A5041995051- Neuroscience and Neuropharmacology Research
- Neurotransmitter Receptor Influence on Behavior
- Genetics and Neurodevelopmental Disorders
- Autism Spectrum Disorder Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Receptor Mechanisms and Signaling
- Tryptophan and brain disorders
- Cholinesterase and Neurodegenerative Diseases
- HIV Research and Treatment
- Nicotinic Acetylcholine Receptors Study
- Nerve injury and regeneration
- Neuroendocrine regulation and behavior
- Amino Acid Enzymes and Metabolism
- Epigenetics and DNA Methylation
- Alzheimer's disease research and treatments
- Infant Health and Development
- Attention Deficit Hyperactivity Disorder
- Cellular transport and secretion
- Endoplasmic Reticulum Stress and Disease
- Hearing, Cochlea, Tinnitus, Genetics
- Cytomegalovirus and herpesvirus research
- Functional Brain Connectivity Studies
- Memory and Neural Mechanisms
- Cannabis and Cannabinoid Research
- Lipid Membrane Structure and Behavior
Colorado State University
2018-2023
Universidade Federal Fluminense
2015-2021
New York University
2020-2021
NYU Langone Health
2016
Beta-amyloid (Aβ) has been recognized as an early trigger in the pathogenesis of Alzheimer's disease (AD) leading to synaptic and cognitive impairments. Aβ can alter neuronal signaling through interactions with nicotinic acetylcholine receptors (nAChRs), contributing dysfunction AD. The three major nAChR subtypes hippocampus are composed α7-, α4β2-, α3β4-nAChRs. selectively affects α7- α4β2-nAChRs, but not α3β4-nAChRs hippocampal neurons, resulting hyperexcitation. However, how subtype...
ABSTRACT Synaptic strength is altered during synaptic plasticity by controlling the number of AMPA receptors (AMPARs) at excitatory synapses. During long-term potentiation and upscaling, AMPARs are accumulated synapses to increase strength. Neuronal activity leads phosphorylation AMPAR subunit GluA1 (also known as GRIA1) subsequent elevation surface expression, either an in receptor forward trafficking membrane or a decrease internalization. However, molecular pathways underlying...
δ-catenin is expressed in excitatory synapses and functions as an anchor for the glutamatergic AMPA receptor (AMPAR) GluA2 subunit postsynaptic density. The glycine 34 to serine (G34S) mutation gene has been found autism spectrum disorder (ASD) patients results loss of at synapses, which presumed underlie ASD pathogenesis humans. However, how G34S causes induce remains unclear. Here, using neuroblastoma cells, we identify that increases glycogen synthase kinase 3β (GSK3β)-dependent...
Over half of individuals infected with human immunodeficiency virus (HIV) suffer from HIV-associated neurocognitive disorders (HANDs), yet the molecular mechanisms leading to neuronal dysfunction are poorly understood. Feline (FIV) naturally infects cats and shares its structure, cell tropism, pathology HIV, including wide-ranging neurological deficits. We employ FIV as a model elucidate pathways underlying HIV-induced dysfunction, in particular, synaptic alteration. Among neuron-damaging...
As the development of combination antiretroviral therapy (cART) against human immunodeficiency virus (HIV) drastically improves lifespan individuals with HIV, many are now entering prime age when Alzheimer's disease (AD)-like symptoms begin to manifest. It has been shown that hyperphosphorylated tau, a known AD pathological characteristic, is prematurely increased in brains HIV-infected as early their 30s and its levels increase age. This suggests HIV infection might lead accelerated...
Phosphorylation of GluA1, a subunit AMPA receptors (AMPARs), is critical for AMPAR synaptic trafficking and control transmission. cGMP-dependent protein kinase II (cGKII) mediates this phosphorylation, cGKII knockout (KO) affects GluA1 phosphorylation alters animal behavior. Notably, in the KO hippocampus increased as functional compensation gene deletion, while such absent prefrontal cortex. Thus, there are brain region-specific effects on trafficking, which could affect Here, we show that...
Methylphenidate (MPD) is one of the most prescribed drugs for alleviating symptoms Attention Deficit/Hyperactivity Disorder (ADHD). However, changes in molecular mechanisms related to MPD withdrawal and susceptibility consumption other psychostimulants normal individuals or with ADHD phenotype are not completely understood. The aims present study were: (i) characterize differences prefrontal dopaminergic system SHR Wistar strains, (ii) establish neurochemical consequences short- (24 hours)...
Abstract Synaptic strength is altered during synaptic plasticity by controlling the number of AMPA receptors (AMPARs) at excitatory synapses. In particular, long-term potentiation and up-scaling, AMPARs are accumulated synapses to increase strength. Neuronal activity leads activity-dependent phosphorylation AMPAR subunit GluA1, subsequent increases in GluA1 surface expression, which can be achieved either an exocytosis or a decrease endocytosis receptors. However, molecular pathways...
δ-catenin is expressed in excitatory synapses and functions as an anchor for the glutamatergic AMPA receptor (AMPAR) GluA2 subunit postsynaptic density. The glycine 34 to serine (G34S) mutation gene found autism spectrum disorder (ASD) patients induces loss of at synapses, which presumed underlie ASD pathogenesis humans. However, how G34S causes induce remains unclear. Here, using neuroblastoma cells, we discover that generates additional phosphorylation site glycogen synthase kinase 3β...
Abstract Valproic acid (VPA) is an effective and commonly prescribed drug for epilepsy bipolar disorder. However, children born from mothers treated with VPA during pregnancy exhibit increased incidence of autism spectrum disorder (ASD). Although may impair brain development at the cellular level, mechanism VPA-induced ASD has not been completely addressed. A previous study found that treatment strongly reduces δ-catenin mRNA levels in cultured human neurons. important control glutamatergic...
Abstract Beta-amyloid (Aβ) has been recognized as an early trigger in the pathogenesis of Alzheimer’s disease (AD) leading to synaptic and cognitive impairments. Aβ can alter neuronal signaling through interactions with nicotinic acetylcholine receptors (nAChRs), contributing dysfunction AD. The three major nAChR subtypes hippocampus are composed α7-, α4β2-, α3β4-nAChRs. selectively affects α7- α4β2-nAChRs, but not α3β4-nAChRs hippocampal neurons, resulting hyperexcitation. However, how...
Abstract As the development of combination antiretroviral therapy (cART) against human immunodeficiency virus (HIV) drastically improves lifespan individuals with HIV, many are now entering prime age when Alzheimer’s disease (AD)-like symptoms begin to manifest. Hyperphosphorylated tau, a known AD pathological characteristic, has been prematurely increased in brains HIV-infected patients as early their 30s and is age. This thus suggests that HIV infection may lead accelerated phenotypes....
Abstract Chromosome 4q21 microdeletion leads to a human syndrome that exhibits restricted growth, facial dysmorphisms, mental retardation, and absent or delayed speech. One of the key genes in affected region chromosome is PRKG2 , which encodes cGMP-dependent protein kinase II (cGKII). Mice lacking cGKII exhibit growth deficits learning memory, as seen syndrome. However, speech/vocalization impairments these mice have not been determined. Moreover, molecular pathway underlying speech...