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Related Experiment Video

Updated: May 16, 2026

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

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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.

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Published on: August 16, 2020

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.