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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 vision for CNDR is to create a world with effective interventions to prevent and cure aging-related neurodegenerative diseases.” – Eddie Lee, MD, PhD, Director of CNDR
John Q. Trojanowski, MD, PhD | 1946 - 2022
In loving memory of John Q. Trojanowski, MD, PhD
Latest Research
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Cerebral perfusion features linking subclinical cardiac and aortic dysfunction to vascular brain injury
Friday, August 21, 2026
INTRODUCTION: Subclinical cardiovascular remodeling may impair cerebral hemodynamics and contribute to dementia, but the perfusion features linking subclinical cardiovascular dysfunction to cerebrovascular injury remain unclear.
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Portable Ultra-Low-Field MRI in Outpatient Neurology: An Examination of Clinical Performance and Patient Experience
Friday, August 21, 2026
CONCLUSIONS: In outpatient neurology practices, pMRI images demonstrated high clinical concordance with sMRI for identifying the presence or absence of structural brain abnormalities and were strongly preferred by patients. These findings support the use of pMRI as a practical point-of-care imaging tool for neurology patients, enabling timely access to structural neuroimaging during the clinical encounter.
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Astrocytes mobilize a broader repertoire of lysosomal repair mechanisms than neurons
Thursday, August 20, 2026
Lysosomal damage impairs proteostasis and contributes to neurodegenerative diseases, yet cell-type-specific differences in lysosomal repair remain unclear. Using a neuron-astrocyte coculture system, we compared responses to lysosomal injury induced by a lysosomotropic methyl ester. Both neurons and astrocytes showed lysosomal damage, marked by Galectin-3 recruitment to lumenal lysosomal β-galactosides, disrupted lysosomal pH, and engagement of lysophagy receptors TAX1BP1 and p62. However,...