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Modeling early phenotypes of Parkinson’s disease by age-induced midbrain-striatum assembloids
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Modeling early phenotypes of Parkinson’s disease by age-induced midbrain-striatum assembloids
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Journal Article
Modeling early phenotypes of Parkinson’s disease by age-induced midbrain-striatum assembloids
2024
Overview
Parkinson’s disease, an aging-associated neurodegenerative disorder, is characterised by nigrostriatal pathway dysfunction caused by the gradual loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain. Human in vitro models are enabling the study of the dopaminergic neurons’ loss, but not the dysregulation within the dopaminergic network in the nigrostriatal pathway. Additionally, these models do not incorporate aging characteristics which potentially contribute to the development of Parkinson’s disease. Here we present a nigrostriatal pathway model based on midbrain-striatum assembloids with inducible aging. We show that these assembloids can develop characteristics of the nigrostriatal connectivity, with catecholamine release from the midbrain to the striatum and synapse formation between midbrain and striatal neurons. Moreover, Progerin-overexpressing assembloids acquire aging traits that lead to early neurodegenerative phenotypes. This model shall help to reveal the contribution of aging as well as nigrostriatal connectivity to the onset and progression of Parkinson’s disease.
Generation of a midbrain-striatum assembloid with progerin overexpression as an in vitro model of possessing aging and senescence characteristics for studying Parkinson’s disease.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 13/107
/ Aging
/ Animals
/ Biomedical and Life Sciences
/ Corpus Striatum - metabolism
/ Dopaminergic Neurons - metabolism
/ Dopaminergic Neurons - pathology
/ Humans
/ Neurons
/ Parkinson Disease - metabolism
/ Parkinson Disease - pathology
/ Parkinson Disease - physiopathology
/ Substantia Nigra - metabolism
