Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome DOI Creative Commons
Costas Papatheodoropoulos

Biology, Journal Year: 2025, Volume and Issue: 14(4), P. 363 - 363

Published: March 31, 2025

The excitation/inhibition (E/I) balance is a critical feature of neural circuits, which crucial for maintaining optimal brain function by ensuring network stability and preventing hyperexcitability. hippocampus exhibits the particularly interesting characteristics having different functions E/I profiles between its dorsal ventral segments. Furthermore, vulnerable to epilepsy implicated in Fragile X Syndrome (FXS), disorders associated with heightened possible deficits GABA-mediated inhibition. In epilepsy, shows susceptibility seizures, while FXS, recent evidence suggests differential alterations excitability inhibition regions. This article explores mechanisms underlying regulation, focusing on emphasizing that may confer homeostatic flexibility balance. Notably, adult FXS models enhanced GABAergic inhibition, resistance epileptiform activity, physiological pattern (sharp wave-ripples, SWRs), potentially representing adaptation. contrast, these more aberrant discharges displays altered SWRs. These findings highlight complex, region-specific nature disruptions neurological suggest possess unique compensatory mechanisms. Specifically, it proposed hippocampus, region most prone hyperexcitability, have adaptive capabilities at cellular levels maintain within normal range prevent transition hyperexcitability preserve function. Investigating responses their developmental trajectories offer novel insights into strategies mitigating imbalances other neuropsychiatric neurodevelopmental disorders.

Language: Английский

Preliminary Evidence for Perturbation‐Based tACS‐EEG Biomarkers of Gamma Activity in Alzheimer's Disease DOI Open Access
Annalisa Palmisano,

Luke R. Pezanko,

Davide Cappon

et al.

International Journal of Geriatric Psychiatry, Journal Year: 2025, Volume and Issue: 40(1)

Published: Jan. 1, 2025

ABSTRACT Background Alzheimer's disease (AD) is characterized by impaired inhibitory circuitry and GABAergic dysfunction, which associated with reduced fast brain oscillations in the gamma band (γ, 30–90 Hz) several animal models. Investigating such activity human patients could lead to identification of novel biomarkers diagnostic prognostic value. The current study aimed test a multimodal “Perturbation‐based” transcranial Alternating Current Stimulation‐Electroencephalography (tACS)‐EEG protocol detect how responses tACS AD correlate patients' clinical phenotype. Methods Fourteen participants mild moderate dementia due underwent baseline assessment including cognitive status, peripheral neuroinflammation, resting‐state (rs)EEG. tACS‐EEG recordings included brief (6′) blocks (i.e., 40 stimulation administered through 4 different montages, Pre/Post 32‐Channels EEG for each block. Changes rsEEG γ power respect were adopted as metric induction compared scores neuroinflammatory biomarkers. Results We found positive correlations between Hz‐induced fronto‐central‐parietal areas patient status negative ones markers. Participants greater impairment exhibited less higher neuroinflammation. same analysis performed spectral from resulted no significant correlations, promoting value tACS‐based perturbation capturing individual differences pathology‐related features. Conclusions Our work suggests link tACS‐induced severity, weaker corresponding more severe clinical/cognitive impairment. This provides preliminary support development physiological therapeutic targets based on severity.

Language: Английский

Citations

0
The role of neuroinflammation in PV interneuron impairments in brain networks; implications for cognitive disorders DOI

Pantea Allami,

Niloufar Yazdanpanah,

Nima Rezaei

et al.

Reviews in the Neurosciences, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 22, 2025

Abstract Fast spiking parvalbumin (PV) interneuron is an inhibitory gamma-aminobutyric acid (GABA)ergic diffused in different brain networks, including the cortex and hippocampus. As a key component of PV interneurons collaborate fundamental functions such as learning memory by regulating excitation inhibition (E/I) balance generating gamma oscillations. The unique characteristics interneurons, like their high metabolic demands long branching axons, make them too vulnerable to stressors. Neuroinflammation one most significant stressors that have adverse, long-lasting impact on interneurons. affects through specialized inflammatory pathways triggered cytokines tumor necrosis factor (TNF) interleukin 6 (IL-6). crucial cells neuroinflammation, microglia, also play role. destructive effect inflammation can comprehensive effects cause neurological disorders schizophrenia, Alzheimer’s disease (AD), autism spectrum disorder (ASD), bipolar disorder. In this article, we provide review mechanisms which neuroinflammation leads hypofunction these diseases. integrated knowledge about role cognitive networks involved impairment pathology diseases help us with better therapeutic interventions.

Language: Английский

Citations

0
GABAergic modulation of beta power enhances motor adaptation in frontotemporal lobar degeneration DOI Creative Commons
Laura E. Hughes, Natalie Adams, Matthew A Rouse

et al.

Alzheimer s & Dementia, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 19, 2025

Abstract INTRODUCTION We examined how abnormal prefrontal neurophysiology and changes in gamma‐aminobutyric acid‐ergic (GABAergic) neurotransmission contribute to behavioral impairments disorders associated with frontotemporal lobar degeneration (FTLD). METHODS recorded magnetoencephalography during an adaptive visuomotor task from 11 people behavioral‐variant dementia, progressive supranuclear palsy, 20 age‐matched controls. used tiagabine, a acid (GABA) re‐uptake inhibitor, as pharmacological probe assess the role of GABA motor‐related beta power changes. RESULTS Task were diminished movement‐related power. Tiagabine facilitated partial recovery neurophysiology, moderated by executive function, such that greatest improvements seen those higher cognitive scores. The right cortex was revealed key site drug interaction. DISCUSSION Behavioral neurophysiological deficits can be mitigated enhancement GABAergic neurotransmission. Clinical trials are warranted test for enduring clinical benefits this restorative‐psychopharmacology strategy. Highlights Event‐related movement altered reuptake tiagabine. In dementia tiagabine enhanced modulation concurrently improved performance, dependent on baseline cognition, diagnosis. effects suggest GABA‐dependent beta‐related mechanism underlies motor control. Restoring selective is potential means improve symptoms patients dementia.

Language: Английский

Citations

0
Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome DOI Creative Commons
Costas Papatheodoropoulos

Biology, Journal Year: 2025, Volume and Issue: 14(4), P. 363 - 363

Published: March 31, 2025

The excitation/inhibition (E/I) balance is a critical feature of neural circuits, which crucial for maintaining optimal brain function by ensuring network stability and preventing hyperexcitability. hippocampus exhibits the particularly interesting characteristics having different functions E/I profiles between its dorsal ventral segments. Furthermore, vulnerable to epilepsy implicated in Fragile X Syndrome (FXS), disorders associated with heightened possible deficits GABA-mediated inhibition. In epilepsy, shows susceptibility seizures, while FXS, recent evidence suggests differential alterations excitability inhibition regions. This article explores mechanisms underlying regulation, focusing on emphasizing that may confer homeostatic flexibility balance. Notably, adult FXS models enhanced GABAergic inhibition, resistance epileptiform activity, physiological pattern (sharp wave-ripples, SWRs), potentially representing adaptation. contrast, these more aberrant discharges displays altered SWRs. These findings highlight complex, region-specific nature disruptions neurological suggest possess unique compensatory mechanisms. Specifically, it proposed hippocampus, region most prone hyperexcitability, have adaptive capabilities at cellular levels maintain within normal range prevent transition hyperexcitability preserve function. Investigating responses their developmental trajectories offer novel insights into strategies mitigating imbalances other neuropsychiatric neurodevelopmental disorders.

Language: Английский

Citations

0