Beneficial effects of physical exercise on cognitive-behavioral impairments and brain-derived neurotrophic factor alteration in the limbic system induced by neurodegeneration

Experimental Gerontology, Год журнала: 2024, Номер 195, С. 112539 - 112539

Опубликована: Авг. 8, 2024

Neurodegenerative diseases (NDDs) are a class of neurological disorders marked by the progressive loss neurons that afflict millions people worldwide. These illnesses affect brain connection, impairing memory, cognition, behavior, sensory perception, and motor function. Alzheimer's, Parkinson's, Huntington's examples common NDDs, which frequently include buildup misfolded proteins. Cognitive-behavioral impairments early markers neurodevelopmental disorders, emphasizing importance detection intervention. Neurotrophins such as brain-derived neurotrophic factor (BDNF) critical for neuron survival synaptic plasticity, is required learning memory. NDDs have been associated with decreased BDNF levels. Physical exercise, non-pharmacological intervention, benefits health increasing levels, lowering cognitive deficits, slowing degradation. Exercise advantages increased well-being, reduced depression, improved skills, neuroprotection amyloid accumulation, oxidative stress, neuroinflammation. This study examines effects physical exercise on cognitive-behavioral deficits levels in limbic system impacted neurodegeneration. The findings highlight necessity including into NDD treatment to improve structure, function, total As research advances, becoming increasingly acknowledged an important technique treating decline neurodegenerative disorders.

Язык: Английский

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Crosstalk Between Dysfunctional Mitochondria and Inflammation in Glaucomatous Neurodegeneration

Frontiers in Pharmacology, Год журнала: 2021, Номер 12

Опубликована: Июль 21, 2021

Mitochondrial dysfunction and excessive inflammatory responses are both sufficient to induce pathology in age-dependent neurodegenerations. However, emerging evidence indicates crosstalk between damaged mitochondrial signaling can exacerbate issues chronic This review discusses for the interaction damage inflammation, with a focus on glaucomatous neurodegeneration, proposes that positive feedback resulting from this drives pathology. exacerbates multiple ways. Damaged DNA is damage-associated molecular pattern, which activates NLRP3 inflammasome; priming activation of inflammasome, liberation IL-1β IL-18 via gasdermin D pore, major pathway enhance responses. The rise reactive oxygen species induced by also pathways, while blockage Complex enzymes increase signaling. Impaired mitophagy contributes inflammation as inability turnover mitochondria timely manner increases levels ROS mtDNA, latter likely stimulate cGAS-STING interferon associated ER membrane contacts mitochondria-associated adaptor molecule MAVS activate inflammasome In addition dysfunctional increasing corollary occurs, reducing function ATP production; downward spiral accelerates degeneration. Evidence several preclinical models including DBA/2J mouse, microbead injection transient elevation IOP, patient data, implicates neurodegeneration. pressure-dependent hypoxia metabolic vulnerability release. Links occur retinal ganglion cells, microglia cells astrocytes. summary, increased enhances implications other complex neurodegenerations like Alzheimer’s Parkinson’s disease.

Язык: Английский

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The natural (poly)phenols as modulators of microglia polarization via TLR4/NF-κB pathway exert anti-inflammatory activity in ischemic stroke

European Journal of Pharmacology, Год журнала: 2021, Номер 914, С. 174660 - 174660

Опубликована: Дек. 1, 2021

Язык: Английский

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Neuroinflammation: A Signature or a Cause of Epilepsy?

International Journal of Molecular Sciences, Год журнала: 2021, Номер 22(13), С. 6981 - 6981

Опубликована: Июнь 29, 2021

Epilepsy can be both a primary pathology and secondary effect of many neurological conditions. Many papers show that neuroinflammation is product epilepsy, in pathological conditions characterized by neuroinflammation, there higher probability to develop epilepsy. However, the bidirectional mechanism reciprocal interaction between epilepsy remains fully understood. Here, we attempt explore discuss relationship inflammation some paradigmatic systemic disorders associated with In particular, have chosen one representative form for each its actual known etiologies. A better understanding mechanistic link would important improve subject-based therapies, prophylaxis treatment

Язык: Английский

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Neuroinflammation in Ischemic Stroke: Focus on MicroRNA-mediated Polarization of Microglia

Frontiers in Molecular Neuroscience, Год журнала: 2021, Номер 13

Опубликована: Янв. 7, 2021

Ischemic stroke is one of the most common causes death and disability worldwide. Neuroinflammation a major pathological event involved in process ischemic injury repair. In particular, microglia play dual role neuroinflammation. During acute phase onset, M2 are dominant phenotype exert protective effects on neuronal cells, whereas permanent M1 contribute to prolonged inflammation detrimental brain tissue. Emerging evidence indicates that microRNAs (miRNAs) may have regulatory microglia-associated inflammation. Thus, we briefly reviewed dynamic response after assessed how specific miRNAs affect behavior reactive microglia. We concluded be useful novel therapeutic targets improve outcomes modulate

Язык: Английский

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The Influence of Gut Microbiota on Neurogenesis: Evidence and Hopes

