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Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

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Updated: Jun 23, 2026

Studying Pre-formed Fibril Induced &#945;-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons
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Cell-Type-Selective Cortical Pathology and Functional Deficits in Synucleinopathy.

Xiaofeng Yang, Changyi Ji, Soomin Song

    Biorxiv : the Preprint Server for Biology
    |June 22, 2026
    PubMed
    Summary
    This summary is machine-generated.

    Alpha-synuclein (α-syn) pathology selectively harms excitatory neurons in the motor cortex during early synucleinopathy. This neuronal vulnerability disrupts brain network balance and causes motor deficits.

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    Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains
    09:27

    Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

    Published on: January 5, 2016

    Area of Science:

    • Neuroscience
    • Pathology
    • Molecular Biology

    Background:

    • Synucleinopathies are characterized by alpha-synuclein (α-syn) aggregates in the cerebral cortex, correlating with motor symptoms and altered neuronal activity.
    • The precise mechanisms linking α-syn pathology to cortical network dysfunction and impaired motor control remain unclear.

    Purpose of the Study:

    • To investigate the pathophysiological characteristics of early-stage synucleinopathy in a mouse model with minimal nigrostriatal degeneration.
    • To elucidate the cell-type-specific alterations in cortical neurons and their contribution to motor deficits.

    Main Methods:

    • Utilized a multi-disciplinary approach including in vivo two-photon imaging and ex vivo whole-cell recordings.
    • Examined transgenic mice expressing mutant human α-syn to assess cortical neuronal activity and α-syn inclusion patterns.

    Main Results:

    • Identified distinct alteration patterns in excitatory and parvalbumin (PV)-expressing inhibitory cortical neurons during fine motor learning.
    • Observed selectively altered intrinsic properties in excitatory neurons, with preferential α-syn accumulation in these cells compared to PV neurons.

    Conclusions:

    • Demonstrated cell-type-selective vulnerability of excitatory neurons in the motor cortex during early synucleinopathy.
    • Concluded that disrupted excitatory/inhibitory balance and dysregulated cortical plasticity in these vulnerable neurons drive early motor symptoms.