This repository is under review for potential modification in compliance with Administration directives.
The AMP PD Knowledge Portal was developed to host and share resources related to Parkinson’s disease research and remains fully operational. We continue to maintain and accept Parkinson’s disease and related disorders data and resources throughout this review process.

Tereza Clarence, Ph.D.

Introduction

My name is Tereza Clarence, and I am a computational neuroscientist working in Dr. Panos Roussos' team at the Icahn School of Medicine at Mount Sinai. My research focuses on cell-type- and brain region-resolved single-cell and multi-omic analyses to understand how molecular programs evolve across PD progression and aging. I integrate transcriptomic, epigenomic, and chromatin conformation data to identify convergent mechanisms of neurodegeneration across neuronal and glial lineages. My broader goal is to build predictive, data-driven models that bridge genetic risk with cellular pathology.

Tereza Clarence, Ph.D.

AMP PD Datasets & the Verily Workbench

We analyzed transcriptomic and whole-genome sequencing data from five brain regions in 97 postmortem donors, comprising over two million single nuclei, generated and deposited by our group in the AMP PD portal [https://www.amp-pd.org/data/postmortem-sequencing-data] (Data Descriptor paper: https://www.nature.com/articles/s41597-024-04117-y). While our initial analyses were performed on local HPC resources, we are now transitioning selected analytical workflows to the Verily Workbench. The main advantage for us is seamless integration with other genetic and genomic datasets, particularly those from the ASAP’s CRN and Global Parkinson’s Genetics Program (GP2) programs.

Impact of the AMP PD Resources in My Work

Our recent study [https://pubmed.ncbi.nlm.nih.gov/40766144/] presents the multi-regional, single-nucleus transcriptomic atlas of Parkinson’s disease, profiling over two million nuclei across five brain regions spanning the Braak spectrum. This work delineates cell-type-specific molecular cascades underlying disease progression, from early neuronal and microglial stress responses to later vascular involvement. Integration of PD GWAS and regulatory networks reveals the convergence of genetic risk on proteostasis and stress-response pathways. By linking genetic architecture to dynamic cellular programs, our study demonstrates the transformative potential of AMP PD’s integrative framework to accelerate mechanistic discovery and therapeutic prioritization in PD.