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Parkinson Disease ll: Pathophysiology

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...

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Related Experiment Video

Updated: Jun 11, 2026

Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

Published on: June 17, 2013

Knockout of Rab27b exacerbates neuropathology in alpha-synuclein mouse models.

Kasandra Scholz, Mary A Gannon, Lehmann Matheny

Biorxiv : the Preprint Server for Biology

|January 9, 2026

Summary

Loss of Rab27b protein exacerbates alpha-synuclein pathology in Parkinson's disease models. This suggests Rab27b is a potential therapeutic target for treating synucleinopathies.

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Last Updated: Jun 11, 2026

Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease

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Development of an Alpha-synuclein Based Rat Model for Parkinson's Disease via Stereotactic Injection of a Recombinant Adeno-associated Viral Vector

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Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

Published on: July 29, 2022

Area of Science:

Neuroscience
Molecular Biology
Cell Biology

Background:

Parkinson's disease (PD) and synucleinopathies involve alpha-synuclein (αsyn) inclusions.
The small GTPase Rab27b regulates lysosomal function and αsyn degradation in neurons.
Rab27b levels are elevated in human synucleinopathies, suggesting a compensatory role.

Purpose of the Study:

To investigate the in vivo role of Rab27b in PD and synucleinopathy mouse models.
To determine if Rab27b deficiency exacerbates αsyn pathology and neurodegeneration.

Main Methods:

Utilized A53T genetic αsyn overexpression and adeno-associated virus (AAV) αsyn overexpression mouse models.
Generated Rab27b knockout (KO) mice crossed with αsyn models.
Assessed motor behavior, survival, αsyn levels (total, proteinase-K resistant, phosphorylated S129), neuroinflammation (astrocyte and microglial activation), and dopaminergic neuron loss.

Main Results:

Rab27b KO did not affect motor behavior or survival in A53T mice.
Rab27b KO increased proteinase-K resistant and phosphorylated S129 αsyn in multiple brain regions of A53T mice.
Rab27b KO led to increased astrocyte and microglial activation in A53T mice.
Rab27b KO accelerated dopaminergic cell loss in the substantia nigra in the AAV αsyn model.

Conclusions:

Loss of Rab27b function significantly elevates neuropathology in PD-relevant brain regions.
Rab27b plays a crucial protective role against αsyn accumulation and neurodegeneration.
Rab27b is validated as a potential therapeutic target for synucleinopathies.