Yelena Y. Grinberg

ORCID: 0000-0003-4255-5293
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Alzheimer's disease research and treatments
  • Neuroscience of respiration and sleep
  • Migraine and Headache Studies
  • Neuroendocrine regulation and behavior
  • Nicotinic Acetylcholine Receptors Study
  • Inflammation biomarkers and pathways
  • Dementia and Cognitive Impairment Research
  • Insect and Arachnid Ecology and Behavior
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Neurological Disease Mechanisms and Treatments
  • Reproductive System and Pregnancy
  • Memory and Neural Mechanisms
  • Circadian rhythm and melatonin
  • Pregnancy and preeclampsia studies
  • Medicinal Plants and Neuroprotection
  • Olfactory and Sensory Function Studies
  • Indoor Air Quality and Microbial Exposure
  • Neonatal and fetal brain pathology
  • Animal Behavior and Reproduction
  • Neurobiology and Insect Physiology Research
  • COVID-19 Impact on Reproduction
  • Zebrafish Biomedical Research Applications
  • Asthma and respiratory diseases
  • Air Quality and Health Impacts

University of California, Riverside
2016-2024

AbbVie (United States)
2020-2024

University of Chicago Medical Center
2011-2017

University of Illinois Urbana-Champaign
2007

Spreading depression (SD), the most likely cause of migraine aura and perhaps migraine, occurs with increased oxidative stress (OS). SD increases reactive oxygen species (ROS), ROS, in turn, can signal to increase neuronal excitability,which includes susceptibility. also elevates tumor necrosis factor-α (TNF-α), which excitability. Accordingly, we probed for cellular origin OS from its relationship TNF-α, might promote SD, using rat hippocampal slice cultures. We observed significantly...

10.1111/jnc.12267 article EN Journal of Neurochemistry 2013-04-15

Spreading depression (SD) is thought to cause migraine aura, and perhaps migraine, includes a transient loss of synaptic activity preceded followed by increased neuronal excitability. Activated microglia influence play an important role in homeostatic scaling via release cytokines. Furthermore, enhanced function activates not only secrete cytokines but also increase the motility their branches, with somata remaining stationary. While SD increases from microglia, effects on microglial...

10.1371/journal.pone.0019294 article EN cc-by PLoS ONE 2011-04-26

Abstract Human microglia are critically involved in Alzheimer’s disease (AD) progression, as shown by genetic and molecular studies. However, their role tau pathology progression human brain has not been well described. Here, we characterized 32 donors along of AD pathology, both time—from early to late pathology—and space—from entorhinal cortex (EC), inferior temporal gyrus (ITG), prefrontal (PFC) visual (V2 V1)—with biochemistry, immunohistochemistry, single nuclei-RNA-sequencing,...

10.1007/s00401-024-02704-2 article EN cc-by Acta Neuropathologica 2024-04-01

J. Neurochem. (2012) 122 , 221–229. Abstract Spreading depression (SD), the likely cause of migraine aura and perhaps migraine, is triggered by widespread unfettered neuronal hyperexcitability. Migraine initiating hyperexcitability seizure, which involve oxidative stress (OS), are interrelated. Environmental enrichment (EE) decreases seizure can reduce migraine. EE’s well‐characterized neuroprotective effect involves insulin‐like growth factor‐1 (IGF‐1). Accordingly, we asked if IGF‐1 could...

10.1111/j.1471-4159.2012.07763.x article EN Journal of Neurochemistry 2012-04-23

This study examined dark microglia-a state linked to central nervous system pathology and neurodegeneration-during postnatal development in the mouse ventral hippocampus, finding that microglia interact with blood vessels synapses perform trogocytosis of pre-synaptic axon terminals. Furthermore, we found notably expressed C-type lectin domain family 7 member A (CLEC7a), lipoprotein lipase (LPL) triggering receptor on myeloid cells 2 (TREM2) required TREM2, differently from other microglia,...

10.1101/2024.10.15.618087 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-10-18

The molecular mechanisms underlying remodeling of neural networks remain largely unknown. In Drosophila, widespread occurs during metamorphosis, and is regulated by ecdysone. Kruppel-homolog 1 (Kr-h1) a zinc finger transcription factor known to play role in orchestrating ecdysone-regulated transcriptional pathways and, furthermore, implicated governing axon morphogenesis. Interestingly, honey bee workers, expression the Apis mellifera homolog Kr-h1 enhanced their transition foraging behavior...

