Area of research
Physiology · Cellular and Molecular Neuroscience
Research interest
Research interests include Alzheimer's disease research and treatments, Neuroscience and Neuropharmacology Research, Cholinesterase and Neurodegenerative Diseases, and Neuroinflammation and Neurodegeneration Mechanisms.
Alzheimer risk-increasing TREM2 variant causes aberrant cortical synapse density and promotes network hyperexcitability in mouse models
TAU ablation in excitatory neurons and postnatal TAU knockdown reduce epilepsy, SUDEP, and autism behaviors in a Dravet syndrome model
Effect of Levetiracetam on Cognition in Patients With Alzheimer Disease With and Without Epileptiform Activity
Tau: Enabler of diverse brain disorders and target of rapidly evolving therapeutic strategies
A second X chromosome contributes to resilience in a mouse model of Alzheimer’s disease
Tau Reduction Prevents Key Features of Autism in Mouse Models
Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer’s disease mutations but not by inhibition of BACE1
Fibrinogen Induces Microglia-Mediated Spine Elimination and Cognitive Impairment in an Alzheimer’s Disease Model
Early neuronal accumulation of DNA double strand breaks in Alzheimer’s disease
Nav1.1-Overexpressing Interneuron Transplants Restore Brain Rhythms and Cognition in a Mouse Model of Alzheimer’s Disease
Fibrin-targeting immunotherapy protects against neuroinflammation and neurodegeneration
Klotho controls the brain–immune system interface in the choroid plexus
The Psychiatric Cell Map Initiative: A Convergent Systems Biological Approach to Illuminating Key Molecular Pathways in Neuropsychiatric Disorders
The mouse as a model for neuropsychiatric drug development
Phosphorylation of tau at Y18, but not tau-fyn binding, is required for tau to modulate NMDA receptor-dependent excitotoxicity in primary neuronal culture
Istradefylline reduces memory deficits in aging mice with amyloid pathology
Incidence and impact of subclinical epileptiform activity in Alzheimer's disease
Expression of A152T human tau causes age‐dependent neuronal dysfunction and loss in transgenic mice
Tau post-translational modifications in wild-type and human amyloid precursor protein transgenic mice
Astrocytic adenosine receptor A2A and Gs-coupled signaling regulate memory
DNA repair factor BRCA1 depletion occurs in Alzheimer brains and impairs cognitive function in mice
Life Extension Factor Klotho Prevents Mortality and Enhances Cognition in hAPP Transgenic Mice
Tau reduction prevents Aβ-induced axonal transport deficits by blocking activation of GSK3β
Dynamin-related protein 1 is required for normal mitochondrial bioenergetic and synaptic function in CA1 hippocampal neurons
Network dysfunction in<i>α</i>‐synuclein transgenic mice and human Lewy body dementia
Life Extension Factor Klotho Enhances Cognition
Tau reduction prevents disease in a mouse model of <scp>D</scp>ravet syndrome
Tau Reduction Diminishes Spatial Learning and Memory Deficits after Mild Repetitive Traumatic Brain Injury in Mice
Seizures and Epileptiform Activity in the Early Stages of Alzheimer Disease
Physiologic brain activity causes DNA double-strand breaks in neurons, with exacerbation by amyloid-β