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
A Statement on Racial Injustice and Recent Events
June 9, 2020
As our nation is currently dealing with an unprecedented mix of significant health, social and financial issues, we want to reach out to the patients and their loved ones who have been participating in our research program. We will continue to update the website as events unfold.
Our nation mourns the tragic and senseless deaths of George Floyd, Breonna Taylor, Ahmaud Arbery, and the countless other black individuals who have lost their lives to police brutality and institutional racism. It is a vivid reminder of the ongoing racial inequalities and unacceptable indignities that so many of our citizens constantly endure. These events should lead everyone to recognize how much more work our society must do to attain liberty and justice for all. As a nation, we have considerable work to do.
Read our full statement, including remarks on COVID-19, here:
Oh brother, where art tau? Amyloid, neurodegeneration, and cognitive decline without elevated tau
Sunday, June 13, 2021
Mild cognitive impairment (MCI) can be an early manifestation of Alzheimer's disease (AD) pathology, other pathologic entities [e.g., cerebrovascular disease, Lewy body disease, LATE (limbic-predominant age-related TDP-43 encephalopathy)], or mixed pathologies, with concomitant AD- and non-AD pathology being particularly common, albeit difficult to identify, in living MCI patients. The National Institute on Aging and Alzheimer's Association (NIA-AA) A/T/(N) [β-Amyloid/Tau/(Neurodegeneration)] AD...
Computational modeling of tau pathology spread reveals patterns of regional vulnerability and the impact of a genetic risk factor
Thursday, June 10, 2021
Neuropathological staging studies have suggested that tau pathology spreads through the brain in Alzheimer's disease (AD) and other tauopathies, but it is unclear how neuroanatomical connections, spatial proximity, and regional vulnerability contribute. In this study, we seed tau pathology in the brains of nontransgenic mice with AD tau and quantify pathology development over 9 months in 134 brain regions. Network modeling of pathology progression shows that diffusion through the connectome is...
Hyperactive LRRK2 kinase impairs the trafficking of axonal autophagosomes
Thursday, June 10, 2021
Parkinson disease (PD)-causing mutations in the LRRK2 (leucine rich repeat kinase 2) gene hyperactivate LRRK2 kinase activity. Here, we discuss our recent work linking LRRK2 hyperactivation to defective axonal autophagosome transport in neurons. In three different models, we observed that expression of the most common causative mutation for PD, LRRK2^(G2019S), disrupts processive autophagosome transport in a kinase-dependent manner. Mechanistically, we found that hyperactive LRRK2 recruits...