Glial Cell Crosstalk in Parkinson's Disease: Mechanisms, Implications, and Therapeutic Strategies DOI Creative Commons

Ning Wang,

Xiao Xiao,

Zi-jiang Chen

и другие.

Fundamental Research, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

Altered glucose metabolism in Alzheimer's disease: Role of mitochondrial dysfunction and oxidative stress DOI
Saikat Dewanjee, Pratik Chakraborty, Hiranmoy Bhattacharya

и другие.

Free Radical Biology and Medicine, Год журнала: 2022, Номер 193, С. 134 - 157

Опубликована: Окт. 4, 2022

Язык: Английский

Процитировано

136

Puerarin: a potential natural neuroprotective agent for neurological disorders DOI Creative Commons

Xue Liu,

Rui Huang, Jiye Wan

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2023, Номер 162, С. 114581 - 114581

Опубликована: Март 24, 2023

Puerarin is an isoflavone compound derived from Pueraria lobata in traditional Chinese medicine. Accumulating evidence has indicated that puerarin demonstrates multiple pharmacological effects and exhibits treatment potential for various neurological disorders. Based on the latest research progress as a neuroprotective agent, its activity, molecular mechanism, therapeutic application were systematically reviewed with emphasis pre-clinical studies. The related information was extracted compiled major scientific databases, including PubMed, ScienceDirect, SpringerLink, National Knowledge Infrastructure, using 'Puerarin', 'Neuroprotection', 'Apoptosis', 'Autophagy', 'Antioxidant', 'Mitochondria', 'Anti-inflammation' keywords. This review complied Preferred Reporting Items Systematic Reviews criteria. Forty-three articles met established inclusion exclusion shown against variety of disorders, ischemic cerebrovascular disease, subarachnoid hemorrhage, epilepsy, cognitive traumatic brain injury, Parkinson's Alzheimer's anxiety, depression, diabetic neuropathy, neuroblastoma/glioblastoma. anti-apoptosis, proinflammatory mediator inhibitory, autophagy regulatory, anti-oxidative stress, mitochondria protection, Ca2+ influx anti-neurodegenerative activities. exerts noticeable models disorders vivo (animal). will contribute to development novel clinical drug candidate However, well-designed, high-quality, large-scale, multicenter randomized studies are needed determine safety utility patients

Язык: Английский

Процитировано

57

Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis DOI Open Access
Eneritz López-Muguruza, Carlos Matute

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(16), С. 12912 - 12912

Опубликована: Авг. 18, 2023

Multiple sclerosis (MS) is a complex autoimmune disease of the central nervous system (CNS), characterized by demyelination and neurodegeneration. Oligodendrocytes play vital role in maintaining integrity myelin, protective sheath around nerve fibres essential for efficient signal transmission. However, MS, oligodendrocytes become dysfunctional, leading to myelin damage axonal degeneration. Emerging evidence suggests that metabolic changes, including mitochondrial dysfunction alterations glucose lipid metabolism, contribute significantly pathogenesis MS. Mitochondrial observed both immune cells within CNS MS patients. Impaired function leads energy deficits, affecting crucial processes such as impulse transmission transport, ultimately contributing Moreover, linked generation reactive oxygen species (ROS), exacerbating inflammation. Altered metabolism affects supply required oligodendrocyte synthesis. Dysregulated results changes composition its stability integrity. Importantly, low levels polyunsaturated fatty acids are associated with upregulated enhanced catabolism. Understanding intricate relationship between these mechanisms developing targeted therapies preserve promote neurological recovery individuals Addressing aspects may offer new insights into potential therapeutic strategies halt progression improve quality life

Язык: Английский

Процитировано

46

Beyond the neuron: Role of non-neuronal cells in stress disorders DOI Creative Commons
Flurin Cathomas, Leanne M. Holt, Eric M. Parise

и другие.

Neuron, Год журнала: 2022, Номер 110(7), С. 1116 - 1138

Опубликована: Фев. 18, 2022

Язык: Английский

Процитировано

51

Chronic stress disrupts the homeostasis and progeny progression of oligodendroglial lineage cells, associating immune oligodendrocytes with prefrontal cortex hypomyelination DOI
Alexandros G. Kokkosis, Miguel M. Madeira,

Matthew Mullahy

и другие.

Molecular Psychiatry, Год журнала: 2022, Номер 27(6), С. 2833 - 2848

Опубликована: Март 17, 2022

Язык: Английский

Процитировано

44

Interlink between the gut microbiota and inflammation in the context of oxidative stress in Alzheimer’s disease progression DOI Creative Commons
Tushar Kanti Das, Bhanu Priya Ganesh

Gut Microbes, Год журнала: 2023, Номер 15(1)

Опубликована: Май 1, 2023

The microbiota-gut-brain axis is an important pathway of communication and may dynamically contribute to Alzheimer's disease (AD) pathogenesis. Pathological commensal gut microbiota alterations, termed as dysbiosis, can influence intestinal permeability break the blood-brain barrier which trigger AD pathogenesis via redox signaling, neuronal, immune, metabolic pathways. Dysbiosis increases oxidative stress. Oxidants affect innate immune system through recognizing microbial-derived pathogens by Toll-like receptors initiating inflammatory process. Most microbiome research work highlights relationship between AD, but contributory connection precise bacteria brain dysfunction in pathology cannot be fully demonstrated. Here, we summarize current information fundamental connections stress, inflammation, dysbiosis AD. This review emphasizes on involvement regulation responses including central peripheral cross-talk. It provides insights for novel preventative therapeutic approaches

Язык: Английский

Процитировано

42

An overall view of the most common experimental models for multiple sclerosis DOI Creative Commons
Simona Dedoni, María Scherma, Chiara Camoglio

и другие.

