Exerkines mitigating Alzheimer's disease progression by regulating inflammation: Focusing on macrophage/microglial NLRP3 inflammasome pathway DOI Creative Commons

Jaehwan Cheon,

Soon-Yong Kwon, Mikyung Kim

et al.

Alzheimer s & Dementia, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 6, 2024

Abstract Recent research highlights the critical role of inflammation in accelerating amyloid beta and phosphorylated tubulin‐associated protein tau cascade Alzheimer's disease (AD) progression. Emerging evidence suggests that exercise influences AD by modulating inflammatory responses. We conducted a comprehensive search across multiple online databases. Our approach focused on previous recent studies exploring links among inflammation, AD, effects exercise, specifically targeting articles books published English. pointed out extends from periphery to central nervous system, facilitated macrophage/microglial NLRP3 (nucleotide‐binding domain, leucine rich–containing family, pyrin domain–containing 3) inflammasome signaling, which exacerbates classical mechanisms. Moreover, we provided further insights into modulation signaling through exerkines, may contribute mitigating development. These deepen our understanding mechanisms offer potential for identifying key therapeutic targets biomarkers crucial effective management treatment. Highlights Inflammation is potentially linked acceleration pathogenesis, including pathways involving tau, mediated pro‐inflammatory cytokines. Inflammation, initiated nucleotide‐binding 3 (NLRP3) pathway within M1‐type macrophages/microglia, neuroinflammation Exercise has reduce development influencing via exerkines.

Language: Английский

Gut–Brain Axis: Focus on Sex Differences in Neuroinflammation DOI Open Access
Mario Caldarelli, Pierluigi Rio, Andrea Marrone

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(10), P. 5377 - 5377

Published: May 15, 2024

In recent years, there has been a growing interest in the concept of “gut–brain axis”. addition to well-studied diseases associated with an imbalance gut microbiota, such as cancer, chronic inflammation, and cardiovascular diseases, research is now exploring potential role microbial dysbiosis onset development brain-related diseases. When function intestinal barrier altered by dysbiosis, aberrant immune system response interacts nervous system, leading state “neuroinflammation”. The microbiota–brain axis mediated inflammatory immunological mechanisms, neurotransmitters, neuroendocrine pathways. This narrative review aims illustrate molecular basis neuroinflammation elaborate on gut–brain virtue analyzing various metabolites produced microbiome how they might impact system. Additionally, current will highlight sex influences these mechanisms. fact, hormones brain–gut microbiota at different levels, central enteric one, enteroendocrine cells. A deeper understanding human health disease crucial guide diagnoses, treatments, preventive interventions.

Language: Английский

Citations

5
NLRP3 inflammasome in Alzheimer’s disease: molecular mechanisms and emerging therapies DOI Creative Commons
Zhitao Li,

Cheng Gong

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: April 7, 2025

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and neuroinflammation, with no definitive cure currently available. The NLRP3 inflammasome, key mediator of has emerged as critical player in AD pathogenesis, contributing to the accumulation β-amyloid (Aβ) plaques, tau hyperphosphorylation, neuronal damage. This review explores mechanisms which inflammasome activated AD, including its interactions Aβ, tau, reactive oxygen species (ROS), pyroptosis. Additionally, it highlights role ubiquitin system, ion channels, autophagy, gut microbiota regulating activation. Therapeutic strategies targeting such IL-1β inhibitors, natural compounds, novel small molecules, are discussed promising approaches mitigate neuroinflammation slow progression. underscores potential inhibition therapeutic avenue for AD.

Language: Английский

Citations

0
Loss of glycine receptors in the nucleus accumbens and ethanol reward in an Alzheimer´s Disease mouse model DOI
Lorena Armijo‐Weingart, Loreto San Martín, Scarlet Gallegos

et al.

Progress in Neurobiology, Journal Year: 2024, Volume and Issue: 237, P. 102616 - 102616

Published: May 7, 2024

Language: Английский

Citations

2
Exerkines mitigating Alzheimer's disease progression by regulating inflammation: Focusing on macrophage/microglial NLRP3 inflammasome pathway DOI Creative Commons

Jaehwan Cheon,

Soon-Yong Kwon, Mikyung Kim

et al.

Alzheimer s & Dementia, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 6, 2024

Abstract Recent research highlights the critical role of inflammation in accelerating amyloid beta and phosphorylated tubulin‐associated protein tau cascade Alzheimer's disease (AD) progression. Emerging evidence suggests that exercise influences AD by modulating inflammatory responses. We conducted a comprehensive search across multiple online databases. Our approach focused on previous recent studies exploring links among inflammation, AD, effects exercise, specifically targeting articles books published English. pointed out extends from periphery to central nervous system, facilitated macrophage/microglial NLRP3 (nucleotide‐binding domain, leucine rich–containing family, pyrin domain–containing 3) inflammasome signaling, which exacerbates classical mechanisms. Moreover, we provided further insights into modulation signaling through exerkines, may contribute mitigating development. These deepen our understanding mechanisms offer potential for identifying key therapeutic targets biomarkers crucial effective management treatment. Highlights Inflammation is potentially linked acceleration pathogenesis, including pathways involving tau, mediated pro‐inflammatory cytokines. Inflammation, initiated nucleotide‐binding 3 (NLRP3) pathway within M1‐type macrophages/microglia, neuroinflammation Exercise has reduce development influencing via exerkines.

Language: Английский

Citations

2