentiation, target innervation and survival during embryonic and postnatal development is analysed, and the implications of these findings are discussed.
PUBLISHER_LOCATION
PUBLISHERMolecular Neurobiology
EDITORS
ISBN_ISSN
EDITION
URL
START_PAGE559
END_PAGE573
DOI_LINK10.1007/s12035-014-8639-3
FUNDING_BODY
GRANT_DETAILS