The existence of individuals who remain cognitively intact despite the presence of neuropathology normally associated with fully symptomatic Alzheimer’s Disease (AD), also called resilient, suggests that there is an intrinsic way for the human brain to resist (or significantly delay) the events that lead to cognitive impairment in AD. Understanding the involved cellular mechanism(s) would thus reveal a very effective target to develop a novel therapeutic concept centered on inducing cognitive resistance in affected patients. With this ultimate goal in mind, the main research focus of Dr. Taglialatela’s group is to determine the molecular basis of brain/cognitive resilience in the face of AD pathology and to explore approaches to induce such resistance in anyone affected by the disease. Dr. Taglialatela’s group uses autoptic human brains, transgenic animal models, and in vitro neuronal systems to interrogate basic molecular mechanisms of synaptic/neuronal resilience and focus on calcineurin inhibitors, neural stem cell-derived exosomes (and their miRNA content) and near-infrared light as viable approaches to elicit it.

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The overall goal of Dr. Dineley`s research program is to better understand the maladaptive neuroplastic changes in the brain related to cognitive deficits that arise in neurological disorders such as Alzheimer’s disease. For the past 15 years, she has been studying neuroplasticity in animal models of neurological and psychiatric disorders, including infectious disease, Alzheimer’s, and Parkinson’s disease. Dr. Dineley has expertise in the design and study of rodent behavioral models for a variety of disease states with special emphasis on quantitative measures of cognitive and motor deficits in addition to the application of pharmacological tools and genetic manipulations to test mechanistic hypotheses. She is a member of the academy for master teachers and Director of the Rodent In Vivo Assessment (RIVA) Core.

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Dr. Fang has extensive research experience in the fields of neurodegenerative diseases, neuroimmunology, lipid metabolism, inflammation, and reactive oxygen species (ROS). His current research focuses on 1) The role of neuroprotective indoles in delaying the onset of cognitive decline; 2) Molecular mechanisms, biomarkers, and therapeutic approach for Myasthenia Gravis (MG); 3) tRNA-derived RNA Fragments and Alzheimer’s disease; 4) Targeting soluble epoxide hydrolase as a novel therapeutic approach for HIV-related pain. His group also is interested in alcohol-induced mitochondrial dysfunction and the role of endogenous cannabinoids in neurodegenerative diseases.

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Dr. Kayed’s area of research focuses on the mechanisms of protein misfolding and aggregation, as well as the toxicity of proteinaceous deposits in neurodegenerative disorders, mainly Alzheimer’s disease, Parkinson’s disease, tauopathies, and amyloidosis. His lab also studies the polymorphism of amyloid and tau species in tauopathies and traumatic brain injury and the development of therapeutic monoclonal antibodies for toxic oligomeric amyloids.

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Dr. Pappolla has extensive research and clinical experience. He holds current board certifications in 5 areas of medicine, all neuroscience-related. His clinical and research expertise contributes to a deep understanding of neurodegenerative diseases in their etiology and clinical practice. His lab and collaborative work were among the first to identify evidence of oxidative stress in Alzheimer's disease brain and hypercholesterolemia as an early risk factor for Alzheimer's disease. His work has led to several patents pertaining to melatonin analogs as neuroprotective drugs. His clinical interests focus on Neuropathology and Interventional Pain management, and translational research in Alzheimer’s disease.

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Dr. Krishnan's lab is interested in the basic mechanism associated with synaptic neurotransmission in central and peripheral nervous systems. His group utilizes electrophysiological, behavioral, and biochemical approaches using different vertebrate and invertebrate animal models to investigate mechanisms underlying synaptic dysfunction. Currently, Dr. Krishnan’s lab has interesting observations associated with neurodegenerative disorders, neuropsychiatric conditions, and the effects of radiation in long-term space flights such as those to Mars. His group is interested in basic mechanisms and preclinical therapeutic strategies with emerging interests in biomarkers for assessments of neurological states.

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Dr. Limon's area of research is focused on elucidating the physiological and pathophysiological processes that underlie synaptic and extrasynaptic remodeling of inhibitory and excitatory signaling in neurological disorders, and how they determine the global excitatory to inhibitory synaptic balance (E/I ratio) that determines the electrical brain activity in the brain. Dr. Limon’s group uses electrophysiological approaches on reactivated human receptors in the context of transcriptomic, proteomic, and clinical information. With this information, it should be possible to advance knowledge of synaptic interactions in health and the rearrangements produced by disease to a point where rational strategies can be developed for effective treatments of brain disorders.

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The Sarkar lab focuses on understanding how microsatellite repeat expansion triggers neurodegeneration in spinocerebellar ataxias, Huntington’s disease (HD), and Parkinson’s disease. The major goal of Dr. Sarkar’s lab is to understand how expanded polyglutamine sequences in the mutant huntingtin protein cause genome instability. His group has discovered that DNA repair is impaired in HD and associated neurodegenerative diseases and is actively trying to understand the contributions of this vital process in many neurodegenerative conditions.

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The Cuevas lab uses pioneering methods to understand the neurovascular and blood-brain barrier role in neurodegenerative diseases, particularly Alzheimer’s Disease (AD).

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