scholarly journals Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Hyuk Sung Kwon ◽  
Seong-Ho Koh

AbstractNeuroinflammation is associated with neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Microglia and astrocytes are key regulators of inflammatory responses in the central nervous system. The activation of microglia and astrocytes is heterogeneous and traditionally categorized as neurotoxic (M1-phenotype microglia and A1-phenotype astrocytes) or neuroprotective (M2-phenotype microglia and A2-phenotype astrocytes). However, this dichotomized classification may not reflect the various phenotypes of microglia and astrocytes. The relationship between these activated glial cells is also very complicated, and the phenotypic distribution can change, based on the progression of neurodegenerative diseases. A better understanding of the roles of microglia and astrocytes in neurodegenerative diseases is essential for developing effective therapies. In this review, we discuss the roles of inflammatory response in neurodegenerative diseases, focusing on the contributions of microglia and astrocytes and their relationship. In addition, we discuss biomarkers to measure neuroinflammation and studies on therapeutic drugs that can modulate neuroinflammation.

2020 ◽  
Vol 26 (7) ◽  
pp. 730-742
Author(s):  
Surendra Gulla ◽  
Dakshayani Lomada ◽  
Anusha Lade ◽  
Reddanna Pallu ◽  
Madhava C. Reddy

: Multiple sclerosis (MS) is an autoimmune demyelinating disorder with chronic inflammation in the central nervous system, manifested by both physical and cognitive disability. Neuroinflammation and neurodegeneration are the phenomena that appear in the central nervous system associated with various neurodegenerative disorders, including MS, Alzheimer’s diseases, amyotrophic lateral sclerosis and Parkinson’s disease. Prostaglandins are one of the major mediators of inflammation that exhibit an important function in enhancing neuroinflammatory and neurodegenerative processes. These mediators would help understand the pathophysiology of MS as the combination of antagonists or agonists of prostaglandins receptors could be beneficial during the treatment of MS. The present review focuses on the role played by different prostaglandins and the enzymes which produced them in the etiopathogenesis of MS.


Loquens ◽  
2017 ◽  
Vol 4 (1) ◽  
pp. 035
Author(s):  
Pedro Gómez Vilda

Neurological deterioration presents different variants depending on their classification criterion, which may be their anatomic localization or their disease clinical features, although there is not a clear cut between both. Anatomically this ample group of disorders may affect the central nervous system (brain and spinal cord), or the peripheral nervous system. Clinically, the neurodegenerative disorders are classified as affecting cognitive functions or neuromotor capabilities. In the group of neurodegenerative diseases of the central nervous system, Alzheimer’s disease (AD) or Fronto-Temporal Dementia (FTD) are to be found, whereas in the second group certain pathologies as Parkinson’s Disease (PD), Amyotrophic Lateral Sclerosis (ALS), Huntington’s Disease (HD) or myasthenia gravis (MG) are among the most frequent ones, although “the number of neurodegenerative diseases is currently estimated to be a few hundred” (Przedborski et al., 2003). All these pathologies produce correlates in speech at different levels: in fluency, in prosody, in articulation or in phonation. Speech technologies offer computer solutions to evaluate objectively detected anomalies in each level, adding statistical robustness, which makes them suitable for their clinical and rehabilitative application. The present issue is devoted to briefly review the characteristics of the diseases mentioned before, defining the foundations of the correlate features present in each one. Some computer solutions available in detecting and monitoring illness progress are reviewed in the contributions of different research groups working in this field.


2019 ◽  
Vol 20 (12) ◽  
pp. 3109 ◽  
Author(s):  
Sarah Hirschberg ◽  
Barbara Gisevius ◽  
Alexander Duscha ◽  
Aiden Haghikia

Within the last century, human lifestyle and dietary behaviors have changed dramatically. These changes, especially concerning hygiene, have led to a marked decrease in some diseases, i.e., infectious diseases. However, other diseases that can be attributed to the so-called ‘Western’ lifestyle have increased, i.e., metabolic and cardiovascular disorders. More recently, multifactorial disorders, such as autoimmune and neurodegenerative diseases, have been associated with changes in diet and the gut microbiome. In particular, short chain fatty acid (SCFA)-producing bacteria are of high interest. SCFAs are the main metabolites produced by bacteria and are often reduced in a dysbiotic state, causing an inflammatory environment. Based on advanced technologies, high-resolution investigations of the abundance and composition of the commensal microbiome are now possible. These techniques enable the assessment of the relationship between the gut microbiome, its metabolome and gut-associated immune and neuronal cells. While a growing number of studies have shown the indirect impact of gut metabolites, mediated by alterations of immune-mediated mechanisms, the direct influence of these compounds on cells of the central nervous system needs to be further elucidated. For instance, the SCFA propionic acid (PA) increases the amount of intestine-derived regulatory T cells, which furthermore can positively affect the central nervous system (CNS), e.g., by increasing remyelination. However, the question of if and how PA can directly interact with CNS-resident cells is a matter of debate. In this review, we discuss the impact of an altered microbiome composition in relation to various diseases and discuss how the commensal microbiome is shaped, starting from the beginning of human life.


