Herpes simplex virus 1 accelerates the progression of Alzheimer’s disease by modulating microglial phagocytosis and activating NLRP3 pathway DOI Creative Commons

Zhimeng Wang,

Jing Liu, Jing Han

et al.

Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)

Published: July 18, 2024

Abstract Accumulating evidence implicates that herpes simplex virus type 1 (HSV-1) has been linked to the development and progression of Alzheimer’s disease (AD). HSV-1 infection induces β-amyloid (Aβ) deposition in vitro vivo, but effect precise mechanism remain elusive. Here, we show brains transgenic 5xFAD mice resulted accelerated Aβ deposition, gliosis, cognitive dysfunction. We demonstrate induced recruitment microglia viral core trigger microglial phagocytosis HSV-GFP-positive neuronal cells. In addition, reveal NLRP3 inflammasome pathway by played a crucial role AD caused infection. Blockade signaling reduces alleviates decline after Our findings support notion is key factor etiology AD, demonstrating activation functions interface AD.

Language: Английский

Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease DOI Creative Commons
Érica Novaes Soares, Ana Carla dos Santos Costa,

Gabriel de Jesus Ferrolho

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(6), P. 474 - 474

Published: March 7, 2024

Parkinson’s disease (PD) is a progressive neurodegenerative characterized by resting tremor, bradykinesia, rigidity, and postural instability that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) the primary neurotransmitter involved in this disease, but cholinergic imbalance has been implicated. Current intervention PD focused on replenishing central DA, which provides remarkable temporary symptomatic relief does not address neuronal loss progression of disease. It well established nicotinic receptors (nAChRs) can regulate DA release nicotine itself may have neuroprotective effects. Recent studies identified nAChRs nonneuronal cell types, including glial cells, where they inflammatory responses. Given crucial role neuroinflammation dopaminergic degeneration involvement microglia astrocytes response, provide novel therapeutic target prevention and/or treatment PD. In review, following brief discussion PD, we focus cells and, specifically, their pathology treatment.

Language: Английский

Citations

10
Neurodegenerative diseases and catechins: (−)-epigallocatechin-3-gallate is a modulator of chronic neuroinflammation and oxidative stress DOI Creative Commons
Siying Li,

Zaoyi Wang,

Gang Liu

et al.

Frontiers in Nutrition, Journal Year: 2024, Volume and Issue: 11

Published: Aug. 1, 2024

Catechins, a class of phytochemicals found in various fruits and tea leaves, have garnered attention for their diverse health-promoting properties, including potential combating neurodegenerative diseases. Among these catechins, (-)-epigallocatechin-3-gallate (EGCG), the most abundant polyphenol green tea, has emerged as promising therapeutic agent due to its potent antioxidant anti-inflammatory effects. Chronic neuroinflammation oxidative stress are key pathological mechanisms diseases such Alzheimer's disease (AD) Parkinson's (PD). EGCG neuroprotective efficacy scavenging free radicals, reducing attenuating neuroinflammatory processes. This review discusses molecular EGCG's anti-oxidative chronic neuroinflammation, emphasizing effects on autoimmune responses, neuroimmune system interactions, focusing related AD PD. By elucidating action impact processes, this underscores intervention AD, PD, possibly other Overall, emerges natural compound stress, offering novel avenues strategies treatment disorders.

Language: Английский

Citations

10
The Dual Role of Amyloid Beta-Peptide in Oxidative Stress and Inflammation: Unveiling Their Connections in Alzheimer’s Disease Etiopathology DOI Creative Commons
Hugo Fanlo-Ucar, Pol Picón-Pagès, Víctor Herrera-Fernández

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(10), P. 1208 - 1208

Published: Oct. 8, 2024

Alzheimer's disease (AD) is a progressive neurodegenerative disease, and it currently the seventh leading cause of death worldwide. It characterized by extracellular aggregation amyloid β-peptide (Aβ) into oligomers fibrils that synaptotoxicity neuronal death. Aβ exhibits dual role in promoting oxidative stress inflammation. This review aims to unravel intricate connection between these processes their contribution AD progression. The delves AD, focusing on involvement metals, mitochondrial dysfunction, biomolecule oxidation. distinct yet overlapping concept nitro-oxidative also discussed, detailing roles nitric oxide, perturbations, cumulative impact production neurotoxicity. Inflammation examined through astroglia microglia function, elucidating response within brain. blood-brain barrier oligodendrocytes are considered context pathophysiology. We current diagnostic methodologies emerging therapeutic strategies aimed at mitigating inflammation, thereby offering potential treatments for halting or slowing comprehensive synthesis underscores pivotal bridging advancing our understanding informing future research treatment paradigms.

Language: Английский

Citations

10
Targeting Microglia in Neuroinflammation: H3 Receptor Antagonists as a Novel Therapeutic Approach for Alzheimer’s Disease, Parkinson’s Disease, and Autism Spectrum Disorder DOI Creative Commons
Shilu Deepa Thomas, Sabna Abdalla, Nermin Eissa

et al.

Pharmaceuticals, Journal Year: 2024, Volume and Issue: 17(7), P. 831 - 831

Published: June 25, 2024

Histamine performs dual roles as an immune regulator and a neurotransmitter in the mammalian brain. The histaminergic system plays vital role regulation of wakefulness, cognition, neuroinflammation, neurogenesis that are substantially disrupted various neurodegenerative neurodevelopmental disorders. H3 receptor (H3R) antagonists inverse agonists potentiate endogenous release brain histamine have been shown to enhance cognitive abilities animal models several Microglial activation subsequent neuroinflammation implicated impacting embryonic adult neurogenesis, contributing development Alzheimer's disease (AD), Parkinson's (PD), autism spectrum disorder (ASD). Acknowledging importance microglia both neurodevelopment, well their by histamine, offers intriguing therapeutic target for these inhibition H3Rs has found facilitate shift from proinflammatory M1 state anti-inflammatory M2 state, leading reduction activity microglial cells. Also, pharmacological studies demonstrated H3R showed positive effects reducing biomarkers, suggesting potential simultaneously modulating crucial neurotransmissions signaling cascades such PI3K/AKT/GSK-3β pathway. In this review, we highlight addressing pathology decline disorders, e.g., AD, PD, ASD, with inflammatory component.

Language: Английский

Citations

9
Herpes simplex virus 1 accelerates the progression of Alzheimer’s disease by modulating microglial phagocytosis and activating NLRP3 pathway DOI Creative Commons

Zhimeng Wang,

Jing Liu, Jing Han

et al.

Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)

Published: July 18, 2024

Abstract Accumulating evidence implicates that herpes simplex virus type 1 (HSV-1) has been linked to the development and progression of Alzheimer’s disease (AD). HSV-1 infection induces β-amyloid (Aβ) deposition in vitro vivo, but effect precise mechanism remain elusive. Here, we show brains transgenic 5xFAD mice resulted accelerated Aβ deposition, gliosis, cognitive dysfunction. We demonstrate induced recruitment microglia viral core trigger microglial phagocytosis HSV-GFP-positive neuronal cells. In addition, reveal NLRP3 inflammasome pathway by played a crucial role AD caused infection. Blockade signaling reduces alleviates decline after Our findings support notion is key factor etiology AD, demonstrating activation functions interface AD.

Language: Английский

Citations

9