Primary Faculty

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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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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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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The Fracassi Lab investigates the cellular mechanisms underlying Alzheimer’s Disease (AD) and the resilience observed in individuals who maintain cognitive function despite Alzheimer’s pathology (NDAN). The lab’s research focuses on key processes such as neuroinflammation, autophagy, and oxidative stress, examining their roles in driving neurodegeneration or supporting cognitive preservation. By studying microglial function, cellular clearance pathways, and antioxidant defenses, the lab aims to uncover critical mechanisms that distinguish resilience from vulnerability. These insights are used to identify therapeutic strategies that promote brain health, enhance resilience, and combat cognitive decline associated with AD.

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Dr. Marino's lab focuses on the following:

• Design and characterization of novel therapeutic interventions against Alzheimer’s disease targeting Reelin and Apolipoprotein E (ApoE) pathway.
• Biomolecular mechanisms of protective genetic variants against Alzheimer’s disease.
• Identification of patient-inspired mechanisms of resilience against Alzheimer’s disease

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The Montalbano Lab focuses on unraveling the molecular mechanisms underlying Alzheimer’s disease and other neurodegenerative disorders. Our research integrates cutting-edge approaches in molecular biology, transcriptomics, and single-cell analysis to investigate the roles of RNA-binding proteins, such as Musashi, TDP-43, hnRNPs, and their interactions with pathological proteins like Tau. We employ a diverse range of experimental models, including human brain tissues, induced pluripotent stem cell (iPSC)-derived neurons, organoids, and transgenic mouse models, to study genome instability, chromatin rearrangements, and epigenetic alterations in neuronal senescence. By bridging molecular insights with translational approaches, our ultimate goal is to uncover therapeutic targets and innovative strategies to counteract Alzheimer's and related dementias.


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