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Updated: Jun 25, 2025

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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
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Cortico-amygdala synaptic structural abnormalities produced by templated aggregation of α-synuclein.
Biorxiv : the Preprint Server for Biology
|May 27, 2024
Summary
Pathologic alpha-synuclein (α-syn) in the basolateral amygdala (BLA) alters synaptic structure, not synapse number, in mice. These changes in synaptic architecture may explain cognitive and emotional impairments in synucleinopathies like Parkinson's disease (PD) and Dementia with Lewy bodies (DLB).
Area of Science:
- Neuroscience
- Synaptic Biology
- Neurodegenerative Diseases
Background:
- Parkinson's disease (PD) and Dementia with Lewy bodies (DLB) feature alpha-synuclein (α-syn) inclusions in the amygdala, impacting cognition and emotion.
- The basolateral amygdala (BLA) is crucial for these functions and receives input from the thalamus and cortex.
- Understanding how α-syn pathology affects the BLA requires animal models.
Conclusions:
- Pathologic α-synuclein causes significant alterations to BLA synaptic architecture, not synapse loss.
- These structural changes may underlie the behavioral and cognitive deficits observed in synucleinopathies.
- Findings align with observations in human DLB cortex and non-human primate PD models.
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