Home
Mission
The mission of the Center for Neurodegenerative Disease Research (CNDR) is to promote and conduct multidisciplinary clinical and basic research to increase the understanding of the causes and mechanisms leading to brain dysfunction and degeneration in neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Lewy body dementia (LBD), Frontotemporal degeneration (FTD), Amyotrophic lateral sclerosis (ALS), Primary lateral sclerosis (PLS), Motor neuron disease (MND), and related disorders that occur increasingly with advancing age. Implicit in the mission of the CNDR are two overarching goals: 1.) Find better ways to cure and treat these disorders, 2. Provide training to the next generation of scientists.
“My goal for CNDR is not only to collaborate with researchers at Penn and from institutions across the globe with the mutual goal of finding better ways to diagnose and treat neurodegenerative diseases, but also to inspire and encourage the next generation of scientists on the importance of investigating these disorders that occur more frequently with advancing age.” – Virginia M.-Y. Lee, PhD, Director, CNDR
John Q. Trojanowski, MD, PhD | 1946 - 2022
In loving memory of John Q. Trojanowski, MD, PhD
Latest Research
-
Individualized Atrophy-Based Prediction of Dementia Progression in Familial Frontotemporal Lobar Degeneration With Bayesian Linear Mixed-Effects Modeling
Thursday, January 29, 2026
OBJECTIVE: Age of symptom onset is highly variable in familial frontotemporal lobar degeneration (f-FTLD). Accurate prediction of onset would inform clinical management and trial enrollment. Prior studies indicate that individualized maps of brain atrophy can predict conversion to dementia in f-FTLD. We used a Bayesian linear mixed-effect (BLME) prediction method for identifying accelerated brain volume loss to predict conversion to dementia.
-
Clinical and Imaging Characteristics of Parkinson's Disease with Negative Alpha-Synuclein Seed Amplification Assay
Wednesday, January 28, 2026
CONCLUSIONS: At baseline, SAA- sPD PPMI participants have a substantially lower rate of hyposmia, but otherwise cannot be readily distinguished from SAA+ participants based on clinical characteristics. However, SAA- participants have a greater degree of subcortical brain atrophy, and approximately one out of seven SAA- participants received a change in diagnosis. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder...
-
Discordance of Dopaminergic Dysfunction and Subcortical Atrophy by alpha-Synuclein Status in Sporadic and Genetic Parkinson's Disease
Wednesday, January 28, 2026
CONCLUSIONS: S+ patients exhibit more dopaminergic deficit, whereas S- patients have more subcortical atrophy across sporadic and genetic PD. Together, our findings reveal structure/function and DAT/MRI discordance, providing insight into biomarkers and pathophysiology of synucleinopathy and PD. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.