2021 ◽  
Vol 22 (9) ◽  
pp. 4630
Author(s):  
Agnieszka Kulczyńska-Przybik ◽  
Piotr Mroczko ◽  
Maciej Dulewicz ◽  
Barbara Mroczko

Reticulons (RTNs) are crucial regulatory factors in the central nervous system (CNS) as well as immune system and play pleiotropic functions. In CNS, RTNs are transmembrane proteins mediating neuroanatomical plasticity and functional recovery after central nervous system injury or diseases. Moreover, RTNs, particularly RTN4 and RTN3, are involved in neurodegeneration and neuroinflammation processes. The crucial role of RTNs in the development of several neurodegenerative diseases, including Alzheimer’s disease (AD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), or other neurological conditions such as brain injury or spinal cord injury, has attracted scientific interest. Reticulons, particularly RTN-4A (Nogo-A), could provide both an understanding of early pathogenesis of neurodegenerative disorders and be potential therapeutic targets which may offer effective treatment or inhibit disease progression. This review focuses on the molecular mechanisms and functions of RTNs and their potential usefulness in clinical practice as a diagnostic tool or therapeutic strategy.


Author(s):  
Giancarlo Logroscino ◽  
Adriano Chiò

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are both progressive neurodegenerative disorders considered part of the same spectrum of overlapping genetic neurological and clinical diseases. ALS involves primarily the motor system, but recent advances consider also the involvement of other parts of the central nervous system (CNS), primarily cognition. FTD presents clinical syndromes with behavioural and language variants, but some subtypes have motor involvement of the motor pathways and/or of some extrapyramidal areas. C9ORF72 is a gene responsible for 7–10% of cases both of sporadic and familial of ALS and FTD as well. Both ALS and FTD are rare diseases with incidence around 3/100,000 for ALS in Europe and FTD probably lower. The data for ALS have been mainly produced in Europe by a system of registries in limited territories. FTD data from populations are sparse. Trauma, smoking, military service, and agricultural occupation are environmental probable risk factors for ALS. No analytic data are available for FTD. FUS, TARDP, SOD 1, and C9ORF72 are the main genes involved in ALS, while C9ORF72, PGR, and TAU have been reported in FTD.


2020 ◽  
Author(s):  
Atefeh Ghahremanloo ◽  
Fariba Mohammadi ◽  
Seyed Isaac Hashemy

Abstract- Tachykinins (TKs) are a family of neuropeptides widely distributed in the human body, especially in the nervous system. TKs have exhibited both neuroprotective and neurodegenerative properties in the central nervous system (CNS) and spinal cord. Also, several studies have shown that substance P (SP), as a pioneering neuropeptide of the TK family, is engaged in the pathogenesis of neurodegenerative disorders (NDs), such as Alzheimer disease, Multiple Sclerosis, Parkinson’s disease, Huntington’s disease, and Amyotrophic lateral sclerosis. However, a huge body of information available about the level of SP in NDs demonstrates that SP and its receptors might be prognostic or diagnostic factors for NDs. The present review article summarizes the roles of TKs in common neurodegenerative disorders.


2012 ◽  
Vol 3 (4) ◽  
Author(s):  
Andrea Diana

AbstractA growing body of research deals with the relationship between the endosomal and autophagic/lysosomal pathways during developmental stages of the central nervous system. This includes their possible influence regarding the onset and progression of specific neurodegenerative disorders. In this review we focus our attention on major alterations affecting two organelles: autophagosomes and multivesicular bodies, both of which are located at the intersection point of their respective pathways.


Author(s):  
Konstantin Gulyabin

Mills' syndrome is a rare neurological disorder. Its nosological nature is currently not completely determined. Nevertheless, Mills' syndrome is considered to be a rare variant of the degenerative pathology of the central nervous system – a variant of focal cortical atrophy. The true prevalence of this pathology is unknown, since this condition is more often of a syndrome type, observed in the clinical picture of a number of neurological diseases (primary lateral sclerosis, frontotemporal dementia, etc.) and is less common in isolated form.


2020 ◽  
Vol 20 (13) ◽  
pp. 1142-1153 ◽  
Author(s):  
Sreyashi Chandra ◽  
Md. Tanjim Alam ◽  
Jhilik Dey ◽  
Baby C. Pulikkaparambil Sasidharan ◽  
Upasana Ray ◽  
...  

Background: The central nervous system (CNS) known to regulate the physiological conditions of human body, also itself gets dynamically regulated by both the physiological as well as pathological conditions of the body. These conditions get changed quite often, and often involve changes introduced into the gut microbiota which, as studies are revealing, directly modulate the CNS via a crosstalk. This cross-talk between the gut microbiota and CNS, i.e., the gut-brain axis (GBA), plays a major role in the pathogenesis of many neurodegenerative disorders such as Parkinson’s disease (PD), Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS) and Huntington’s disease (HD). Objective: We aim to discuss how gut microbiota, through GBA, regulate neurodegenerative disorders such as PD, AD, ALS, MS and HD. Methods: In this review, we have discussed the present understanding of the role played by the gut microbiota in neurodegenerative disorders and emphasized the probable therapeutic approaches being explored to treat them. Results: In the first part, we introduce the GBA and its relevance, followed by the changes occurring in the GBA during neurodegenerative disorders and then further discuss its role in the pathogenesis of these diseases. Finally, we discuss its applications in possible therapeutics of these diseases and the current research improvements being made to better investigate this interaction. Conclusion: We concluded that alterations in the intestinal microbiota modulate various activities that could potentially lead to CNS disorders through interactions via the GBA.


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