Common threads in neurodegenerative disorders of aging

@article{Beal2006CommonTI,
  title={Common threads in neurodegenerative disorders of aging},
  author={M. Flint Beal and Ella Bossy‐Wetzel and Steven Finkbeiner and Gary Fiskum and Benoit I. Giasson and Carl Johnson and Zaven S. Khachaturian and Virginia M. -Y. Lee and David Nicholls and Hemachandra Reddy and Ian Reynolds and David B. Teplow and Leon Thal and John Q. Trojanowski and Dominic M. Walsh and Ronald Wetzel and Nancy S Wexler and Anne B. Young and Lisa J Bain},
  journal={Alzheimer's \& Dementia},
  year={2006},
  volume={2},
  pages={322-326}
}

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References

SHOWING 1-8 OF 8 REFERENCES

Common mechanisms of amyloid oligomer pathogenesis in degenerative disease

  • C. Glabe
  • Biology
    Neurobiology of Aging
  • 2006

Mitochondria take center stage in aging and neurodegeneration

  • M. Beal
  • Biology
    Annals of neurology
  • 2005
There is strong evidence from genetics and transgenic mouse models that mitochondrial dysfunction results in neurodegeneration and may contribute to the pathogenesis of Alzheimer’s disease, Parkinson's disease, Huntington's Disease, amyotrophic lateral sclerosis, hereditary spastic paraplegia, and cerebellar degenerations.

Neurodegenerative diseases: new concepts of pathogenesis and their therapeutic implications.

A perspective on pathogenesis suggests that a wide variety of neurodegenerative diseases can be grouped mechanistically as brain amyloidoses, an outlook that yields novel insights into potential therapeutic approaches that may be applicable across the broad spectrum of neuro degenerative disease.

What is the role of protein aggregation in neurodegeneration?

It is suggested that protein aggregation is pathogenic, but several lines of evidence indicate that inclusion bodies are not the main cause of toxicity, and probably represent a cellular protective response.

Nitric oxide‐induced mitochondrial fission is regulated by dynamin‐related GTPases in neurons

It is reported that mitochondria undergo profound fission in response to nitric oxide in cortical neurons of primary cultures and persistent mitochondrial fission may play a causal role in NO‐mediated neurotoxicity.

In Situ Respiration and Bioenergetic Status of Mitochondria in Primary Cerebellar Granule Neuronal Cultures Exposed Continuously to Glutamate*

It is concluded that excitotoxicity under these conditions is not because of an ATP deficit or uncoupling, and mitochondria maintain the same respiratory capacity as in control cells.

Automated microscope system for determining factors that predict neuronal fate.

An automated imaging and analysis system that enables us to follow the fates of individual cells and intracellular proteins over time and adapted survival analysis methods to determine whether and how factors measured during longitudinal analysis predict a particular biological outcome are determined.