Cells, Год журнала: 2022, Номер 11(3), С. 382 - 382

Опубликована: Янв. 23, 2022

Adult neurogenesis (i.e., the life-long generation of new neurons from undifferentiated neuronal precursors in adult brain) may contribute to brain repair after damage, and participates plasticity-related processes including memory, cognition, mood sensory functions. Among many intrinsic (oxidative stress, inflammation, ageing), extrinsic (environmental pollution, lifestyle, diet) factors deemed impact neurogenesis, significant attention has been recently attracted by myriad saprophytic microorganismal communities inhabiting intestinal ecosystem collectively referred as gut microbiota. A growing body evidence, mainly animal studies, reveal influence microbiota its disease-associated imbalances on neural stem cell proliferative differentiative activities neurogenic niches. On other hand, long-claimed pro-neurogenic activity natural dietary compounds endowed with antioxidants anti-inflammatory properties (such polyphenols, polyunsaturated fatty acids, or pro/prebiotics) be mediated, at least part, their action microflora. The purpose this review is summarise available information regarding analyse possible underlying mechanisms, discuss potential implications emerging knowledge for fight against neurodegeneration ageing.

Язык: Английский

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Anti-Inflammatory Effects of GLP-1 Receptor Activation in the Brain in Neurodegenerative Diseases

International Journal of Molecular Sciences, Год журнала: 2022, Номер 23(17), С. 9583 - 9583

Опубликована: Авг. 24, 2022

The glucagon-like peptide-1 (GLP-1) is a pleiotropic hormone well known for its incretin effect in the glucose-dependent stimulation of insulin secretion. However, GLP-1 also produced brain and displays critical role neuroprotection inflammation by activating receptor signaling pathways. Several studies vivo vitro using preclinical models neurodegenerative diseases show that GLP-1R activation has anti-inflammatory properties. This review explores molecular mechanistic action RAS relation to brain. These findings update our knowledge potential benefits GLP-1RAS actions reducing inflammatory response. molecules emerge as therapeutic tool treating neuroinflammatory pathologies.

Язык: Английский

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The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation

Molecular Neurobiology, Год журнала: 2022, Номер 60(3), С. 1369 - 1390

Опубликована: Ноя. 29, 2022

Abstract Sepsis is a leading cause of intensive care unit admission and death worldwide. Most surviving patients show acute or chronic mental disorders, which are known as sepsis-associated encephalopathy (SAE). Although accumulating studies in the past two decades focused on pathogenesis SAE, systematic review retrospective exclusively focuses inflammatory mechanisms SAE has been lacking yet. This summarizes recent advance field neuroinflammation sheds light activation microglia SAE. Activation predominates neuroinflammation. As gene expression profile changes, heterogeneous characterizations throughout all stages Here, we summarize systemic inflammation following sepsis also relationship microglial diversity Moreover, collection neuroinflammation-related dysfunction reviewed to illustrate possible for In addition, promising pharmacological non-pharmacological therapeutic strategies, especially those target microglia, concluded final part this review. Collectively, clarification vital between SAE-related disorders would significantly improve our understanding pathophysiological therefore provide potential targets therapies aimed at inhibiting

Язык: Английский

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Microglia-Astrocyte Communication in Alzheimer’s Disease

Journal of Alzheimer s Disease, Год журнала: 2023, Номер 95(3), С. 785 - 803

Опубликована: Авг. 25, 2023

Microglia and astrocytes are regarded as active participants in the central nervous system under various neuropathological conditions, including Alzheimer's disease (AD). Both microglia astrocyte activation have been reported to occur with a spatially temporarily distinct pattern. Acting double-edged sword, glia-mediated neuroinflammation may be both detrimental beneficial brain. In variety of neuropathologies, activated before astrocytes, which facilitates activation. Yet reactive can also prevent adjacent addition helping them become activated. Studies describe changes genetic profile well cellular molecular responses these two types glial cells that contribute dysfunctional immune crosstalk AD. this paper, we construct current knowledge microglia-astrocyte communication, highlighting multifaceted functions their role A thorough comprehension communication could hasten creation novel AD treatment approaches.

Язык: Английский

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Microglia-containing cerebral organoids derived from induced pluripotent stem cells for the study of neurological diseases

iScience, Год журнала: 2023, Номер 26(3), С. 106267 - 106267

Опубликована: Фев. 25, 2023

Microglia play an important role in neuroinflammation and neurodegeneration. Here, we report approach for generating microglia-containing cerebral organoids derived from human pluripotent stem cells involving the supplementation of growth factors (FGF, EGF, heparin) 10% CO2 culture conditions. Using this platform, Western Pacific Amyotrophic Lateral Sclerosis Parkinsonism-Dementia Complex (ALS-PDC) were generated patient-derived induced (iPSCs). These ALS-PDC-affected had more reactive astrocytes M1 microglia, fewer M2 microglia than their unaffected counterparts, leading to impaired microglia-mediated phagocytosis. RNA-seq analysis ALS-PDC control indicated that most significant changes microglia- astrocyte-related genes (IFITM1/2, TGF-β, GFAP). The significantly downregulated pathway was type I interferon signaling. Interferon-gamma increased IFITM expression, enhanced phagocytosis, reduced beta-amyloid accumulation network. results demonstrated feasibility using study neurodegenerative diseases.

Язык: Английский

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