Neurobiology of Disease, Год журнала: 2023, Номер 184, С. 106230 - 106230

Опубликована: Июль 13, 2023

Multiple sclerosis (MS) is a complex chronic disease with an unknown etiology. It considered inflammatory demyelinating and neurodegenerative disorder of the central nervous system (CNS) characterized, in most cases, by unpredictable onset relapse remission phases. The generally starts subjects under 40; it has higher incidence women described as multifactorial due to interaction between genetic environmental risk factors. Unfortunately, there currently no definitive cure for MS. Still, therapies can modify disease's natural history, reducing rate slowing progression or managing symptoms. limited access human CNS tissue slows down. limits research on This limit been partially overcome over years developing various experimental models study this disease. Animal autoimmune demyelination, such encephalomyelitis (EAE) viral toxin transgenic MS models, represent significant part approaches. These have now complemented ex vivo studies, using organotypic brain slice cultures vitro, through induced Pluripotent Stem cells (iPSCs). We will discuss which clinical features disorders might be reproduced investigated vivo, vitro commonly used understand processes behind neuropathological events occurring patients. primary purpose review give reader global view main paradigms research, spacing from classical animal mice 2D 3D cultures.

Язык: Английский

Процитировано

36

Neurodegeneration cell per cell DOI Creative Commons
Sriram Balusu, Roman Praschberger, Elsa Lauwers

и другие.

Neuron, Год журнала: 2023, Номер 111(6), С. 767 - 786

Опубликована: Фев. 13, 2023

Язык: Английский

Процитировано

32

Oligodendrocyte progenitor cells in Alzheimer’s disease: from physiology to pathology DOI Creative Commons

Peibin Zou,

Chongyun Wu,

Timon Cheng‐Yi Liu

и другие.

Translational Neurodegeneration, Год журнала: 2023, Номер 12(1)

Опубликована: Ноя. 14, 2023

Abstract Oligodendrocyte progenitor cells (OPCs) play pivotal roles in myelin formation and phagocytosis, communicating with neighboring contributing to the integrity of blood–brain barrier (BBB). However, under pathological circumstances Alzheimer’s disease (AD), brain’s microenvironment undergoes detrimental changes that significantly impact OPCs their functions. Starting OPC functions, we delve into transformation myelin-producing oligodendrocytes, intricate signaling interactions other central nervous system (CNS), fascinating process which influences function affects CNS homeostasis. Moreover, discuss essential role BBB highlight critical contribution forming CNS-protective barriers. In context AD, deterioration local brain is discussed, mainly focusing on neuroinflammation, oxidative stress, accumulation toxic proteins. The disturb delicate balance brain, impacting regenerative capacity compromising integrity. Under conditions, experience significant alterations migration proliferation, leading impaired differentiation a reduced ability produce mature oligodendrocytes. degeneration become increasingly active progressive neurodegeneration. Finally, summarize current therapeutic approaches targeting AD. Strategies revitalize senescence, modulate pathways enhance differentiation, explore potential avenues are promising alleviating AD function. conclusion, this review highlights indispensable involvement pathogenesis interplay between underscores complexity neurodegenerative diseases. Insights from studying conditions provide foundation for innovative strategies fostering Future research will advance our understanding management diseases, ultimately offering hope effective treatments improved quality life those affected by related disorders.

Язык: Английский

Процитировано

29

Inflammation as common link to progressive neurological diseases DOI Creative Commons
Ana Dias-Carvalho, Susana I. Sá, Félix Carvalho

и другие.

Archives of Toxicology, Год журнала: 2023, Номер 98(1), С. 95 - 119

Опубликована: Ноя. 15, 2023

Abstract Life expectancy has increased immensely over the past decades, bringing new challenges to health systems as advanced age increases predisposition for many diseases. One of those is burden neurologic disorders. While hypotheses have been placed explain aging mechanisms, it widely accepted that increasing pro-inflammatory status with or “inflammaging” a main determinant biological aging. Furthermore, inflammaging at cornerstone age-related diseases and its involvement in disorders an exciting hypothesis. Indeed, development elderly seem share some basic pathways fundamentally converge on inflammation. Peripheral inflammation significantly influences brain function contributes neurological disorders, including Alzheimer’s disease, Parkinson’s multiple sclerosis. Understanding role pathogenesis progressive crucial importance developing effective treatments interventions can slow down prevent disease progression, therefore, decreasing social economic burden.

Язык: Английский

Процитировано

28