10.1002/dneu.20537 article EN Developmental Neurobiology 2007-06-11

Abstract Alzheimer’s disease (AD) is a common neurodegenerative with poor prognosis. New options for drug discovery targets are needed. We developed an imaging based arrayed CRISPR method to interrogate the human genome modulation of in vitro correlates AD features, and used this assess 1525 genes related tau aggregation, autophagy mitochondria. This work revealed (I) network aggregation modulators including NF-κB pathway inflammatory signaling, (II) correlation between mitochondrial...

10.1038/s41598-021-82658-7 article EN cc-by Scientific Reports 2021-02-03

Abstract Seventy‐five percent of all traumatic brain injuries are mild and do not cause readily visible abnormalities on routine medical imaging making it difficult to predict which individuals will develop unwanted clinical sequelae. Microglia brain‐resident macrophages early responders insults. Their activation is associated with changes in morphology or expression phenotypic markers including P2Y12 major histocompatibility complex class II. Using a murine model unrestrained closed head...

10.1111/jnc.13402 article EN cc-by-nc-nd Journal of Neurochemistry 2016-01-01

Migraine and its transformation to chronic migraine are healthcare burdens in need of improved treatment options. We seek define how neural immune signaling modulates the susceptibility migraine, modeled vitro using spreading depression (SD), as a means develop novel therapeutic targets for episodic migraine. SD is likely cause aura pain. It paroxysmal loss neuronal function triggered by initially increased activity, which slowly propagates within susceptible brain regions. Normal...

10.3791/2910 article EN Journal of Visualized Experiments 2011-06-13

Continuous exposure to aerosolized fine (particle size ≤2.5 µm) and ultrafine ≤0.1 particulates can trigger innate inflammatory responses in the lung brain depending on particle composition. Most studies of manmade toxicants use inhalation routes, whereas most allergens soluble solutions administered via intranasal or injection routes. Here, we tested whether continuous Alternaria alternata (a common fungal allergen associated with asthma) would induce brain. By designing a new environmental...

10.1177/1759091418782304 article EN cc-by-nc ASN NEURO 2018-01-01

Rare sequence variants in the microglial cell surface receptor TREM2 have been shown to increase risk for Alzheimer's disease (AD). Disease-linked mutations seem confer a partial loss of function, and increasing expression thereby its function(s) might therapeutic benefit AD. However, druggable targets that could modulate are not known. To identify such targets, we conducted screen small molecule compounds with known pharmacology using human myeloid cells, searching those enhance protein at...

10.1074/jbc.ra120.014352 article EN cc-by Journal of Biological Chemistry 2020-12-23

Migraine and its transformation to chronic migraine are healthcare burdens in need of improved treatment options. We seek define how neural immune signaling modulates the susceptibility migraine, modeled vitro using spreading depression (SD), as a means develop novel therapeutic targets for episodic migraine. SD is likely cause aura pain. It paroxysmal loss neuronal function triggered by initially increased activity, which slowly propagates within susceptible brain regions. Normal...

10.3791/2910-v article EN Journal of Visualized Experiments 2011-06-13

Abstract Background In Alzheimer’s disease (AD) progression, amyloid beta load uniformly increases across the brain cortex, while neurofibrillary tangles progressively spread in a stereotypical pattern from entorhinal to visual cortex. AD is known have strong genetic link microglia and recently, expression profiling at single cell resolution has identified disease‐associated populations with differential amyloid‐beta vs. tau pathology association human brain. However, prior studies focusing...

10.1002/alz.062092 article EN Alzheimer s & Dementia 2023-06-01

Abstract Background Tau pathology is known as a primary driver of neurodegeneration in Alzheimer’s disease (AD). Understanding its underlying molecular mechanism critical expanding our knowledge AD pathogenesis and developing novel therapeutic strategies. However, interrogating tau induced neurotoxicity mechanisms has been difficult due to heterogeneous susceptibility neurons pathology. Here, we aim identify the most vulnerable neuronal subpopulation reveal more clear...

10.1002/alz.063430 article EN Alzheimer s & Dementia 2022-12-01
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