K
Kathryn A. Lindl
Researcher at University of Pennsylvania
Publications - 12
Citations - 1254
Kathryn A. Lindl is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Neurodegeneration & Neurotoxicity. The author has an hindex of 10, co-authored 12 publications receiving 1100 citations.
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Journal ArticleDOI
Expression of Nrf2 in Neurodegenerative Diseases
Chenere P. Ramsey,Charles A. Glass,Marshall B. Montgomery,Kathryn A. Lindl,Gillian P. Ritson,Luis A. Chia,Ronald L. Hamilton,Charleen T. Chu,Kelly L. Jordan-Sciutto +8 more
TL;DR: It is suggested that Nrf2-mediated transcription is not induced in neurons in AD despite the presence of oxidative stress, and in PD, nuclear localization of NRF2 is strongly induced, but this response may be insufficient to protect neurons from degeneration.
Journal ArticleDOI
HIV-associated neurocognitive disorder: pathogenesis and therapeutic opportunities.
TL;DR: By considering the specific mechanisms and consequences of HIV neuropathogenesis, unified approaches for neuroprotection will likely emerge using a tailored, combined, and non-invasive approach.
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Antiretroviral drugs induce oxidative stress and neuronal damage in the central nervous system.
Cagla Akay,Michael Cooper,Akinleye O. Odeleye,Brigid K. Jensen,Michael G. White,Fair M. Vassoler,Patrick J. Gannon,Joseph L. Mankowski,Jamie L. Dorsey,Alison M. Buch,Stephanie A. Cross,Denise R. Cook,Michelle Marie Peña,Emily S. Andersen,Melpo Christofidou-Solomidou,Kathryn A. Lindl,M. Christine Zink,Janice E. Clements,R. Christopher Pierce,Dennis L. Kolson,Kelly L. Jordan-Sciutto +20 more
TL;DR: It is shown that ARVs are neurotoxic in the CNS in both pigtail macaques and rats in vivo and implicate oxidative stress as a contributor to the underlying mechanisms of ARV-induced neurotoxicity and will provide an access point for adjunctive therapies to complement ARV therapy and reduce neurotoxicity in this patient population.
Journal ArticleDOI
Expression of the endoplasmic reticulum stress response marker, BiP, in the central nervous system of HIV-positive individuals.
TL;DR: Data presented here indicate for the first time that numbers of macrophages/microglia increase in brains of MCMD patients, as has been observed in HAD, and suggest that ER stress response is activated in HIV‐infected cortex.
Journal ArticleDOI
Activation of cyclin-dependent kinase 5 by calpains contributes to human immunodeficiency virus-induced neurotoxicity.
Ying Wang,Michael G. White,Cagla Akay,Rebecca A. Chodroff,Jonathan Robinson,Kathryn A. Lindl,Marc A. Dichter,Yang Qian,Zixu Mao,Dennis L. Kolson,Kelly L. Jordan-Sciutto +10 more
TL;DR: The data suggest calpain activation of CDK5, a pathway activated in HIV‐infected individuals, can mediate neuronal damage and death in a model of HIV‐induced neurotoxicity.