The Role of Exosomes as Mediators of Neuroinflammation in the Pathogenesis and Treatment of Alzheimer’s Disease

Frontiers in Aging Neuroscience, Journal Year: 2022, Volume and Issue: 14

Published: June 28, 2022

Alzheimer’s disease (AD) is a common neurodegenerative characterized by progressive dementia. Accumulation of β–amyloid peptide 1–42 and phosphorylation tau protein in the brain are two main pathological features AD. However, comprehensive studies have shown that neuroinflammation also plays crucial role pathogenesis Neuroinflammation associated with neuronal death abnormal aggregation promotes process β-amyloid protein. The inflammatory components AD include glial cells, complement system, cytokines chemokines. In recent years, some researchers focused on exosomes, type membrane nano vesicles. Exosomes can transport proteins, lipids, microRNAs other signaling molecules to participate variety pathways for signal transmission or immune response, affecting activity target cells participating important pathophysiological processes. Therefore, exosomes play an essential intercellular communication may mediate promote development This paper reviews occurrence AD, providing deeper understanding Furthermore, treatment further described, demonstrating their potential as therapeutic targets future.

Language: Английский

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NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders

Progress in Neurobiology, Journal Year: 2023, Volume and Issue: 231, P. 102539 - 102539

Published: Oct. 12, 2023

Neurodegenerative diseases (NDDs) causing cognitive impairment and dementia are difficult to treat due the lack of understanding primary initiating factors. Meanwhile, major sporadic NDDs share many risk factors exhibit similar pathologies in their early stages, indicating existence common initiation pathways. Glucose hypometabolism associated with oxidative stress is one such primary, shared pathology, a likely cause detrimental disease-associated cascades; targeting this pathology may therefore be an effective preventative strategy for most NDDs. However, its exact trigger remain unclear. Recent research suggests that caused by NADPH oxidase (NOX) activation mechanism among could prove long-sought ubiquitous NDD trigger. We focus on two - Alzheimer's disease (AD) Parkinson's (PD), as well acquired epilepsy which increasingly recognized comorbidity also discuss available data suggesting relevance proposed mechanisms other delve into commonalities these neuroinflammation NOX involvement identify potential therapeutic targets gain deeper underlying causes

Language: Английский

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Natural Disaster-induced Dementia and Cognitive Decline: A Meta-analysis and Systematic Review

Social Science & Medicine, Journal Year: 2025, Volume and Issue: 371, P. 117898 - 117898

Published: Feb. 26, 2025

Language: Английский

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Innovative approaches in breast cancer therapy: repurposing nanocarriers for enhanced outcomes

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

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Emerging roles of GPR109A in regulation of neuroinflammation in neurological diseases and pain

Neural Regeneration Research, Journal Year: 2022, Volume and Issue: 18(4), P. 763 - 763

Published: Sept. 21, 2022

Neuroinflammation plays a critical role in the pathological process of multiple neurological disorders and pain conditions. GPR109A, Gi protein-coupled receptor, has emerged as an important therapeutic target for controlling inflammation various tissues organs. In this review, we summarized current data about GPR109A neuroinflammation. Specifically, focused on pharmacological features signaling pathways used by to ameliorate neuroinflammation symptoms Alzheimer’s disease, Parkinson’s sclerosis, stroke,

Language: Английский

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Nicotinic Acetylcholine Receptors and Microglia as Therapeutic and Imaging Targets in Alzheimer’s Disease

Molecules, Journal Year: 2022, Volume and Issue: 27(9), P. 2780 - 2780

Published: April 27, 2022

Amyloid-β (Aβ) accumulation and tauopathy are considered the pathological hallmarks of Alzheimer’s disease (AD), but attenuation in choline signaling, including decreased nicotinic acetylcholine receptors (nAChRs), is evident early phase AD. Currently, there no drugs that can suppress progression AD due to a limited understanding pathophysiology. For this, diagnostic methods assess non-invasively before onset symptoms essential, it would be valuable incorporate concept neurotheranostics, which simultaneously enables diagnosis treatment. The neuroprotective pathways activated by nAChRs attractive targets as these may regulate microglial-mediated neuroinflammation. Microglia exhibit both pro- anti-inflammatory functions could modulated mitigate pathogenesis. single-cell analysis identifying microglial subpopulations have specific different stages pathologies. Thus, ability image microglia according stage living brain lead development new therapeutic methods. In this review, we summarize discuss recent findings on microglia, well their for live imaging context diagnosis, prophylaxis, therapy

