Abstract
The accumulation and aggregation of alpha-synuclein (α-syn) in several tissue including the brain is a major pathological hallmark in Parkinson’s disease (PD). In this study, we show that α-syn can be taken up by primary human cortical neurons, astrocytes and skin-derived fibroblasts in vitro. Our findings that brain and peripheral cells exposed to α-syn can lead to impaired mitochondrial function, leading to cellular degeneration and cell death, provides additional evidence for the involvement of mitochondrial dysfunction as a mechanism of toxicity of α-syn in human cells.
Highlights
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease (AD) [1]
Time dependent uptake of α-syn in cultured human cortical neurons, astrocytes and skin-derived fibroblasts To reaffirm the uptake of extracellular α-syn aggregates in human astrocytes, cortical neurons and fibroblasts, primary cultures were incubated with cell culture media containing Alexa-Fluor-488 labelled α-syn
Using the same dose and exposure time, we investigated the cytotoxic effect of recombinant α-syn in human astrocytes, cortical neurons and fibroblasts
Summary
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease (AD) [1] This debilitating degenerative movement disorder is characterized symptomatically by resting tremor, bradykinesia, muscle tone rigidity and impaired autonomic, sensory and cognitive function. These motor deficits are attributed to the selective loss of dopaminergic neurons projecting from the substantia nigra to the midbrain. Familial forms of PD are associated with either missense of gene mutations in the SNCA gene encoding for α-syn [8]. Mutations in the αsyn gene locus represents an important risk factor for PD in several genome-wide association studies using large cohorts worldwide [9]
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