Adipose tissue as a therapeutic target for vascular damage in Alzheimer's disease DOI Creative Commons
Miriam Bettinetti‐Luque, Laura Trujillo‐Estrada, Eduardo Garcı́a-Fuentes

et al.

British Journal of Pharmacology, Journal Year: 2023, Volume and Issue: 181(6), P. 840 - 878

Published: Sept. 14, 2023

Adipose tissue has recently been recognized as an important endocrine organ that plays a crucial role in energy metabolism and the immune response many metabolic tissues. With this regard, emerging evidence indicates crosstalk exists between adipose brain. However, contribution of to development age-related diseases, including Alzheimer's disease, remains poorly defined. New studies suggest modulates brain function through range endogenous biologically active factors known adipokines, which can cross blood-brain barrier reach target areas or regulate barrier. In review, we discuss effects several adipokines on physiology barrier, their disease therapeutic potential. LINKED ARTICLES: This article is part themed issue From Disease Vascular Dementia: Different Roads Leading Cognitive Decline. To view other articles section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.6/issuetoc.

Language: Английский

The effects of microglia-associated neuroinflammation on Alzheimer’s disease DOI Creative Commons
Cuicui Wang, Shuai Zong, Xiaolin Cui

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Feb. 22, 2023

Alzheimer’s disease (AD) is defined as a severe chronic degenerative neurological in human. The pathogenic mechanism of AD has been convincingly elucidated by the “amyloid cascade hypothesis” with main focus pathological accretion β-amyloid (Aβ) peptides outside cell. However, increasing evidence suggests that this hypothesis weak explaining pathogenesis AD. Neuroinflammation crucial development AD, which proven elevated levels inflammatory markers and identification risk genes relevant to innate immune function. Here, we summarize effects microglia-mediated neuroinflammation on focusing temporal spatial changes microglial phenotype, interactions among microglia, Aβ, tau, neurons, prospects recent advances diagnostic therapeutic target

Language: Английский

Citations

129
Glial Cell-Mediated Neuroinflammation in Alzheimer’s Disease DOI Open Access

Nour F. Al-Ghraiybah,

Junwei Wang, Amer E. Alkhalifa

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(18), P. 10572 - 10572

Published: Sept. 12, 2022

Alzheimer's disease (AD) is a progressive neurodegenerative disorder; it the most common cause of dementia and has no treatment. It characterized by two pathological hallmarks, extracellular deposits amyloid beta (Aβ) intraneuronal Neurofibrillary tangles (NFTs). Yet, those hallmarks do not explain full pathology seen with AD, suggesting involvement other mechanisms. Neuroinflammation could offer another explanation for progression disease. This review provides an overview recent advances on role immune cells' microglia astrocytes in neuroinflammation. In become reactive several mechanisms leading to release proinflammatory cytokines that further neuronal damage. We then provide updates neuroinflammation diagnostic markers investigational therapeutics currently clinical trials target

Language: Английский

Citations

92
Cornuside alleviates cognitive impairments induced by Aβ1−42 through attenuating NLRP3-mediated neurotoxicity by promoting mitophagy DOI Creative Commons

Fulin Zhou,

Wenwen Lian,

Xiaotang Yuan

et al.

Alzheimer s Research & Therapy, Journal Year: 2025, Volume and Issue: 17(1)

Published: Feb. 19, 2025

Language: Английский

Citations

4
IGF2BP2 Regulates the Progression of Alzheimer's Disease Through m6A‐Mediated NLRP3 Inflammasome DOI Creative Commons

Wu Jingrui,

Haihui Yang,

Yan Jinjin

et al.

Immunity Inflammation and Disease, Journal Year: 2025, Volume and Issue: 13(1)

Published: Jan. 1, 2025

ABSTRACT Background Recent studies show that N6‐methyladenosine (m6A) plays an important role in the pathogenesis of Alzheimer's disease (AD), while mechanisms involved were studied insufficiently. Aims The present study aimed to explore effect human insulin‐like growth factor 2 (IGF2) mRNA binding proteins (IGF2BP2), one m6A‐binding on progression AD. Materials & Methods and protein expression level determined using RT‐qPCR western blot, respectively. MTT assay was carried out evaluate cell viability. content ROS, antioxidant enzymes, IL‐1β pyroptosis, as well m6A contents relative commercial kit. AD models built Aβ1‐42 ‐stimulated hippocampal neuron vitro mice vivo. Results Our results showed IGF2BP2 significantly upregulated neuron. inhibition reversed decreased viability increased apoptosis induced by Aβ1‐42. siRNA transfection alleviated pyroptosis pyroptosis‐related upregulation. we also found downregulated NLRP3 through methylation. Furthermore, overexpression partly ‐induced injury. In addition, improved cognitive function neuronal injury Conclusion Knockdown inhibit damage hippocampus cells, improve m6A‐mediated inflammasome.

Language: Английский

Citations

1
Role of Peripheral NLRP3 Inflammasome in Cognitive Impairments: Insights of Non-central Factors DOI
Min Qiao, Junjun Ni,

Hong Qing

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 25, 2025

Language: Английский

Citations

1
Microglial autophagy in Alzheimer’s disease and Parkinson’s disease DOI Creative Commons
Zhifu Wang, Qi Wang, Shihua Li

et al.

