A stem cell-based assay platform demonstrates alpha-synuclein dependent synaptic dysfunction in patient-derived cortical neurons.
Andrew J WhiteKaris A ClarkKellianne D AlexanderNagendran RamalingamTracy L Young-PearseUlf DettmerDennis J SelkoeGary P H HoPublished in: NPJ Parkinson's disease (2024)
Alpha-synuclein (αS)-rich Lewy bodies and neurites in the cerebral cortex correlate with the presence of dementia in Parkinson disease (PD) and Dementia with Lewy bodies (DLB), but whether αS influences synaptic vesicle dynamics in human cortical neurons is unknown. Using a new iPSC-based assay platform for measuring synaptic vesicle cycling, we found that in human cortical glutamatergic neurons, increased αS from either transgenic expression or triplication of the endogenous locus in patient-derived neurons reduced synaptic vesicle cycling under both stimulated and spontaneous conditions. Thus, using a robust, easily adopted assay platform, we show for the first time αS-induced synaptic dysfunction in human cortical neurons, a key cellular substrate for PD dementia and DLB.
Keyphrases
- parkinson disease
- high throughput
- endothelial cells
- spinal cord
- induced pluripotent stem cells
- mild cognitive impairment
- stem cells
- prefrontal cortex
- cognitive impairment
- deep brain stimulation
- high glucose
- pluripotent stem cells
- oxidative stress
- high intensity
- spinal cord injury
- mesenchymal stem cells
- brain injury
- long non coding rna
- cell therapy
- stress induced