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Mutant alpha-synuclein causes age-dependent neuropathology in monkey brain.

Weili Yang1, Guohao Wang2, Chuan-En Wang3

  • 1State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|May 29, 2015
PubMed
Summary

Aging rhesus monkeys show increased alpha-synuclein and neurodegeneration, mirroring Parkinson's disease (PD) pathology. Mutant alpha-synuclein exacerbates these age-related changes, highlighting primate models for PD research.

Keywords:
Parkinson'sagingdegenerationneuriteprimate

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Area of Science:

  • Neuroscience
  • Aging Research
  • Neurodegenerative Diseases

Background:

  • Parkinson's disease (PD) is an age-dependent neurodegenerative disorder.
  • Rodent models have limitations in studying age-related PD pathology due to short lifespans.
  • Key genes implicated in PD include Parkin, PINK1, and alpha-synuclein.

Purpose of the Study:

  • To investigate age-dependent changes in PD-related protein expression in nonhuman primate brains.
  • To examine the neuropathological effects of mutant alpha-synuclein (A53T) in aged monkeys.
  • To explore the interaction between A53T and neurofascin in the context of aging and PD.

Main Methods:

  • Analysis of brain tissues from rhesus monkeys of varying ages (2-3, 7-8, and >15 years).
  • Examination of protein expression levels for Parkin, PINK1, and alpha-synuclein.
  • Stereotaxic injection of lentiviral vectors expressing mutant A53T alpha-synuclein into the substantia nigra.
  • Investigation of A53T interaction with neurofascin in vivo and in cultured neuronal cells.

Main Results:

  • Alpha-synuclein levels increased with age in monkey brains, while Parkin and PINK1 decreased or remained unchanged.
  • Aging exacerbated the accumulation of A53T in neurites and associated neuropathology, including reactive astrocytes and axonal degeneration.
  • Aged monkey brains showed increased interaction between A53T and neurofascin.
  • Overexpression of A53T induced neuritic toxicity, which was mitigated by neurofascin.

Conclusions:

  • Nonhuman primate brains exhibit age-dependent pathological and molecular alterations relevant to Parkinson's disease.
  • Mutant alpha-synuclein's toxicity is amplified by aging in primate models.
  • Neurofascin plays a role in modulating A53T-induced neuritic toxicity, suggesting potential therapeutic targets.