Frontiers in Aging Neuroscience, Journal Year: 2023, Volume and Issue: 14

Published: Jan. 10, 2023

Alzheimer’s disease (AD) and Parkinson’s (PD) are the most common neurodegenerative diseases, characterized by gradual selective loss of neurons in central nervous system. They affect more than 50 million people worldwide, their incidence increases with age. Although cases AD PD sporadic, some caused genetic mutations that inherited. Both sporadic familial display complex neuropathology represent perplexing neurological disorders. Because undefined pathogenesis clinical manifestations, there is still no effective treatment for both PD. Understanding these important diseases developing successful therapies. Increasing evidence suggests microglial autophagy associated PD, its dysfunction has been implicated progression. In this review, we focus on function microglia models an attempt to help our understanding identifying new therapeutic targets

Language: Английский

Citations

20
Mitochondrial DNA and Inflammation in Alzheimer’s Disease DOI Creative Commons
Giacoma Galizzi, Marta Di Carlo

Current Issues in Molecular Biology, Journal Year: 2023, Volume and Issue: 45(11), P. 8586 - 8606

Published: Oct. 25, 2023

Mitochondrial dysfunction and neuroinflammation are implicated in the pathogenesis of most neurodegenerative diseases, such as Alzheimer’s disease (AD). In fact, although a growing number studies show crosstalk between these two processes, there remain numerous gaps our knowledge mechanisms involved, which requires further clarification. On one hand, mitochondrial may lead to release damage-associated molecular patterns (mtDAMPs) recognized by microglial immune receptors contribute progression. other inflammatory molecules released glial cells can influence regulate function. A deeper understanding help identify biomarkers targets useful for treatment diseases. This review works published recent years is focused on description contribution neurodegeneration, with particular attention DNA (mtDNA) AD.

Language: Английский

Citations

18
Research progress of NLRP3 inflammasome and its inhibitors with aging diseases DOI Creative Commons

Zhuo Yuan,

Dongke Yu,

Tingting Gou

et al.

European Journal of Pharmacology, Journal Year: 2023, Volume and Issue: 957, P. 175931 - 175931

Published: July 24, 2023

Language: Английский

Citations

17
Neuroprotective effects of gemfibrozil in neurological disorders: Focus on inflammation and molecular mechanisms DOI Creative Commons
Mehraveh Sadeghi Ivraghi, Mohammad Yasin Zamanian, Reena Gupta

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2023, Volume and Issue: 30(3)

Published: Oct. 30, 2023

Abstract Background Gemfibrozil (Gem) is a drug that has been shown to activate PPAR‐α, nuclear receptor plays key role in regulating lipid metabolism. Gem used lower the levels of triglycerides and reduce risk coronary heart disease patients. Experimental studies vitro vivo have can prevent or slow progression neurological disorders (NDs), including cerebral ischemia (CI), Alzheimer's (AD), Parkinson's (PD), multiple sclerosis (MS). Neuroinflammation known play significant these disorders. Method The literature review for this study was conducted by searching Scopus, Science Direct, PubMed, Google Scholar databases. Result results show neuroprotective effects through several cellular molecular mechanisms such as: (1) ability upregulate pro‐survival factors (PGC‐1α TFAM), promoting survival function mitochondria brain, (2) strongly inhibits activation NF‐κB, AP‐1, C/EBPβ cytokine‐stimulated astroglial cells, which are increase expression iNOS production NO response proinflammatory cytokines, (3) protects dopamine neurons MPTP mouse model PD increasing PPARα, turn stimulates GDNF astrocytes, (4) reduces amyloid plaque pathology, activity glial improves memory, (5) increases myelin genes (MBP CNPase) via PPAR‐β, (6) hippocampal BDNF counteract depression. Conclusion According study, investigated its potential therapeutic effect NDs. Further research needed fully understand

Language: Английский

Citations

17
Neuroinflammation: A Critical Factor in Neurodegenerative Disorders DOI Open Access

Zahieh Suleiman Khoury,

Fatima Sohail,

Jada Wang

et al.

Cureus, Journal Year: 2024, Volume and Issue: unknown

Published: June 13, 2024

This review offers a comprehensive of the signals and paramount role neuroinflammation plays in neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis. The study explores sophisticated interactions between microglial, astrocytic, dendritic cells how affects long-term neuronal damage dysfunction. There are specific pathways related to mentioned inflammatory processes, including Janus kinases/signal transducer activator transcriptions, nuclear factor-κB, mitogen-activated protein kinases pathways. Neuroinflammation is argued be double-edged sword, being not only protective agent that prevents further neuron but also causative factor more cell injury development. concept contrasting inflammation with neuroprotection advocates for use therapeutic techniques seek modulate neuroinflammatory responses part neurodegeneration treatment. recent research findings integrated established knowledge help present image neuroinflammation's impact on its implications future therapy.

Language: Английский

Citations

7