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Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation
Published on: June 26, 2018
Age-dependent α-synuclein aggregation in the Microcebus murinus lemur primate.
Marie-Hélène Canron1, Martine Perret, Anne Vital
1Univ. de Bordeaux, Institut des Maladies Neurodégénératives , UMR 5293, F-33000 Bordeaux, France.
Scientific Reports
|December 4, 2012
Summary
Mouse lemur primates naturally develop alpha-synuclein aggregates with age, mirroring human synucleinopathies. This finding suggests Microcebus murinus as a valuable model for studying age-related diseases like Alzheimer's and Parkinson's.
Area of Science:
- Neuroscience
- Primate Models
- Aging Research
Background:
- Age-dependent amyloid-beta deposition is known in Microcebus murinus.
- This suggests potential for modeling other age-related neurological disorders.
Purpose of the Study:
- To investigate Microcebus murinus as a model for age-related synucleinopathy.
- To characterize the distribution of alpha-synuclein and its modified forms in aging primate brains.
Main Methods:
- Brain tissue analysis of Microcebus murinus aged 1.5 to 10 years.
- Characterization of amyloid-beta, alpha-synuclein, phospho-Ser129 alpha-synuclein, and nitrated alpha-synuclein.
Main Results:
- Intracytoplasmic alpha-synuclein aggregates were found exclusively in aged animals.
- These aggregates were immunoreactive for phospho-Ser129 and nitrated alpha-synuclein.
- Age-dependent alpha-synuclein aggregation occurs spontaneously in this primate model.
Conclusions:
- Microcebus murinus exhibits spontaneous, age-dependent alpha-synuclein aggregation.
- This primate species serves as a potential model for studying age-associated synucleinopathies.
- It may also be useful for preclinical testing of therapeutics for Alzheimer's and Parkinson's diseases.
