Senescence and PD-linked gene mutations have reciprocal pathological interactions where (i) senescence causes PD-relevant neuropathology; (ii) PD-linked mutant genes (alpha-synuclein, LRRK2, Vps35) cause premature senescence; and (iii) senescence participates in neuropathology caused by PD-linked genes. First, we will use novel mouse models of premature senescence to test whether premature senescence in specific cell types causes PD-like neuropathology. Second, we will combine mouse models of senescence and familial PD to test whether senescence participates in neuropathology caused by mutant PD-linked genes. Specifically, we will determine if pathology in a PD mouse model causes premature senescence and whether removing senescent cells from brain can prevent PD pathology. Finally, we will perform gene expression analysis of PD brains and mouse brains, at a single-cell level, to gain high-resolution insights about cellular processes that link aging and PD pathology.
Here is an overview of how this team’s article findings have contributed to the PD field as of June 2025. There are two different categorizations of these contributions – one by impact to the PD community and a second by scientific category.
Impact
Category
Members of the team have been recognized for their contributions.
Network Spotlights
Updates will be posted when available.
Members of the CRN work diligently to advance our understanding of Parkinson’s disease. Learn more about recent CRN discoveries and achievements.