Language: Английский

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Anti-inflammatory effects of cannabidiol in early stages of neuroinflammation induced by high-fat diet in cerebral cortex of rats

Toxicology and Applied Pharmacology, Journal Year: 2024, Volume and Issue: 484, P. 116856 - 116856

Published: Feb. 7, 2024

High-fat diet (HFD) contributes to neuroinflammation forming, hence it is crucial find safe and effective substances that are able counteract its progress. The anti-inflammatory properties of phytocannabinoids acquired from the Cannabis plant have been widely acknowledged. We evaluated effects cannabidiol (CBD) treatment on induced by applying HFD early stages in Wistar rat cerebral cortex. In our 7-week experiment, CBD was injected intraperitoneally over last 14days at a dose 10 mg/kg body weight once day. level arachidonic acid, precursor pro-inflammatory eicosanoids, decreased all analysed lipid classes after administration group. Moreover, extent diminishing activity omega-6 (n-6) fatty acid pathway greatest diacylglycerols phospholipids. Surprisingly, also capable downregulating omega-3 (n-3) pathway. expression enzymes involved synthesis eicosanoids significantly increased group subsequently lowered CBD. Significant changes various cytokines levels were discovered. Our results strongly suggest ability reduce formation inflammation precursors cortex, as primary event development neurodegenerative diseases. This can raise hopes for future use this cannabinoid therapeutic purposes since substance lacking lasting severe side effects.

Language: Английский

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Anti-inflammatory activities of novel heat shock protein 90 isoform selective inhibitors in BV-2 microglial cells

Frontiers in Molecular Biosciences, Journal Year: 2024, Volume and Issue: 11

Published: May 2, 2024

Heat shock protein 90 (Hsp90) is a family of chaperone proteins that consists four isoforms: Hsp90α, Hsp90β, glucose-regulated 94 (Grp94), and tumor necrosis factor type 1 receptor-associated (TRAP1). They are involved in modulating the folding, maturation, activation their client to regulate numerous intracellular signaling pathways. Previous studies demonstrated pan-Hsp90 inhibitors reduce inflammatory pathways resulting reduction inflammation pain but show toxicities cancer-related clinical trials. Further, role Hsp90 isoforms remains poorly understood. This study aimed determine anti-inflammatory activities selective on lipopolysaccharide (LPS)-induced BV-2 cells, murine microglial cell line. The production mediators such as nitric oxide (NO), interleukin beta (IL-1β), factor-alpha (TNF-α) was measured. We also investigated impact isoform nuclear kappa B (NF-κB), erythroid 2-related 2 (Nrf2), mitogen-activated kinases (MAPKs). found Hsp90β reduced LPS-induced NO, IL-1β, TNF-α via diminishing NF-κB Extracellular signal-regulated (ERK) MAPK. Grp94, TRAP1 had limited effect mediators. These findings suggest key player neuroinflammation. Thereby providing more drug target for development medications management can potentially contribute adverse side effects associated with pan inhibitors.

Language: Английский

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Mechanism of microglia-mediated neuroinflammation, associated cognitive dysfunction, and therapeutic updates in Alzheimer's disease

hLife, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

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Heat shock protein 70 in Alzheimer's disease and other dementias: A possible alternative therapeutic

Journal of Alzheimer s Disease Reports, Journal Year: 2025, Volume and Issue: 9

Published: Jan. 1, 2025

Alzheimer's disease (AD) is considered a global health issue with high social burden due to the level of disability it causes in those who suffer from it. In absence therapeutic alternative for this disease, we will follow one biochemical pathways involved development AD, which related molecular chaperones. The molecules are responsible eliminating toxins and misfolded proteins at cerebral level. These chaperones set heat shock (HSPs) family, which, among their functions, help maintain homeostasis protect cells against stress. Various authors have described activity HSPs different neurodegenerative diseases, highlighting protein 70 (HSP70) presence aberrant characteristic neurodegeneration, such as amyloid-β (Aβ) tau. role HSP70 AD other dementias lies its mechanism, along HSP has capacity eliminate Aβ aggregates by promoting catalytic pathways. review, explore biological potential use.

Language: Английский

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