Missing pieces in the Parkinson's disease puzzle

@article{Obeso2010MissingPI,
  title={Missing pieces in the Parkinson's disease puzzle},
  author={Jose A. Obeso and Maria C. Rodriguez-Oroz and Christopher G. Goetz and Concepci{\'o} Mar{\'i}n and Jeffrey H. Kordower and Manuel Rodriguez and Etienne C. Hirsch and Matthew J Farrer and Anthony H. V. Schapira and Glenda M. Halliday},
  journal={Nature Medicine},
  year={2010},
  volume={16},
  pages={653-661}
}
Parkinson's disease is a neurodegenerative process characterized by numerous motor and nonmotor clinical manifestations for which effective, mechanism-based treatments remain elusive. Here we discuss a series of critical issues that we think researchers need to address to stand a better chance of solving the different challenges posed by this pathology. 

Epidemiology of Parkinson's disease.

Molecular Targets for Improvement of Parkinson's Disease Therapy

An overview of molecular targets whose attack can contribute to improve the therapy of Parkinson’s disease and putative targets for new therapeutical measures are presented.

Parkinson disease: Parkinson disease clinical subtypes and their implications

A new study supports distinct clinical subtypes of Parkinson disease that could have implications for understanding the etiology of this condition.

[Future drug targets for Parkinson's disease].

  • E. Hirsch
  • Biology, Psychology
    Bulletin de l'Academie nationale de medecine
  • 2012

Animal models of neurodegenerative diseases.

The purpose of this review is to present the main animal models for AD, PD, and Huntington's disease.

Ten Unsolved Questions About Neuroinflammation in Parkinson's Disease

  • E. HirschD. Standaert
  • Psychology, Biology
    Movement disorders : official journal of the Movement Disorder Society
  • 2020
10 unanswered questions related to neuroinflammatory processes in Parkinson's disease are reviewed with the goal of stimulating research in the field and accelerating the clinical development of neuroprotective therapies based on anti‐inflammatory strategies.

Etiology and pathogenesis of Parkinson's disease

  • A. SchapiraP. Jenner
  • Biology, Medicine
    Movement disorders : official journal of the Movement Disorder Society
  • 2011
Focusing on those events that characterize Parkinson's disease, namely, mitochondrial dysfunction and Lewy body formation, may be the key to further advancing the understanding of pathogenesis and to taking these mechanisms forward as a means of defining targets for neuroprotection.

Brain‐derived neurotrophic factor attenuates cognitive impairment and motor deficits in a mouse model of Parkinson's disease

The neuroprotective roles of brain‐derived neurotrophic factor (BDNF) in PD mice are investigated and the underlying mechanisms are revealed via the injection of adeno‐associated viruses with BDNF gene.

Can Parkinson's disease pathology be propagated from one neuron to another?

...

References

SHOWING 1-10 OF 126 REFERENCES

What causes cell death in Parkinson's disease?

Many of the advances in the last decade regarding the identification of new targets for the treatment of PD based on understanding the molecular mechanisms of how mutations in genes linked to PD cause neurodegeneration are reviewed.

Molecular basis of Parkinson's disease.

This work discusses what has been learnt in the study of these genes and how these genes may contribute to the pathogenesis of Parkinson's disease through different molecular pathways, and considers how these pathways might converge to lead to the onset of Parkinson’s disease.

Genetics of Parkinson disease: paradigm shifts and future prospects

  • M. Farrer
  • Biology, Medicine
    Nature Reviews Genetics
  • 2006
Genetic insights provide the rationale for new strategies for prevention or therapy, and have led to animal models of disease in which these strategies can be tested.

Is Parkinson's disease a prion disorder?

It is demonstrated that nerve cells that overexpress tagged α-synuclein can transmit the protein to neural stem cells in both in vitro and in vivo models, which could explain the remarkable finding that human embryonic dopamine nerve cells implanted into the striatum of patients with Parkinson's disease develop PD pathology with loss of dopamine markers and classic Lewy bodies.

Research in motion: the enigma of Parkinson's disease pathology spread

The paper discusses the possible underlying mechanisms and their implications for how pathology spreads in Parkinson's disease and demonstrates that grafted healthy neurons can gradually develop the same pathology as host neurons in the diseased brains.

Neurobiology and treatment of Parkinson's disease.

  • A. Schapira
  • Biology, Medicine
    Trends in pharmacological sciences
  • 2009

The genetics of Parkinson's syndromes: a critical review.

α-Synuclein Locus Triplication Causes Parkinson's Disease

Mutations in the α-synuclein gene ( SNCA ) in the Contursi kindred ([ 1 ][1]) implicated this gene in Parkinson's disease (PD). Subsequently, α-synuclein was identified as the major component of Lewy

Dopamine neurons implanted into people with Parkinson's disease survive without pathology for 14 years

Postmortem analysis of five subjects with Parkinson's disease 9–14 years after transplantation of fetal midbrain cell suspensions revealed surviving grafts that included dopamine and serotonin

Lewy body–like pathology in long-term embryonic nigral transplants in Parkinson's disease

Fourteen years after transplantation into the striatum of an individual with Parkinson's disease, grafted nigral neurons were found to have Lewy body–like inclusions that stained positively for
...