Results 11 to 20 of about 3,292 (66)

Moderation of treatment outcomes by polygenic risk for alcohol‐related traits in placebo‐controlled trials of topiramate

open access: yesAlcohol, Clinical and Experimental Research, Volume 49, Issue 6, Page 1297-1305, June 2025.
In a secondary analysis of data from two randomized controlled trials of topiramate in 285 individuals with alcohol use disorder (AUD), measures of genetic risk for problematic alcohol use (PAU) and time to relapse to any drinking (TR) and heavy drinking (THR) significantly moderated topiramate's effect on alcohol‐related problems.
Henry R. Kranzler   +8 more
wiley   +1 more source

Multi‐ancestry genome‐wide association study of topiramate's effects on heavy alcohol use

open access: yesAlcohol, Clinical and Experimental Research, Volume 49, Issue 6, Page 1197-1205, June 2025.
Topiramate reduces alcohol consumption, but genetic predictors of treatment response have not been identified. We conducted a GWAS in 8386 individuals from the Million Veteran Program, evaluating genetic variants associated with the change in alcohol consumption before and after initiating topiramate.
Christal N. Davis   +4 more
wiley   +1 more source

Targeting Excitatory Glutamate Receptors for Morphine Tolerance: A Narrative Review

open access: yesCNS Neuroscience &Therapeutics, Volume 31, Issue 6, June 2025.
Schematic diagram for the excitatory glutamate receptors for morphine tolerance and drugs targeting glutamate receptors in morphine tolerance. This figure illustrates the main mechanisms by which the major ionic and metabotropic glutamatergic receptors are involved in the process of morphine tolerance.
Min Huang   +6 more
wiley   +1 more source

Hippocampal‐Specific Insulin Resistance Elicits Synaptic Effects on Glutamate Neurotransmission

open access: yesJournal of Neurochemistry, Volume 169, Issue 6, June 2025.
In animals with hippocampal‐specific insulin resistance, reduced vGluT2 and synaptophysin expression resulted in lowered synaptic glutamate concentrations. These animals also exhibited reduced serine phosphorylation of GluA1 (green postsynaptic receptor) and reduced expression of GluN2B (purple postsynaptic receptor).
Jennifer M. Erichsen   +5 more
wiley   +1 more source

Multi‐Omic Analysis of Glutamate Excitotoxicity in Primary Neuronal Cultures

open access: yesJournal of Neurochemistry, Volume 169, Issue 6, June 2025.
Our study on rat neuron cells found 250 μM glutamate to be toxic, causing neuron death. We identified genes in pathways linked to apoptosis, neuron plasticity, and cell signaling, along with proteins regulating the cell cycle and tumor proliferation.
Jennifer H. Nguyen   +13 more
wiley   +1 more source

A Bird's‐Eye View of Glycolytic Upregulation in Activated Brain: The Major Fate of Lactate Is Release From Activated Tissue, Not Shuttling to Nearby Neurons

open access: yesJournal of Neurochemistry, Volume 169, Issue 6, June 2025.
During brain activation triggered by sensory stimulation, mental activity, or physical work, nonoxidative metabolism of glucose (CMRglc‐non‐ox, where subscripts ‐n and ‐a denote the rate in neurons and astrocytes, respectively) and glycogen are disproportionately upregulated compared with the cellular rates of oxidative metabolism of glucose (CMRglc‐ox)
Gerald A. Dienel   +2 more
wiley   +1 more source

Role of Glutamate Excitotoxicity in Glioblastoma Growth and Its Implications in Treatment

open access: yesCell Biology International, Volume 49, Issue 5, Page 421-434, May 2025.
ABSTRACT Glioblastoma is a highly malignant and invasive type of primary brain tumor that originates from astrocytes. Glutamate, a neurotransmitter in the brain plays a crucial role in excitotoxic cell death. Excessive glutamate triggers a pathological process known as glutamate excitotoxicity, leading to neuronal damage.
Colin Moriarty   +2 more
wiley   +1 more source

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