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Full-Text Articles in Medicine and Health Sciences
Fosinopril, Kaitlyn Alessi, Mayur S. Parmar
Indinavir, Eliyah B. Pollak, Mayur S. Parmar
Pramipexole, Raman Singh, Mayur S. Parmar
Tolterodine, Shreya Narain, Mayur S. Parmar
387. Gene Delivery Of Apoe2 Reduces Amyloid Pathology In Transgenic Mouse Models Of Alzheimer's Disease, Lingzhi Zhao, Andrew J. Gottesdiener, Mayur S. Parmar, Christine Grevstad, David Havlicek, Jonathan Rosenberg, Stephen Kaminsky, Maria Chiuchiolo, Dolan Sondhi, Ronald G. Crystal, Steven M. Paul
387. Gene Delivery Of Apoe2 Reduces Amyloid Pathology In Transgenic Mouse Models Of Alzheimer's Disease, Lingzhi Zhao, Andrew J. Gottesdiener, Mayur S. Parmar, Christine Grevstad, David Havlicek, Jonathan Rosenberg, Stephen Kaminsky, Maria Chiuchiolo, Dolan Sondhi, Ronald G. Crystal, Steven M. Paul
HPD Articles
The deposition of amyloid β-peptides (Aβ), cleavage products of the amyloid precursor protein (APP) by β- and γ-secretases, in brain represents a pathological hallmark of Alzheimer's disease (AD). Apolipoprotein E (APOE) ε4 allele carriers have an increased risk to develop AD and an earlier age of onset, whereas carriers of the ε2 allele have reduced risk and a delayed age of onset. APOE is also a major determinant of brain Aβ and amyloid burden in humans and in several transgenic mouse models of AD (E4>E3>E2). We have previously reported that lentivirus-mediated intraparenchymal gene delivery of APOE2 significantly reduces …
Ros-Mediated Oxidative Stress Influence Anti-Apoptotic Genes And Cyt C Release In Hyperglycemic Mouse Kidneys To Initiate Late Nephropathic Complications, Krina Shah, Mayur S. Parmar, Sidhartha D. Ray
Ros-Mediated Oxidative Stress Influence Anti-Apoptotic Genes And Cyt C Release In Hyperglycemic Mouse Kidneys To Initiate Late Nephropathic Complications, Krina Shah, Mayur S. Parmar, Sidhartha D. Ray
HPD Articles
Decades of intense research has shown that hyperglycemiainduced ROS production can lead to a redox-imbalance causing oxidative stress (OS) in a variety of target organs in vivo. In the absence of an efficient antioxidant counteracting system, massive OS often leads to activation of stress-responsive signaling pathways resulting in deregulated expression of pro-survival and/or pro-death genes. Persistent deregulation of such pathways eventually masterminds late complications of diabetes. Most studies hold hyperglycemia-induced OS as the ‘cause’, and premature onset of apoptosis as the ‘effect’. This ‘cause and effect’ axis ultimately initiates the development and progression of macro and microvascular complications including diabetic …